--- _id: '15146' abstract: - lang: eng text: The extracellular matrix (ECM) serves as a scaffold for cells and plays an essential role in regulating numerous cellular processes, including cell migration and proliferation. Due to limitations in specimen preparation for conventional room-temperature electron microscopy, we lack structural knowledge on how ECM components are secreted, remodeled, and interact with surrounding cells. We have developed a 3D-ECM platform compatible with sample thinning by cryo-focused ion beam milling, the lift-out extraction procedure, and cryo-electron tomography. Our workflow implements cell-derived matrices (CDMs) grown on EM grids, resulting in a versatile tool closely mimicking ECM environments. This allows us to visualize ECM for the first time in its hydrated, native context. Our data reveal an intricate network of extracellular fibers, their positioning relative to matrix-secreting cells, and previously unresolved structural entities. Our workflow and results add to the structural atlas of the ECM, providing novel insights into its secretion and assembly. acknowledged_ssus: - _id: LifeSc - _id: ScienComp - _id: EM-Fac - _id: M-Shop acknowledgement: "Open Access funding provided by IST Austria. We thank Armel Nicolas and his team at the ISTA proteomics facility, Alois Schloegl, Stefano Elefante, and colleagues at the ISTA Scientific Computing facility, Tommaso Constanzo and Ludek Lovicar at the Electron Microsocpy Facility (EMF), and Thomas Menner at the Miba Machine shop for their support. We also thank Wanda Kukulski (University of Bern) as well as Darío Porley, Andreas Thader, and other members of the Schur group for helpful discussions. Matt Swulius and Jessica Heebner provided great support in using Dragonfly. We thank Dorotea Fracciolla (Art & Science) for support in figure illustration.\r\n\r\nThis research was supported by the Scientific Service Units of ISTA through resources provided by Scientific Computing, the Lab Support Facility, and the Electron Microscopy Facility. We acknowledge funding support from the following sources: Austrian Science Fund (FWF) grant P33367 (to F.K.M. Schur), the Federation of European Biochemical Societies (to F.K.M. Schur), Niederösterreich (NÖ) Fonds (to B. Zens), FWF grant E435 (to J.M. Hansen), European Research Council under the European Union’s Horizon 2020 research (grant agreement No. 724373) (to M. Sixt), and Jenny and Antti Wihuri Foundation (to J. Alanko). This publication has been made possible in part by CZI grant DAF2021-234754 and grant DOI https://doi.org/10.37921/812628ebpcwg from the Chan Zuckerberg Initiative DAF, an advised fund of Silicon Valley Community Foundation (to F.K.M. Schur)." article_number: e202309125 article_processing_charge: Yes (via OA deal) article_type: original author: - first_name: Bettina full_name: Zens, Bettina id: 45FD126C-F248-11E8-B48F-1D18A9856A87 last_name: Zens - first_name: Florian full_name: Fäßler, Florian id: 404F5528-F248-11E8-B48F-1D18A9856A87 last_name: Fäßler orcid: 0000-0001-7149-769X - first_name: Jesse full_name: Hansen, Jesse id: 1063c618-6f9b-11ec-9123-f912fccded63 last_name: Hansen - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Julia full_name: Datler, Julia id: 3B12E2E6-F248-11E8-B48F-1D18A9856A87 last_name: Datler orcid: 0000-0002-3616-8580 - first_name: Victor-Valentin full_name: Hodirnau, Victor-Valentin id: 3661B498-F248-11E8-B48F-1D18A9856A87 last_name: Hodirnau - first_name: Vanessa full_name: Zheden, Vanessa id: 39C5A68A-F248-11E8-B48F-1D18A9856A87 last_name: Zheden orcid: 0000-0002-9438-4783 - first_name: Jonna H full_name: Alanko, Jonna H id: 2CC12E8C-F248-11E8-B48F-1D18A9856A87 last_name: Alanko orcid: 0000-0002-7698-3061 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Florian KM full_name: Schur, Florian KM id: 48AD8942-F248-11E8-B48F-1D18A9856A87 last_name: Schur orcid: 0000-0003-4790-8078 citation: ama: Zens B, Fäßler F, Hansen J, et al. Lift-out cryo-FIBSEM and cryo-ET reveal the ultrastructural landscape of extracellular matrix. Journal of Cell Biology. 2024;223(6). doi:10.1083/jcb.202309125 apa: Zens, B., Fäßler, F., Hansen, J., Hauschild, R., Datler, J., Hodirnau, V.-V., … Schur, F. K. (2024). Lift-out cryo-FIBSEM and cryo-ET reveal the ultrastructural landscape of extracellular matrix. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.202309125 chicago: Zens, Bettina, Florian Fäßler, Jesse Hansen, Robert Hauschild, Julia Datler, Victor-Valentin Hodirnau, Vanessa Zheden, Jonna H Alanko, Michael K Sixt, and Florian KM Schur. “Lift-out Cryo-FIBSEM and Cryo-ET Reveal the Ultrastructural Landscape of Extracellular Matrix.” Journal of Cell Biology. Rockefeller University Press, 2024. https://doi.org/10.1083/jcb.202309125. ieee: B. Zens et al., “Lift-out cryo-FIBSEM and cryo-ET reveal the ultrastructural landscape of extracellular matrix,” Journal of Cell Biology, vol. 223, no. 6. Rockefeller University Press, 2024. ista: Zens B, Fäßler F, Hansen J, Hauschild R, Datler J, Hodirnau V-V, Zheden V, Alanko JH, Sixt MK, Schur FK. 2024. Lift-out cryo-FIBSEM and cryo-ET reveal the ultrastructural landscape of extracellular matrix. Journal of Cell Biology. 223(6), e202309125. mla: Zens, Bettina, et al. “Lift-out Cryo-FIBSEM and Cryo-ET Reveal the Ultrastructural Landscape of Extracellular Matrix.” Journal of Cell Biology, vol. 223, no. 6, e202309125, Rockefeller University Press, 2024, doi:10.1083/jcb.202309125. short: B. Zens, F. Fäßler, J. Hansen, R. Hauschild, J. Datler, V.-V. Hodirnau, V. Zheden, J.H. Alanko, M.K. Sixt, F.K. Schur, Journal of Cell Biology 223 (2024). date_created: 2024-03-21T06:45:51Z date_published: 2024-03-20T00:00:00Z date_updated: 2024-03-25T13:03:57Z day: '20' ddc: - '570' department: - _id: FlSc - _id: MiSi - _id: Bio - _id: EM-Fac doi: 10.1083/jcb.202309125 ec_funded: 1 external_id: pmid: - '38506714' file: - access_level: open_access checksum: 90d1984a93660735e506c2a304bc3f73 content_type: application/pdf creator: dernst date_created: 2024-03-25T12:52:04Z date_updated: 2024-03-25T12:52:04Z file_id: '15188' file_name: 2024_JCB_Zens.pdf file_size: 11907016 relation: main_file success: 1 file_date_updated: 2024-03-25T12:52:04Z has_accepted_license: '1' intvolume: ' 223' issue: '6' language: - iso: eng license: https://creativecommons.org/licenses/by/4.0/ month: '03' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 9B954C5C-BA93-11EA-9121-9846C619BF3A grant_number: P33367 name: Structure and isoform diversity of the Arp2/3 complex - _id: 7bd318a1-9f16-11ee-852c-cc9217763180 grant_number: E435 name: In Situ Actin Structures via Hybrid Cryo-electron Microscopy - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 059B463C-7A3F-11EA-A408-12923DDC885E name: NÖ-Fonds Preis für die Jungforscherin des Jahres am IST Austria - _id: 2615199A-B435-11E9-9278-68D0E5697425 grant_number: '21317' name: Spatiotemporal regulation of chemokine-induced signalling in leukocyte chemotaxis - _id: 62909c6f-2b32-11ec-9570-e1476aab5308 grant_number: CZI01 name: CryoMinflux-guided in-situ visual proteomics and structure determination publication: Journal of Cell Biology publication_identifier: eissn: - 1540-8140 issn: - 0021-9525 publication_status: published publisher: Rockefeller University Press quality_controlled: '1' scopus_import: '1' status: public title: Lift-out cryo-FIBSEM and cryo-ET reveal the ultrastructural landscape of extracellular matrix tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 223 year: '2024' ... --- _id: '13052' abstract: - lang: eng text: Imaging of the immunological synapse (IS) between dendritic cells (DCs) and T cells in suspension is hampered by suboptimal alignment of cell-cell contacts along the vertical imaging plane. This requires optical sectioning that often results in unsatisfactory resolution in time and space. Here, we present a workflow where DCs and T cells are confined between a layer of glass and polydimethylsiloxane (PDMS) that orients the cells along one, horizontal imaging plane, allowing for fast en-face-imaging of the DC-T cell IS. acknowledged_ssus: - _id: Bio - _id: NanoFab - _id: M-Shop acknowledgement: 'A.L. was funded by an Erwin Schrödinger postdoctoral fellowship of the Austrian Science Fund (FWF, project number: J4542-B) and is an EMBO non-stipendiary postdoctoral fellow. This work was supported by a European Research Council grant ERC-CoG-72437 to M.S. We thank the Imaging & Optics facility, the Nanofabrication facility, and the Miba Machine Shop of ISTA for their excellent support.' alternative_title: - Methods in Molecular Biology article_processing_charge: No author: - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Leithner AF, Merrin J, Sixt MK. En-Face Imaging of T Cell-Dendritic Cell Immunological Synapses. In: Baldari C, Dustin M, eds. The Immune Synapse. Vol 2654. MIMB. New York, NY: Springer Nature; 2023:137-147. doi:10.1007/978-1-0716-3135-5_9' apa: 'Leithner, A. F., Merrin, J., & Sixt, M. K. (2023). En-Face Imaging of T Cell-Dendritic Cell Immunological Synapses. In C. Baldari & M. Dustin (Eds.), The Immune Synapse (Vol. 2654, pp. 137–147). New York, NY: Springer Nature. https://doi.org/10.1007/978-1-0716-3135-5_9' chicago: 'Leithner, Alexander F, Jack Merrin, and Michael K Sixt. “En-Face Imaging of T Cell-Dendritic Cell Immunological Synapses.” In The Immune Synapse, edited by Cosima Baldari and Michael Dustin, 2654:137–47. MIMB. New York, NY: Springer Nature, 2023. https://doi.org/10.1007/978-1-0716-3135-5_9.' ieee: 'A. F. Leithner, J. Merrin, and M. K. Sixt, “En-Face Imaging of T Cell-Dendritic Cell Immunological Synapses,” in The Immune Synapse, vol. 2654, C. Baldari and M. Dustin, Eds. New York, NY: Springer Nature, 2023, pp. 137–147.' ista: 'Leithner AF, Merrin J, Sixt MK. 2023.En-Face Imaging of T Cell-Dendritic Cell Immunological Synapses. In: The Immune Synapse. Methods in Molecular Biology, vol. 2654, 137–147.' mla: Leithner, Alexander F., et al. “En-Face Imaging of T Cell-Dendritic Cell Immunological Synapses.” The Immune Synapse, edited by Cosima Baldari and Michael Dustin, vol. 2654, Springer Nature, 2023, pp. 137–47, doi:10.1007/978-1-0716-3135-5_9. short: A.F. Leithner, J. Merrin, M.K. Sixt, in:, C. Baldari, M. Dustin (Eds.), The Immune Synapse, Springer Nature, New York, NY, 2023, pp. 137–147. date_created: 2023-05-22T08:41:48Z date_published: 2023-04-28T00:00:00Z date_updated: 2023-10-17T08:44:53Z day: '28' department: - _id: MiSi - _id: NanoFab doi: 10.1007/978-1-0716-3135-5_9 ec_funded: 1 editor: - first_name: Cosima full_name: Baldari, Cosima last_name: Baldari - first_name: Michael full_name: Dustin, Michael last_name: Dustin external_id: pmid: - '37106180' intvolume: ' 2654' language: - iso: eng month: '04' oa_version: None page: 137-147 place: New York, NY pmid: 1 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients publication: The Immune Synapse publication_identifier: eisbn: - '9781071631355' eissn: - 1940-6029 isbn: - '9781071631348' issn: - 1064-3745 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' series_title: MIMB status: public title: En-Face Imaging of T Cell-Dendritic Cell Immunological Synapses type: book_chapter user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 2654 year: '2023' ... --- _id: '14555' abstract: - lang: eng text: The intricate regulatory processes behind actin polymerization play a crucial role in cellular biology, including essential mechanisms such as cell migration or cell division. However, the self-organizing principles governing actin polymerization are still poorly understood. In this perspective article, we compare the Belousov-Zhabotinsky (BZ) reaction, a classic and well understood chemical oscillator known for its self-organizing spatiotemporal dynamics, with the excitable dynamics of polymerizing actin. While the BZ reaction originates from the domain of inorganic chemistry, it shares remarkable similarities with actin polymerization, including the characteristic propagating waves, which are influenced by geometry and external fields, and the emergent collective behavior. Starting with a general description of emerging patterns, we elaborate on single droplets or cell-level dynamics, the influence of geometric confinements and conclude with collective interactions. Comparing these two systems sheds light on the universal nature of self-organization principles in both living and inanimate systems. acknowledgement: The author(s) declare that no financial support was received for the research, authorship, and/or publication of this article. article_number: '1287420' article_processing_charge: Yes article_type: original author: - first_name: Michael full_name: Riedl, Michael id: 3BE60946-F248-11E8-B48F-1D18A9856A87 last_name: Riedl orcid: 0000-0003-4844-6311 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Riedl M, Sixt MK. The excitable nature of polymerizing actin and the Belousov-Zhabotinsky reaction. Frontiers in Cell and Developmental Biology. 2023;11. doi:10.3389/fcell.2023.1287420 apa: Riedl, M., & Sixt, M. K. (2023). The excitable nature of polymerizing actin and the Belousov-Zhabotinsky reaction. Frontiers in Cell and Developmental Biology. Frontiers. https://doi.org/10.3389/fcell.2023.1287420 chicago: Riedl, Michael, and Michael K Sixt. “The Excitable Nature of Polymerizing Actin and the Belousov-Zhabotinsky Reaction.” Frontiers in Cell and Developmental Biology. Frontiers, 2023. https://doi.org/10.3389/fcell.2023.1287420. ieee: M. Riedl and M. K. Sixt, “The excitable nature of polymerizing actin and the Belousov-Zhabotinsky reaction,” Frontiers in Cell and Developmental Biology, vol. 11. Frontiers, 2023. ista: Riedl M, Sixt MK. 2023. The excitable nature of polymerizing actin and the Belousov-Zhabotinsky reaction. Frontiers in Cell and Developmental Biology. 11, 1287420. mla: Riedl, Michael, and Michael K. Sixt. “The Excitable Nature of Polymerizing Actin and the Belousov-Zhabotinsky Reaction.” Frontiers in Cell and Developmental Biology, vol. 11, 1287420, Frontiers, 2023, doi:10.3389/fcell.2023.1287420. short: M. Riedl, M.K. Sixt, Frontiers in Cell and Developmental Biology 11 (2023). date_created: 2023-11-19T23:00:55Z date_published: 2023-10-31T00:00:00Z date_updated: 2023-11-20T08:44:17Z day: '31' ddc: - '570' department: - _id: MiSi doi: 10.3389/fcell.2023.1287420 file: - access_level: open_access checksum: 61857fc3ebf019354932e7ee684658ce content_type: application/pdf creator: dernst date_created: 2023-11-20T08:41:15Z date_updated: 2023-11-20T08:41:15Z file_id: '14561' file_name: 2023_FrontiersCellDevBio_Riedl.pdf file_size: 2047622 relation: main_file success: 1 file_date_updated: 2023-11-20T08:41:15Z has_accepted_license: '1' intvolume: ' 11' language: - iso: eng month: '10' oa: 1 oa_version: Published Version publication: Frontiers in Cell and Developmental Biology publication_identifier: eissn: - 2296-634X publication_status: published publisher: Frontiers quality_controlled: '1' scopus_import: '1' status: public title: The excitable nature of polymerizing actin and the Belousov-Zhabotinsky reaction tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 11 year: '2023' ... --- _id: '14361' abstract: - lang: eng text: Whether one considers swarming insects, flocking birds, or bacterial colonies, collective motion arises from the coordination of individuals and entails the adjustment of their respective velocities. In particular, in close confinements, such as those encountered by dense cell populations during development or regeneration, collective migration can only arise coordinately. Yet, how individuals unify their velocities is often not understood. Focusing on a finite number of cells in circular confinements, we identify waves of polymerizing actin that function as a pacemaker governing the speed of individual cells. We show that the onset of collective motion coincides with the synchronization of the wave nucleation frequencies across the population. Employing a simpler and more readily accessible mechanical model system of active spheres, we identify the synchronization of the individuals’ internal oscillators as one of the essential requirements to reach the corresponding collective state. The mechanical ‘toy’ experiment illustrates that the global synchronous state is achieved by nearest neighbor coupling. We suggest by analogy that local coupling and the synchronization of actin waves are essential for the emergent, self-organized motion of cell collectives. acknowledged_ssus: - _id: Bio - _id: LifeSc - _id: M-Shop acknowledgement: We thank K. O’Keeffe, E. Hannezo, P. Devreotes, C. Dessalles, and E. Martens for discussion and/or critical reading of the manuscript; the Bioimaging Facility of ISTA for excellent support, as well as the Life Science Facility and the Miba Machine Shop of ISTA. This work was supported by the European Research Council (ERC StG 281556 and CoG 724373) to M.S. article_number: '5633' article_processing_charge: Yes article_type: original author: - first_name: Michael full_name: Riedl, Michael id: 3BE60946-F248-11E8-B48F-1D18A9856A87 last_name: Riedl orcid: 0000-0003-4844-6311 - first_name: Isabelle D full_name: Mayer, Isabelle D id: 61763940-15b2-11ec-abd3-cfaddfbc66b4 last_name: Mayer - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Björn full_name: Hof, Björn id: 3A374330-F248-11E8-B48F-1D18A9856A87 last_name: Hof orcid: 0000-0003-2057-2754 citation: ama: Riedl M, Mayer ID, Merrin J, Sixt MK, Hof B. Synchronization in collectively moving inanimate and living active matter. Nature Communications. 2023;14. doi:10.1038/s41467-023-41432-1 apa: Riedl, M., Mayer, I. D., Merrin, J., Sixt, M. K., & Hof, B. (2023). Synchronization in collectively moving inanimate and living active matter. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-023-41432-1 chicago: Riedl, Michael, Isabelle D Mayer, Jack Merrin, Michael K Sixt, and Björn Hof. “Synchronization in Collectively Moving Inanimate and Living Active Matter.” Nature Communications. Springer Nature, 2023. https://doi.org/10.1038/s41467-023-41432-1. ieee: M. Riedl, I. D. Mayer, J. Merrin, M. K. Sixt, and B. Hof, “Synchronization in collectively moving inanimate and living active matter,” Nature Communications, vol. 14. Springer Nature, 2023. ista: Riedl M, Mayer ID, Merrin J, Sixt MK, Hof B. 2023. Synchronization in collectively moving inanimate and living active matter. Nature Communications. 14, 5633. mla: Riedl, Michael, et al. “Synchronization in Collectively Moving Inanimate and Living Active Matter.” Nature Communications, vol. 14, 5633, Springer Nature, 2023, doi:10.1038/s41467-023-41432-1. short: M. Riedl, I.D. Mayer, J. Merrin, M.K. Sixt, B. Hof, Nature Communications 14 (2023). date_created: 2023-09-24T22:01:10Z date_published: 2023-09-13T00:00:00Z date_updated: 2023-12-13T12:29:41Z day: '13' ddc: - '530' - '570' department: - _id: MiSi - _id: NanoFab - _id: BjHo doi: 10.1038/s41467-023-41432-1 ec_funded: 1 external_id: isi: - '001087583700030' pmid: - '37704595' file: - access_level: open_access checksum: 82d2d4ad736cc8493db8ce45cd313f7b content_type: application/pdf creator: dernst date_created: 2023-09-25T08:32:37Z date_updated: 2023-09-25T08:32:37Z file_id: '14366' file_name: 2023_NatureComm_Riedl.pdf file_size: 2317272 relation: main_file success: 1 file_date_updated: 2023-09-25T08:32:37Z has_accepted_license: '1' intvolume: ' 14' isi: 1 language: - iso: eng month: '09' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients publication: Nature Communications publication_identifier: eissn: - 2041-1723 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Synchronization in collectively moving inanimate and living active matter tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 14 year: '2023' ... --- _id: '14360' abstract: - lang: eng text: To navigate through diverse tissues, migrating cells must balance persistent self-propelled motion with adaptive behaviors to circumvent obstacles. We identify a curvature-sensing mechanism underlying obstacle evasion in immune-like cells. Specifically, we propose that actin polymerization at the advancing edge of migrating cells is inhibited by the curvature-sensitive BAR domain protein Snx33 in regions with inward plasma membrane curvature. The genetic perturbation of this machinery reduces the cells’ capacity to evade obstructions combined with faster and more persistent cell migration in obstacle-free environments. Our results show how cells can read out their surface topography and utilize actin and plasma membrane biophysics to interpret their environment, allowing them to adaptively decide if they should move ahead or turn away. On the basis of our findings, we propose that the natural diversity of BAR domain proteins may allow cells to tune their curvature sensing machinery to match the shape characteristics in their environment. acknowledgement: "We thank Jan Ellenberg, Leanne Strauss, Anusha Gopalan, and Jia Hui Li for critical feedback on the manuscript and the Life Science Editors for editing assistance. The plasmid with hSnx33 was a kind gift from Duanqing Pei. Cell line with GFP-tagged IRSp53 was a kind gift from Orion Weiner. We thank Brian Graziano for providing protocols, reagents, and key advice to generate CRISPR knockout HL-60 cells. We thank the EMBL flow cytometry core facility, the EMBL advanced light microscopy facility, the EMBL proteomics facility, and the EMBL genomics core facility for support and advice. We thank Anusha Gopalan and Martin Bergert for their support during mechanical measurements by AFM. We thank Estela Sosa Osorio for technical assistance for the co-immunoprecipitation. We thank the EMBL genome biology computational support (and specially Charles Girardot and Jelle Scholtalbers) for critical assistance during RNAseq analysis. We thank Hans Kristian Hannibal‐Bach for his technical assistance during the lipidomic analysis of plasma membrane isolates. We thank Steffen Burgold for their support with LLS7 microscope in the ZEISS Microscopy Customer Center Europe. We acknowledge the financial support of the European Molecular Biology Laboratory (EMBL) to A.D.-M., Y.S., A.K., and A.E., the EMBL Interdisciplinary Postdocs (EIPOD) program under Marie Sklodowska-Curie COFUND actions MSCA-COFUND-FP to M.S.B. and M. S. (grant agreement number: 847543), the BEST program funding by FCT (SFRH/BEST/150300/2019) to S.D.A. and the Joachim Herz Stiftung Add-on Fellowship for Interdisciplinary Science to E.S.\r\nOpen Access funding enabled and organized by Projekt DEAL." article_number: '5644' article_processing_charge: Yes (via OA deal) article_type: original author: - first_name: Ewa full_name: Sitarska, Ewa last_name: Sitarska - first_name: Silvia Dias full_name: Almeida, Silvia Dias last_name: Almeida - first_name: Marianne Sandvold full_name: Beckwith, Marianne Sandvold last_name: Beckwith - first_name: Julian A full_name: Stopp, Julian A id: 489E3F00-F248-11E8-B48F-1D18A9856A87 last_name: Stopp - first_name: Jakub full_name: Czuchnowski, Jakub last_name: Czuchnowski - first_name: Marc full_name: Siggel, Marc last_name: Siggel - first_name: Rita full_name: Roessner, Rita last_name: Roessner - first_name: Aline full_name: Tschanz, Aline last_name: Tschanz - first_name: Christer full_name: Ejsing, Christer last_name: Ejsing - first_name: Yannick full_name: Schwab, Yannick last_name: Schwab - first_name: Jan full_name: Kosinski, Jan last_name: Kosinski - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Anna full_name: Kreshuk, Anna last_name: Kreshuk - first_name: Anna full_name: Erzberger, Anna last_name: Erzberger - first_name: Alba full_name: Diz-Muñoz, Alba last_name: Diz-Muñoz citation: ama: Sitarska E, Almeida SD, Beckwith MS, et al. Sensing their plasma membrane curvature allows migrating cells to circumvent obstacles. Nature Communications. 2023;14. doi:10.1038/s41467-023-41173-1 apa: Sitarska, E., Almeida, S. D., Beckwith, M. S., Stopp, J. A., Czuchnowski, J., Siggel, M., … Diz-Muñoz, A. (2023). Sensing their plasma membrane curvature allows migrating cells to circumvent obstacles. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-023-41173-1 chicago: Sitarska, Ewa, Silvia Dias Almeida, Marianne Sandvold Beckwith, Julian A Stopp, Jakub Czuchnowski, Marc Siggel, Rita Roessner, et al. “Sensing Their Plasma Membrane Curvature Allows Migrating Cells to Circumvent Obstacles.” Nature Communications. Springer Nature, 2023. https://doi.org/10.1038/s41467-023-41173-1. ieee: E. Sitarska et al., “Sensing their plasma membrane curvature allows migrating cells to circumvent obstacles,” Nature Communications, vol. 14. Springer Nature, 2023. ista: Sitarska E, Almeida SD, Beckwith MS, Stopp JA, Czuchnowski J, Siggel M, Roessner R, Tschanz A, Ejsing C, Schwab Y, Kosinski J, Sixt MK, Kreshuk A, Erzberger A, Diz-Muñoz A. 2023. Sensing their plasma membrane curvature allows migrating cells to circumvent obstacles. Nature Communications. 14, 5644. mla: Sitarska, Ewa, et al. “Sensing Their Plasma Membrane Curvature Allows Migrating Cells to Circumvent Obstacles.” Nature Communications, vol. 14, 5644, Springer Nature, 2023, doi:10.1038/s41467-023-41173-1. short: E. Sitarska, S.D. Almeida, M.S. Beckwith, J.A. Stopp, J. Czuchnowski, M. Siggel, R. Roessner, A. Tschanz, C. Ejsing, Y. Schwab, J. Kosinski, M.K. Sixt, A. Kreshuk, A. Erzberger, A. Diz-Muñoz, Nature Communications 14 (2023). date_created: 2023-09-24T22:01:10Z date_published: 2023-09-13T00:00:00Z date_updated: 2023-12-21T14:30:01Z day: '13' ddc: - '570' department: - _id: MiSi doi: 10.1038/s41467-023-41173-1 external_id: isi: - '001087583700008' pmid: - '37704612' file: - access_level: open_access checksum: ad670e3b3c64fc585675948370f6b149 content_type: application/pdf creator: dernst date_created: 2023-09-25T08:22:58Z date_updated: 2023-09-25T08:22:58Z file_id: '14365' file_name: 2023_NatureComm_Sitarska.pdf file_size: 2725421 relation: main_file success: 1 file_date_updated: 2023-09-25T08:22:58Z has_accepted_license: '1' intvolume: ' 14' isi: 1 language: - iso: eng month: '09' oa: 1 oa_version: Published Version pmid: 1 publication: Nature Communications publication_identifier: eissn: - 2041-1723 publication_status: published publisher: Springer Nature quality_controlled: '1' related_material: record: - id: '14697' relation: dissertation_contains status: public scopus_import: '1' status: public title: Sensing their plasma membrane curvature allows migrating cells to circumvent obstacles tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 14 year: '2023' ... --- _id: '14274' abstract: - lang: eng text: Immune responses rely on the rapid and coordinated migration of leukocytes. Whereas it is well established that single-cell migration is often guided by gradients of chemokines and other chemoattractants, it remains poorly understood how these gradients are generated, maintained, and modulated. By combining experimental data with theory on leukocyte chemotaxis guided by the G protein–coupled receptor (GPCR) CCR7, we demonstrate that in addition to its role as the sensory receptor that steers migration, CCR7 also acts as a generator and a modulator of chemotactic gradients. Upon exposure to the CCR7 ligand CCL19, dendritic cells (DCs) effectively internalize the receptor and ligand as part of the canonical GPCR desensitization response. We show that CCR7 internalization also acts as an effective sink for the chemoattractant, dynamically shaping the spatiotemporal distribution of the chemokine. This mechanism drives complex collective migration patterns, enabling DCs to create or sharpen chemotactic gradients. We further show that these self-generated gradients can sustain the long-range guidance of DCs, adapt collective migration patterns to the size and geometry of the environment, and provide a guidance cue for other comigrating cells. Such a dual role of CCR7 as a GPCR that both senses and consumes its ligand can thus provide a novel mode of cellular self-organization. acknowledgement: "We thank I. de Vries and the Scientific Service Units (Life Sciences, Bioimaging, Nanofabrication, Preclinical and Miba Machine Shop) of the Institute of Science and Technology Austria for excellent support, as well as all the rotation students assisting in the laboratory work (B. Zens, H. Schön, and D. Babic).\r\nThis work was supported by grants from the European Research Council under the European Union’s Horizon 2020 research to M.S. (grant agreement no. 724373) and to E.H. (grant agreement no. 851288), and a grant by the Austrian Science Fund (DK Nanocell W1250-B20) to M.S. J.A. was supported by the Jenny and Antti Wihuri Foundation and Research Council of Finland's Flagship Programme InFLAMES (decision number: 357910). M.C.U. was supported by the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 754411." article_number: adc9584 article_processing_charge: No article_type: original author: - first_name: Jonna H full_name: Alanko, Jonna H id: 2CC12E8C-F248-11E8-B48F-1D18A9856A87 last_name: Alanko orcid: 0000-0002-7698-3061 - first_name: Mehmet C full_name: Ucar, Mehmet C id: 50B2A802-6007-11E9-A42B-EB23E6697425 last_name: Ucar orcid: 0000-0003-0506-4217 - first_name: Nikola full_name: Canigova, Nikola id: 3795523E-F248-11E8-B48F-1D18A9856A87 last_name: Canigova orcid: 0000-0002-8518-5926 - first_name: Julian A full_name: Stopp, Julian A id: 489E3F00-F248-11E8-B48F-1D18A9856A87 last_name: Stopp - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Edouard B full_name: Hannezo, Edouard B id: 3A9DB764-F248-11E8-B48F-1D18A9856A87 last_name: Hannezo orcid: 0000-0001-6005-1561 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Alanko JH, Ucar MC, Canigova N, et al. CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective leukocyte migration. Science Immunology. 2023;8(87). doi:10.1126/sciimmunol.adc9584 apa: Alanko, J. H., Ucar, M. C., Canigova, N., Stopp, J. A., Schwarz, J., Merrin, J., … Sixt, M. K. (2023). CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective leukocyte migration. Science Immunology. American Association for the Advancement of Science. https://doi.org/10.1126/sciimmunol.adc9584 chicago: Alanko, Jonna H, Mehmet C Ucar, Nikola Canigova, Julian A Stopp, Jan Schwarz, Jack Merrin, Edouard B Hannezo, and Michael K Sixt. “CCR7 Acts as Both a Sensor and a Sink for CCL19 to Coordinate Collective Leukocyte Migration.” Science Immunology. American Association for the Advancement of Science, 2023. https://doi.org/10.1126/sciimmunol.adc9584. ieee: J. H. Alanko et al., “CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective leukocyte migration,” Science Immunology, vol. 8, no. 87. American Association for the Advancement of Science, 2023. ista: Alanko JH, Ucar MC, Canigova N, Stopp JA, Schwarz J, Merrin J, Hannezo EB, Sixt MK. 2023. CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective leukocyte migration. Science Immunology. 8(87), adc9584. mla: Alanko, Jonna H., et al. “CCR7 Acts as Both a Sensor and a Sink for CCL19 to Coordinate Collective Leukocyte Migration.” Science Immunology, vol. 8, no. 87, adc9584, American Association for the Advancement of Science, 2023, doi:10.1126/sciimmunol.adc9584. short: J.H. Alanko, M.C. Ucar, N. Canigova, J.A. Stopp, J. Schwarz, J. Merrin, E.B. Hannezo, M.K. Sixt, Science Immunology 8 (2023). date_created: 2023-09-06T08:07:51Z date_published: 2023-09-01T00:00:00Z date_updated: 2023-12-21T14:30:01Z day: '01' department: - _id: MiSi - _id: EdHa - _id: NanoFab doi: 10.1126/sciimmunol.adc9584 ec_funded: 1 external_id: isi: - '001062110600003' pmid: - '37656776' intvolume: ' 8' isi: 1 issue: '87' keyword: - General Medicine - Immunology language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1126/sciimmunol.adc9584 month: '09' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 05943252-7A3F-11EA-A408-12923DDC885E call_identifier: H2020 grant_number: '851288' name: Design Principles of Branching Morphogenesis - _id: 265E2996-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: W01250-B20 name: Nano-Analytics of Cellular Systems - _id: 260C2330-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '754411' name: ISTplus - Postdoctoral Fellowships publication: Science Immunology publication_identifier: issn: - 2470-9468 publication_status: published publisher: American Association for the Advancement of Science quality_controlled: '1' related_material: record: - id: '14279' relation: research_data status: public - id: '14697' relation: dissertation_contains status: public scopus_import: '1' status: public title: CCR7 acts as both a sensor and a sink for CCL19 to coordinate collective leukocyte migration type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 8 year: '2023' ... --- _id: '9794' abstract: - lang: eng text: 'Lymph nodes (LNs) comprise two main structural elements: fibroblastic reticular cells that form dedicated niches for immune cell interaction and capsular fibroblasts that build a shell around the organ. Immunological challenge causes LNs to increase more than tenfold in size within a few days. Here, we characterized the biomechanics of LN swelling on the cellular and organ scale. We identified lymphocyte trapping by influx and proliferation as drivers of an outward pressure force, causing fibroblastic reticular cells of the T-zone (TRCs) and their associated conduits to stretch. After an initial phase of relaxation, TRCs sensed the resulting strain through cell matrix adhesions, which coordinated local growth and remodeling of the stromal network. While the expanded TRC network readopted its typical configuration, a massive fibrotic reaction of the organ capsule set in and countered further organ expansion. Thus, different fibroblast populations mechanically control LN swelling in a multitier fashion.' acknowledged_ssus: - _id: Bio - _id: EM-Fac - _id: PreCl - _id: LifeSc acknowledgement: This research was supported by the Scientific Service Units of IST Austria through resources provided by the Imaging and Optics, Electron Microscopy, Preclinical and Life Science Facilities. We thank C. Moussion for providing anti-PNAd antibody and D. Critchley for Talin1-floxed mice, and E. Papusheva for providing a custom 3D channel alignment script. This work was supported by a European Research Council grant ERC-CoG-72437 to M.S. M.H. was supported by Czech Sciencundation GACR 20-24603Y and Charles University PRIMUS/20/MED/013. article_processing_charge: No article_type: original author: - first_name: Frank P full_name: Assen, Frank P id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87 last_name: Assen orcid: 0000-0003-3470-6119 - first_name: Jun full_name: Abe, Jun last_name: Abe - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Shayan full_name: Shamipour, Shayan id: 40B34FE2-F248-11E8-B48F-1D18A9856A87 last_name: Shamipour - first_name: Walter full_name: Kaufmann, Walter id: 3F99E422-F248-11E8-B48F-1D18A9856A87 last_name: Kaufmann orcid: 0000-0001-9735-5315 - first_name: Tommaso full_name: Costanzo, Tommaso id: D93824F4-D9BA-11E9-BB12-F207E6697425 last_name: Costanzo orcid: 0000-0001-9732-3815 - first_name: Gabriel full_name: Krens, Gabriel id: 2B819732-F248-11E8-B48F-1D18A9856A87 last_name: Krens orcid: 0000-0003-4761-5996 - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Burkhard full_name: Ludewig, Burkhard last_name: Ludewig - first_name: Simon full_name: Hippenmeyer, Simon id: 37B36620-F248-11E8-B48F-1D18A9856A87 last_name: Hippenmeyer orcid: 0000-0003-2279-1061 - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 - first_name: Wolfgang full_name: Weninger, Wolfgang last_name: Weninger - first_name: Edouard B full_name: Hannezo, Edouard B id: 3A9DB764-F248-11E8-B48F-1D18A9856A87 last_name: Hannezo orcid: 0000-0001-6005-1561 - first_name: Sanjiv A. full_name: Luther, Sanjiv A. last_name: Luther - first_name: Jens V. full_name: Stein, Jens V. last_name: Stein - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-4561-241X citation: ama: Assen FP, Abe J, Hons M, et al. Multitier mechanics control stromal adaptations in swelling lymph nodes. Nature Immunology. 2022;23:1246-1255. doi:10.1038/s41590-022-01257-4 apa: Assen, F. P., Abe, J., Hons, M., Hauschild, R., Shamipour, S., Kaufmann, W., … Sixt, M. K. (2022). Multitier mechanics control stromal adaptations in swelling lymph nodes. Nature Immunology. Springer Nature. https://doi.org/10.1038/s41590-022-01257-4 chicago: Assen, Frank P, Jun Abe, Miroslav Hons, Robert Hauschild, Shayan Shamipour, Walter Kaufmann, Tommaso Costanzo, et al. “Multitier Mechanics Control Stromal Adaptations in Swelling Lymph Nodes.” Nature Immunology. Springer Nature, 2022. https://doi.org/10.1038/s41590-022-01257-4. ieee: F. P. Assen et al., “Multitier mechanics control stromal adaptations in swelling lymph nodes,” Nature Immunology, vol. 23. Springer Nature, pp. 1246–1255, 2022. ista: Assen FP, Abe J, Hons M, Hauschild R, Shamipour S, Kaufmann W, Costanzo T, Krens G, Brown M, Ludewig B, Hippenmeyer S, Heisenberg C-PJ, Weninger W, Hannezo EB, Luther SA, Stein JV, Sixt MK. 2022. Multitier mechanics control stromal adaptations in swelling lymph nodes. Nature Immunology. 23, 1246–1255. mla: Assen, Frank P., et al. “Multitier Mechanics Control Stromal Adaptations in Swelling Lymph Nodes.” Nature Immunology, vol. 23, Springer Nature, 2022, pp. 1246–55, doi:10.1038/s41590-022-01257-4. short: F.P. Assen, J. Abe, M. Hons, R. Hauschild, S. Shamipour, W. Kaufmann, T. Costanzo, G. Krens, M. Brown, B. Ludewig, S. Hippenmeyer, C.-P.J. Heisenberg, W. Weninger, E.B. Hannezo, S.A. Luther, J.V. Stein, M.K. Sixt, Nature Immunology 23 (2022) 1246–1255. date_created: 2021-08-06T09:09:11Z date_published: 2022-07-11T00:00:00Z date_updated: 2023-08-02T06:53:07Z day: '11' ddc: - '570' department: - _id: SiHi - _id: CaHe - _id: EdHa - _id: EM-Fac - _id: Bio - _id: MiSi doi: 10.1038/s41590-022-01257-4 ec_funded: 1 external_id: isi: - '000822975900002' file: - access_level: open_access checksum: 628e7b49809f22c75b428842efe70c68 content_type: application/pdf creator: dernst date_created: 2022-07-25T07:11:32Z date_updated: 2022-07-25T07:11:32Z file_id: '11642' file_name: 2022_NatureImmunology_Assen.pdf file_size: 11475325 relation: main_file success: 1 file_date_updated: 2022-07-25T07:11:32Z has_accepted_license: '1' intvolume: ' 23' isi: 1 language: - iso: eng month: '07' oa: 1 oa_version: Published Version page: 1246-1255 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients publication: Nature Immunology publication_identifier: eissn: - 1529-2916 issn: - 1529-2908 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Multitier mechanics control stromal adaptations in swelling lymph nodes tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 23 year: '2022' ... --- _id: '11843' abstract: - lang: eng text: A key attribute of persistent or recurring bacterial infections is the ability of the pathogen to evade the host’s immune response. Many Enterobacteriaceae express type 1 pili, a pre-adapted virulence trait, to invade host epithelial cells and establish persistent infections. However, the molecular mechanisms and strategies by which bacteria actively circumvent the immune response of the host remain poorly understood. Here, we identified CD14, the major co-receptor for lipopolysaccharide detection, on mouse dendritic cells (DCs) as a binding partner of FimH, the protein located at the tip of the type 1 pilus of Escherichia coli. The FimH amino acids involved in CD14 binding are highly conserved across pathogenic and non-pathogenic strains. Binding of the pathogenic strain CFT073 to CD14 reduced DC migration by overactivation of integrins and blunted expression of co-stimulatory molecules by overactivating the NFAT (nuclear factor of activated T-cells) pathway, both rate-limiting factors of T cell activation. This response was binary at the single-cell level, but averaged in larger populations exposed to both piliated and non-piliated pathogens, presumably via the exchange of immunomodulatory cytokines. While defining an active molecular mechanism of immune evasion by pathogens, the interaction between FimH and CD14 represents a potential target to interfere with persistent and recurrent infections, such as urinary tract infections or Crohn’s disease. acknowledged_ssus: - _id: Bio - _id: PreCl - _id: EM-Fac acknowledgement: We thank Ulrich Dobrindt for providing UPEC strains CFT073, UTI89, and 536, Frank Assen, Vlad Gavra, Maximilian Götz, Bor Kavčič, Jonna Alanko, and Eva Kiermaier for help with experiments and Robert Hauschild, Julian Stopp, and Saren Tasciyan for help with data analysis. We thank the IST Austria Scientific Service Units, especially the Bioimaging facility, the Preclinical facility and the Electron microscopy facility for technical support, Jakob Wallner and all members of the Guet and Sixt lab for fruitful discussions and Daria Siekhaus for critically reading the manuscript. This work was supported by grants from the Austrian Research Promotion Agency (FEMtech 868984) to IG, the European Research Council (CoG 724373), and the Austrian Science Fund (FWF P29911) to MS. article_number: e78995 article_processing_charge: Yes article_type: original author: - first_name: Kathrin full_name: Tomasek, Kathrin id: 3AEC8556-F248-11E8-B48F-1D18A9856A87 last_name: Tomasek - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner - first_name: Ivana full_name: Glatzová, Ivana id: 727b3c7d-4939-11ec-89b3-b9b0750ab74d last_name: Glatzová - first_name: Michael S. full_name: Lukesch, Michael S. last_name: Lukesch - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. eLife. 2022;11. doi:10.7554/eLife.78995 apa: Tomasek, K., Leithner, A. F., Glatzová, I., Lukesch, M. S., Guet, C. C., & Sixt, M. K. (2022). Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.78995 chicago: Tomasek, Kathrin, Alexander F Leithner, Ivana Glatzová, Michael S. Lukesch, Calin C Guet, and Michael K Sixt. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack the Host Immune Response by Binding to CD14.” ELife. eLife Sciences Publications, 2022. https://doi.org/10.7554/eLife.78995. ieee: K. Tomasek, A. F. Leithner, I. Glatzová, M. S. Lukesch, C. C. Guet, and M. K. Sixt, “Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14,” eLife, vol. 11. eLife Sciences Publications, 2022. ista: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. 2022. Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. eLife. 11, e78995. mla: Tomasek, Kathrin, et al. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack the Host Immune Response by Binding to CD14.” ELife, vol. 11, e78995, eLife Sciences Publications, 2022, doi:10.7554/eLife.78995. short: K. Tomasek, A.F. Leithner, I. Glatzová, M.S. Lukesch, C.C. Guet, M.K. Sixt, ELife 11 (2022). date_created: 2022-08-14T22:01:46Z date_published: 2022-07-26T00:00:00Z date_updated: 2023-08-03T12:54:21Z day: '26' ddc: - '570' department: - _id: MiSi - _id: CaGu doi: 10.7554/eLife.78995 ec_funded: 1 external_id: isi: - '000838410200001' file: - access_level: open_access checksum: 002a3c7c7ea5caa9af9cfbea308f6ea4 content_type: application/pdf creator: cchlebak date_created: 2022-08-16T08:57:37Z date_updated: 2022-08-16T08:57:37Z file_id: '11861' file_name: 2022_eLife_Tomasek.pdf file_size: 2057577 relation: main_file success: 1 file_date_updated: 2022-08-16T08:57:37Z has_accepted_license: '1' intvolume: ' 11' isi: 1 language: - iso: eng month: '07' oa: 1 oa_version: Published Version project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 26018E70-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29911 name: Mechanical adaptation of lamellipodial actin publication: eLife publication_identifier: eissn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' related_material: record: - id: '10316' relation: earlier_version status: public scopus_import: '1' status: public title: Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14 tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 11 year: '2022' ... --- _id: '12133' abstract: - lang: eng text: Social distancing is an effective way to prevent the spread of disease in societies, whereas infection elimination is a key element of organismal immunity. Here, we discuss how the study of social insects such as ants — which form a superorganism of unconditionally cooperative individuals and thus represent a level of organization that is intermediate between a classical society of individuals and an organism of cells — can help to determine common principles of disease defence across levels of organization. article_processing_charge: No article_type: letter_note author: - first_name: Sylvia full_name: Cremer, Sylvia id: 2F64EC8C-F248-11E8-B48F-1D18A9856A87 last_name: Cremer orcid: 0000-0002-2193-3868 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Cremer S, Sixt MK. Principles of disease defence in organisms, superorganisms and societies. Nature Reviews Immunology. 2022;22(12):713-714. doi:10.1038/s41577-022-00797-y apa: Cremer, S., & Sixt, M. K. (2022). Principles of disease defence in organisms, superorganisms and societies. Nature Reviews Immunology. Springer Nature. https://doi.org/10.1038/s41577-022-00797-y chicago: Cremer, Sylvia, and Michael K Sixt. “Principles of Disease Defence in Organisms, Superorganisms and Societies.” Nature Reviews Immunology. Springer Nature, 2022. https://doi.org/10.1038/s41577-022-00797-y. ieee: S. Cremer and M. K. Sixt, “Principles of disease defence in organisms, superorganisms and societies,” Nature Reviews Immunology, vol. 22, no. 12. Springer Nature, pp. 713–714, 2022. ista: Cremer S, Sixt MK. 2022. Principles of disease defence in organisms, superorganisms and societies. Nature Reviews Immunology. 22(12), 713–714. mla: Cremer, Sylvia, and Michael K. Sixt. “Principles of Disease Defence in Organisms, Superorganisms and Societies.” Nature Reviews Immunology, vol. 22, no. 12, Springer Nature, 2022, pp. 713–14, doi:10.1038/s41577-022-00797-y. short: S. Cremer, M.K. Sixt, Nature Reviews Immunology 22 (2022) 713–714. date_created: 2023-01-12T12:03:14Z date_published: 2022-12-01T00:00:00Z date_updated: 2023-08-04T08:53:32Z day: '01' department: - _id: SyCr - _id: MiSi doi: 10.1038/s41577-022-00797-y external_id: isi: - '000871836300001' pmid: - '36284178' intvolume: ' 22' isi: 1 issue: '12' keyword: - Energy Engineering and Power Technology - Fuel Technology language: - iso: eng month: '12' oa_version: None page: 713-714 pmid: 1 publication: Nature Reviews Immunology publication_identifier: eissn: - 1474-1741 issn: - 1474-1733 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Principles of disease defence in organisms, superorganisms and societies type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 22 year: '2022' ... --- _id: '12272' abstract: - lang: eng text: Reading, interpreting and crawling along gradients of chemotactic cues is one of the most complex questions in cell biology. In this issue, Georgantzoglou et al. (2022. J. Cell. Biol.https://doi.org/10.1083/jcb.202103207) use in vivo models to map the temporal sequence of how neutrophils respond to an acutely arising gradient of chemoattractant. article_number: e202206127 article_processing_charge: No article_type: original author: - first_name: Julian A full_name: Stopp, Julian A id: 489E3F00-F248-11E8-B48F-1D18A9856A87 last_name: Stopp - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Stopp JA, Sixt MK. Plan your trip before you leave: The neutrophils’ search-and-run journey. Journal of Cell Biology. 2022;221(8). doi:10.1083/jcb.202206127' apa: 'Stopp, J. A., & Sixt, M. K. (2022). Plan your trip before you leave: The neutrophils’ search-and-run journey. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.202206127' chicago: 'Stopp, Julian A, and Michael K Sixt. “Plan Your Trip before You Leave: The Neutrophils’ Search-and-Run Journey.” Journal of Cell Biology. Rockefeller University Press, 2022. https://doi.org/10.1083/jcb.202206127.' ieee: 'J. A. Stopp and M. K. Sixt, “Plan your trip before you leave: The neutrophils’ search-and-run journey,” Journal of Cell Biology, vol. 221, no. 8. Rockefeller University Press, 2022.' ista: 'Stopp JA, Sixt MK. 2022. Plan your trip before you leave: The neutrophils’ search-and-run journey. Journal of Cell Biology. 221(8), e202206127.' mla: 'Stopp, Julian A., and Michael K. Sixt. “Plan Your Trip before You Leave: The Neutrophils’ Search-and-Run Journey.” Journal of Cell Biology, vol. 221, no. 8, e202206127, Rockefeller University Press, 2022, doi:10.1083/jcb.202206127.' short: J.A. Stopp, M.K. Sixt, Journal of Cell Biology 221 (2022). date_created: 2023-01-16T10:01:08Z date_published: 2022-07-20T00:00:00Z date_updated: 2023-12-21T14:30:01Z day: '20' ddc: - '570' department: - _id: MiSi doi: 10.1083/jcb.202206127 external_id: isi: - '000874717200001' pmid: - '35856919' file: - access_level: open_access checksum: 6b1620743669679b48b9389bb40f5a11 content_type: application/pdf creator: dernst date_created: 2023-01-30T10:39:34Z date_updated: 2023-01-30T10:39:34Z file_id: '12451' file_name: 2022_JourCellBiology_Stopp.pdf file_size: 969969 relation: main_file success: 1 file_date_updated: 2023-01-30T10:39:34Z has_accepted_license: '1' intvolume: ' 221' isi: 1 issue: '8' keyword: - Cell Biology language: - iso: eng license: https://creativecommons.org/licenses/by-nc-sa/4.0/ month: '07' oa: 1 oa_version: Published Version pmid: 1 publication: Journal of Cell Biology publication_identifier: eissn: - 1540-8140 issn: - 0021-9525 publication_status: published publisher: Rockefeller University Press quality_controlled: '1' related_material: record: - id: '14697' relation: dissertation_contains status: public scopus_import: '1' status: public title: 'Plan your trip before you leave: The neutrophils’ search-and-run journey' tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 221 year: '2022' ... --- _id: '10703' abstract: - lang: eng text: 'When crawling through the body, leukocytes often traverse tissues that are densely packed with extracellular matrix and other cells, and this raises the question: How do leukocytes overcome compressive mechanical loads? Here, we show that the actin cortex of leukocytes is mechanoresponsive and that this responsiveness requires neither force sensing via the nucleus nor adhesive interactions with a substrate. Upon global compression of the cell body as well as local indentation of the plasma membrane, Wiskott-Aldrich syndrome protein (WASp) assembles into dot-like structures, providing activation platforms for Arp2/3 nucleated actin patches. These patches locally push against the external load, which can be obstructing collagen fibers or other cells, and thereby create space to facilitate forward locomotion. We show in vitro and in vivo that this WASp function is rate limiting for ameboid leukocyte migration in dense but not in loose environments and is required for trafficking through diverse tissues such as skin and lymph nodes.' acknowledged_ssus: - _id: LifeSc - _id: Bio - _id: EM-Fac acknowledgement: We thank N. Darwish-Miranda, F. Leite, F.P. Assen, and A. Eichner for advice and help with experiments. We thank J. Renkawitz, E. Kiermaier, A. Juanes Garcia, and M. Avellaneda for critical reading of the manuscript. We thank M. Driscoll for advice on fluorescent labeling of collagen gels. This research was supported by the Scientific Service Units (SSUs) of IST Austria through resources provided by Molecular Biology Services/Lab Support Facility (LSF)/Bioimaging Facility/Electron Microscopy Facility. This work was funded by grants from the European Research Council ( CoG 724373 ) and the Austrian Science Foundation (FWF) to M.S. F.G. received funding from the European Union’s Horizon 2020 research and innovation program under the Marie Skłodowska-Curie grant agreement no. 747687. article_processing_charge: No article_type: original author: - first_name: Florian full_name: Gaertner, Florian last_name: Gaertner - first_name: Patricia full_name: Reis-Rodrigues, Patricia last_name: Reis-Rodrigues - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Juan full_name: Aguilera, Juan last_name: Aguilera - first_name: Michael full_name: Riedl, Michael id: 3BE60946-F248-11E8-B48F-1D18A9856A87 last_name: Riedl orcid: 0000-0003-4844-6311 - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Saren full_name: Tasciyan, Saren id: 4323B49C-F248-11E8-B48F-1D18A9856A87 last_name: Tasciyan orcid: 0000-0003-1671-393X - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Vanessa full_name: Zheden, Vanessa id: 39C5A68A-F248-11E8-B48F-1D18A9856A87 last_name: Zheden orcid: 0000-0002-9438-4783 - first_name: Walter full_name: Kaufmann, Walter id: 3F99E422-F248-11E8-B48F-1D18A9856A87 last_name: Kaufmann orcid: 0000-0001-9735-5315 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Gaertner F, Reis-Rodrigues P, de Vries I, et al. WASp triggers mechanosensitive actin patches to facilitate immune cell migration in dense tissues. Developmental Cell. 2022;57(1):47-62.e9. doi:10.1016/j.devcel.2021.11.024 apa: Gaertner, F., Reis-Rodrigues, P., de Vries, I., Hons, M., Aguilera, J., Riedl, M., … Sixt, M. K. (2022). WASp triggers mechanosensitive actin patches to facilitate immune cell migration in dense tissues. Developmental Cell. Cell Press ; Elsevier. https://doi.org/10.1016/j.devcel.2021.11.024 chicago: Gaertner, Florian, Patricia Reis-Rodrigues, Ingrid de Vries, Miroslav Hons, Juan Aguilera, Michael Riedl, Alexander F Leithner, et al. “WASp Triggers Mechanosensitive Actin Patches to Facilitate Immune Cell Migration in Dense Tissues.” Developmental Cell. Cell Press ; Elsevier, 2022. https://doi.org/10.1016/j.devcel.2021.11.024. ieee: F. Gaertner et al., “WASp triggers mechanosensitive actin patches to facilitate immune cell migration in dense tissues,” Developmental Cell, vol. 57, no. 1. Cell Press ; Elsevier, p. 47–62.e9, 2022. ista: Gaertner F, Reis-Rodrigues P, de Vries I, Hons M, Aguilera J, Riedl M, Leithner AF, Tasciyan S, Kopf A, Merrin J, Zheden V, Kaufmann W, Hauschild R, Sixt MK. 2022. WASp triggers mechanosensitive actin patches to facilitate immune cell migration in dense tissues. Developmental Cell. 57(1), 47–62.e9. mla: Gaertner, Florian, et al. “WASp Triggers Mechanosensitive Actin Patches to Facilitate Immune Cell Migration in Dense Tissues.” Developmental Cell, vol. 57, no. 1, Cell Press ; Elsevier, 2022, p. 47–62.e9, doi:10.1016/j.devcel.2021.11.024. short: F. Gaertner, P. Reis-Rodrigues, I. de Vries, M. Hons, J. Aguilera, M. Riedl, A.F. Leithner, S. Tasciyan, A. Kopf, J. Merrin, V. Zheden, W. Kaufmann, R. Hauschild, M.K. Sixt, Developmental Cell 57 (2022) 47–62.e9. date_created: 2022-01-30T23:01:33Z date_published: 2022-01-10T00:00:00Z date_updated: 2024-03-27T23:30:23Z day: '10' ddc: - '570' department: - _id: MiSi - _id: EM-Fac - _id: NanoFab - _id: BjHo doi: 10.1016/j.devcel.2021.11.024 ec_funded: 1 external_id: isi: - '000768933800005' pmid: - '34919802' intvolume: ' 57' isi: 1 issue: '1' language: - iso: eng license: https://creativecommons.org/licenses/by-nc-nd/4.0/ main_file_link: - open_access: '1' url: https://www.sciencedirect.com/science/article/pii/S1534580721009497 month: '01' oa: 1 oa_version: Published Version page: 47-62.e9 pmid: 1 project: - _id: 260AA4E2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '747687' name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients publication: Developmental Cell publication_identifier: eissn: - 1878-1551 issn: - 1534-5807 publication_status: published publisher: Cell Press ; Elsevier quality_controlled: '1' related_material: record: - id: '12726' relation: dissertation_contains status: public - id: '14530' relation: dissertation_contains status: public - id: '12401' relation: dissertation_contains status: public scopus_import: '1' status: public title: WASp triggers mechanosensitive actin patches to facilitate immune cell migration in dense tissues tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 57 year: '2022' ... --- _id: '9259' abstract: - lang: eng text: Gradients of chemokines and growth factors guide migrating cells and morphogenetic processes. Migration of antigen-presenting dendritic cells from the interstitium into the lymphatic system is dependent on chemokine CCL21, which is secreted by endothelial cells of the lymphatic capillary, binds heparan sulfates and forms gradients decaying into the interstitium. Despite the importance of CCL21 gradients, and chemokine gradients in general, the mechanisms of gradient formation are unclear. Studies on fibroblast growth factors have shown that limited diffusion is crucial for gradient formation. Here, we used the mouse dermis as a model tissue to address the necessity of CCL21 anchoring to lymphatic capillary heparan sulfates in the formation of interstitial CCL21 gradients. Surprisingly, the absence of lymphatic endothelial heparan sulfates resulted only in a modest decrease of CCL21 levels at the lymphatic capillaries and did neither affect interstitial CCL21 gradient shape nor dendritic cell migration toward lymphatic capillaries. Thus, heparan sulfates at the level of the lymphatic endothelium are dispensable for the formation of a functional CCL21 gradient. acknowledgement: "This work was supported by Sigrid Juselius fellowship (KV), University of Helsinki 3-year research grant (KV), Academy of Finland Research fellow funding (315710, to KV), the European Research Council (ERC CoG 724373 to MS), and by the Austrian Science foundation (FWF) (Y564-B12 START award to MS).\r\nTaija Mäkinen is acknowledged for providing Prox1CreERT2 transgenic mice and Yu Yamaguchi for providing the conditional Ext1 mouse strain." article_number: '630002' article_processing_charge: No article_type: original author: - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Christine full_name: Moussion, Christine id: 3356F664-F248-11E8-B48F-1D18A9856A87 last_name: Moussion - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Vaahtomeri K, Moussion C, Hauschild R, Sixt MK. Shape and function of interstitial chemokine CCL21 gradients are independent of heparan sulfates produced by lymphatic endothelium. Frontiers in Immunology. 2021;12. doi:10.3389/fimmu.2021.630002 apa: Vaahtomeri, K., Moussion, C., Hauschild, R., & Sixt, M. K. (2021). Shape and function of interstitial chemokine CCL21 gradients are independent of heparan sulfates produced by lymphatic endothelium. Frontiers in Immunology. Frontiers. https://doi.org/10.3389/fimmu.2021.630002 chicago: Vaahtomeri, Kari, Christine Moussion, Robert Hauschild, and Michael K Sixt. “Shape and Function of Interstitial Chemokine CCL21 Gradients Are Independent of Heparan Sulfates Produced by Lymphatic Endothelium.” Frontiers in Immunology. Frontiers, 2021. https://doi.org/10.3389/fimmu.2021.630002. ieee: K. Vaahtomeri, C. Moussion, R. Hauschild, and M. K. Sixt, “Shape and function of interstitial chemokine CCL21 gradients are independent of heparan sulfates produced by lymphatic endothelium,” Frontiers in Immunology, vol. 12. Frontiers, 2021. ista: Vaahtomeri K, Moussion C, Hauschild R, Sixt MK. 2021. Shape and function of interstitial chemokine CCL21 gradients are independent of heparan sulfates produced by lymphatic endothelium. Frontiers in Immunology. 12, 630002. mla: Vaahtomeri, Kari, et al. “Shape and Function of Interstitial Chemokine CCL21 Gradients Are Independent of Heparan Sulfates Produced by Lymphatic Endothelium.” Frontiers in Immunology, vol. 12, 630002, Frontiers, 2021, doi:10.3389/fimmu.2021.630002. short: K. Vaahtomeri, C. Moussion, R. Hauschild, M.K. Sixt, Frontiers in Immunology 12 (2021). date_created: 2021-03-21T23:01:20Z date_published: 2021-02-25T00:00:00Z date_updated: 2023-08-07T14:18:26Z day: '25' ddc: - '570' department: - _id: MiSi - _id: Bio doi: 10.3389/fimmu.2021.630002 ec_funded: 1 external_id: isi: - '000627134400001' pmid: - '33717158' file: - access_level: open_access checksum: 663f5a48375e42afa4bfef58d42ec186 content_type: application/pdf creator: dernst date_created: 2021-03-22T12:08:26Z date_updated: 2021-03-22T12:08:26Z file_id: '9277' file_name: 2021_FrontiersImmumo_Vaahtomeri.pdf file_size: 3740146 relation: main_file success: 1 file_date_updated: 2021-03-22T12:08:26Z has_accepted_license: '1' intvolume: ' 12' isi: 1 language: - iso: eng month: '02' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and force transduction of migrating leukocytes publication: Frontiers in Immunology publication_identifier: eissn: - 1664-3224 publication_status: published publisher: Frontiers quality_controlled: '1' scopus_import: '1' status: public title: Shape and function of interstitial chemokine CCL21 gradients are independent of heparan sulfates produced by lymphatic endothelium tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 12 year: '2021' ... --- _id: '9294' abstract: - lang: eng text: In this issue of Developmental Cell, Doyle and colleagues identify periodic anterior contraction as a characteristic feature of fibroblasts and mesenchymal cancer cells embedded in 3D collagen gels. This contractile mechanism generates a matrix prestrain required for crawling in fibrous 3D environments. article_processing_charge: No article_type: original author: - first_name: Florian R full_name: Gärtner, Florian R id: 397A88EE-F248-11E8-B48F-1D18A9856A87 last_name: Gärtner orcid: 0000-0001-6120-3723 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Gärtner FR, Sixt MK. Engaging the front wheels to drive through fibrous terrain. Developmental Cell. 2021;56(6):723-725. doi:10.1016/j.devcel.2021.03.002 apa: Gärtner, F. R., & Sixt, M. K. (2021). Engaging the front wheels to drive through fibrous terrain. Developmental Cell. Elsevier. https://doi.org/10.1016/j.devcel.2021.03.002 chicago: Gärtner, Florian R, and Michael K Sixt. “Engaging the Front Wheels to Drive through Fibrous Terrain.” Developmental Cell. Elsevier, 2021. https://doi.org/10.1016/j.devcel.2021.03.002. ieee: F. R. Gärtner and M. K. Sixt, “Engaging the front wheels to drive through fibrous terrain,” Developmental Cell, vol. 56, no. 6. Elsevier, pp. 723–725, 2021. ista: Gärtner FR, Sixt MK. 2021. Engaging the front wheels to drive through fibrous terrain. Developmental Cell. 56(6), 723–725. mla: Gärtner, Florian R., and Michael K. Sixt. “Engaging the Front Wheels to Drive through Fibrous Terrain.” Developmental Cell, vol. 56, no. 6, Elsevier, 2021, pp. 723–25, doi:10.1016/j.devcel.2021.03.002. short: F.R. Gärtner, M.K. Sixt, Developmental Cell 56 (2021) 723–725. date_created: 2021-03-28T22:01:41Z date_published: 2021-03-22T00:00:00Z date_updated: 2023-08-07T14:26:47Z day: '22' department: - _id: MiSi doi: 10.1016/j.devcel.2021.03.002 external_id: isi: - '000631681200004' pmid: - '33756118' intvolume: ' 56' isi: 1 issue: '6' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.devcel.2021.03.002 month: '03' oa: 1 oa_version: Published Version page: 723-725 pmid: 1 publication: Developmental Cell publication_identifier: eissn: - '18781551' issn: - '15345807' publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Engaging the front wheels to drive through fibrous terrain type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 56 year: '2021' ... --- _id: '9822' abstract: - lang: eng text: Attachment of adhesive molecules on cell culture surfaces to restrict cell adhesion to defined areas and shapes has been vital for the progress of in vitro research. In currently existing patterning methods, a combination of pattern properties such as stability, precision, specificity, high-throughput outcome, and spatiotemporal control is highly desirable but challenging to achieve. Here, we introduce a versatile and high-throughput covalent photoimmobilization technique, comprising a light-dose-dependent patterning step and a subsequent functionalization of the pattern via click chemistry. This two-step process is feasible on arbitrary surfaces and allows for generation of sustainable patterns and gradients. The method is validated in different biological systems by patterning adhesive ligands on cell-repellent surfaces, thereby constraining the growth and migration of cells to the designated areas. We then implement a sequential photopatterning approach by adding a second switchable patterning step, allowing for spatiotemporal control over two distinct surface patterns. As a proof of concept, we reconstruct the dynamics of the tip/stalk cell switch during angiogenesis. Our results show that the spatiotemporal control provided by our “sequential photopatterning” system is essential for mimicking dynamic biological processes and that our innovative approach has great potential for further applications in cell science. acknowledgement: We would like to thank Charlott Leu for the production of our chromium wafers, Louise Ritter for her contribution of the IF stainings in Figure 4, Shokoufeh Teymouri for her help with the Bioinert coated slides, and finally Prof. Dr. Joachim Rädler for his valuable scientific guidance. article_processing_charge: Yes (in subscription journal) article_type: original author: - first_name: Themistoklis full_name: Zisis, Themistoklis last_name: Zisis - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Miriam full_name: Balles, Miriam last_name: Balles - first_name: Maibritt full_name: Kretschmer, Maibritt last_name: Kretschmer - first_name: Maria full_name: Nemethova, Maria id: 34E27F1C-F248-11E8-B48F-1D18A9856A87 last_name: Nemethova - first_name: Remy P full_name: Chait, Remy P id: 3464AE84-F248-11E8-B48F-1D18A9856A87 last_name: Chait orcid: 0000-0003-0876-3187 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Janina full_name: Lange, Janina last_name: Lange - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-4561-241X - first_name: Stefan full_name: Zahler, Stefan last_name: Zahler citation: ama: Zisis T, Schwarz J, Balles M, et al. Sequential and switchable patterning for studying cellular processes under spatiotemporal control. ACS Applied Materials and Interfaces. 2021;13(30):35545–35560. doi:10.1021/acsami.1c09850 apa: Zisis, T., Schwarz, J., Balles, M., Kretschmer, M., Nemethova, M., Chait, R. P., … Zahler, S. (2021). Sequential and switchable patterning for studying cellular processes under spatiotemporal control. ACS Applied Materials and Interfaces. American Chemical Society. https://doi.org/10.1021/acsami.1c09850 chicago: Zisis, Themistoklis, Jan Schwarz, Miriam Balles, Maibritt Kretschmer, Maria Nemethova, Remy P Chait, Robert Hauschild, et al. “Sequential and Switchable Patterning for Studying Cellular Processes under Spatiotemporal Control.” ACS Applied Materials and Interfaces. American Chemical Society, 2021. https://doi.org/10.1021/acsami.1c09850. ieee: T. Zisis et al., “Sequential and switchable patterning for studying cellular processes under spatiotemporal control,” ACS Applied Materials and Interfaces, vol. 13, no. 30. American Chemical Society, pp. 35545–35560, 2021. ista: Zisis T, Schwarz J, Balles M, Kretschmer M, Nemethova M, Chait RP, Hauschild R, Lange J, Guet CC, Sixt MK, Zahler S. 2021. Sequential and switchable patterning for studying cellular processes under spatiotemporal control. ACS Applied Materials and Interfaces. 13(30), 35545–35560. mla: Zisis, Themistoklis, et al. “Sequential and Switchable Patterning for Studying Cellular Processes under Spatiotemporal Control.” ACS Applied Materials and Interfaces, vol. 13, no. 30, American Chemical Society, 2021, pp. 35545–35560, doi:10.1021/acsami.1c09850. short: T. Zisis, J. Schwarz, M. Balles, M. Kretschmer, M. Nemethova, R.P. Chait, R. Hauschild, J. Lange, C.C. Guet, M.K. Sixt, S. Zahler, ACS Applied Materials and Interfaces 13 (2021) 35545–35560. date_created: 2021-08-08T22:01:28Z date_published: 2021-08-04T00:00:00Z date_updated: 2023-08-10T14:22:48Z day: '04' ddc: - '620' - '570' department: - _id: MiSi - _id: GaTk - _id: Bio - _id: CaGu doi: 10.1021/acsami.1c09850 ec_funded: 1 external_id: isi: - '000683741400026' pmid: - '34283577' file: - access_level: open_access checksum: b043a91d9f9200e467b970b692687ed3 content_type: application/pdf creator: asandaue date_created: 2021-08-09T09:44:03Z date_updated: 2021-08-09T09:44:03Z file_id: '9833' file_name: 2021_ACSAppliedMaterialsAndInterfaces_Zisis.pdf file_size: 7123293 relation: main_file success: 1 file_date_updated: 2021-08-09T09:44:03Z has_accepted_license: '1' intvolume: ' 13' isi: 1 issue: '30' language: - iso: eng month: '08' oa: 1 oa_version: Published Version page: 35545–35560 pmid: 1 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients publication: ACS Applied Materials and Interfaces publication_identifier: eissn: - '19448252' issn: - '19448244' publication_status: published publisher: American Chemical Society quality_controlled: '1' scopus_import: '1' status: public title: Sequential and switchable patterning for studying cellular processes under spatiotemporal control tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 13 year: '2021' ... --- _id: '10834' abstract: - lang: eng text: Hematopoietic-specific protein 1 (Hem1) is an essential subunit of the WAVE regulatory complex (WRC) in immune cells. WRC is crucial for Arp2/3 complex activation and the protrusion of branched actin filament networks. Moreover, Hem1 loss of function in immune cells causes autoimmune diseases in humans. Here, we show that genetic removal of Hem1 in macrophages diminishes frequency and efficacy of phagocytosis as well as phagocytic cup formation in addition to defects in lamellipodial protrusion and migration. Moreover, Hem1-null macrophages displayed strong defects in cell adhesion despite unaltered podosome formation and concomitant extracellular matrix degradation. Specifically, dynamics of both adhesion and de-adhesion as well as concomitant phosphorylation of paxillin and focal adhesion kinase (FAK) were significantly compromised. Accordingly, disruption of WRC function in non-hematopoietic cells coincided with both defects in adhesion turnover and altered FAK and paxillin phosphorylation. Consistently, platelets exhibited reduced adhesion and diminished integrin αIIbβ3 activation upon WRC removal. Interestingly, adhesion phenotypes, but not lamellipodia formation, were partially rescued by small molecule activation of FAK. A full rescue of the phenotype, including lamellipodia formation, required not only the presence of WRCs but also their binding to and activation by Rac. Collectively, our results uncover that WRC impacts on integrin-dependent processes in a FAK-dependent manner, controlling formation and dismantling of adhesions, relevant for properly grabbing onto extracellular surfaces and particles during cell edge expansion, like in migration or phagocytosis. acknowledgement: We are grateful to Silvia Prettin, Ina Schleicher, and Petra Hagendorff for expert technical assistance; David Dettbarn for animal keeping and breeding; and Lothar Gröbe and Maria Höxter for cell sorting. We also thank Werner Tegge for peptides and Giorgio Scita for antibodies. This work was supported, in part, by the Deutsche Forschungsgemeinschaft (DFG), Priority Programm SPP1150 (to T.E.B.S., K.R., and M. Sixt), and by DFG grant GRK2223/1 (to K.R.). T.E.B.S. acknowledges support by the Helmholtz Society through HGF impulse fund W2/W3-066 and M. Schnoor by the Mexican Council for Science and Technology (CONACyT, 284292 ), Fund SEP-Cinvestav ( 108 ), and the Royal Society, UK (Newton Advanced Fellowship, NAF/R1/180017 ). article_processing_charge: No article_type: original author: - first_name: Stephanie full_name: Stahnke, Stephanie last_name: Stahnke - first_name: Hermann full_name: Döring, Hermann last_name: Döring - first_name: Charly full_name: Kusch, Charly last_name: Kusch - first_name: David J.J. full_name: de Gorter, David J.J. last_name: de Gorter - first_name: Sebastian full_name: Dütting, Sebastian last_name: Dütting - first_name: Aleks full_name: Guledani, Aleks last_name: Guledani - first_name: Irina full_name: Pleines, Irina last_name: Pleines - first_name: Michael full_name: Schnoor, Michael last_name: Schnoor - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Robert full_name: Geffers, Robert last_name: Geffers - first_name: Manfred full_name: Rohde, Manfred last_name: Rohde - first_name: Mathias full_name: Müsken, Mathias last_name: Müsken - first_name: Frieda full_name: Kage, Frieda last_name: Kage - first_name: Anika full_name: Steffen, Anika last_name: Steffen - first_name: Jan full_name: Faix, Jan last_name: Faix - first_name: Bernhard full_name: Nieswandt, Bernhard last_name: Nieswandt - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner - first_name: Theresia E.B. full_name: Stradal, Theresia E.B. last_name: Stradal citation: ama: Stahnke S, Döring H, Kusch C, et al. Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis, and integrin-mediated adhesion. Current Biology. 2021;31(10):2051-2064.e8. doi:10.1016/j.cub.2021.02.043 apa: Stahnke, S., Döring, H., Kusch, C., de Gorter, D. J. J., Dütting, S., Guledani, A., … Stradal, T. E. B. (2021). Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis, and integrin-mediated adhesion. Current Biology. Elsevier. https://doi.org/10.1016/j.cub.2021.02.043 chicago: Stahnke, Stephanie, Hermann Döring, Charly Kusch, David J.J. de Gorter, Sebastian Dütting, Aleks Guledani, Irina Pleines, et al. “Loss of Hem1 Disrupts Macrophage Function and Impacts Migration, Phagocytosis, and Integrin-Mediated Adhesion.” Current Biology. Elsevier, 2021. https://doi.org/10.1016/j.cub.2021.02.043. ieee: S. Stahnke et al., “Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis, and integrin-mediated adhesion,” Current Biology, vol. 31, no. 10. Elsevier, p. 2051–2064.e8, 2021. ista: Stahnke S, Döring H, Kusch C, de Gorter DJJ, Dütting S, Guledani A, Pleines I, Schnoor M, Sixt MK, Geffers R, Rohde M, Müsken M, Kage F, Steffen A, Faix J, Nieswandt B, Rottner K, Stradal TEB. 2021. Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis, and integrin-mediated adhesion. Current Biology. 31(10), 2051–2064.e8. mla: Stahnke, Stephanie, et al. “Loss of Hem1 Disrupts Macrophage Function and Impacts Migration, Phagocytosis, and Integrin-Mediated Adhesion.” Current Biology, vol. 31, no. 10, Elsevier, 2021, p. 2051–2064.e8, doi:10.1016/j.cub.2021.02.043. short: S. Stahnke, H. Döring, C. Kusch, D.J.J. de Gorter, S. Dütting, A. Guledani, I. Pleines, M. Schnoor, M.K. Sixt, R. Geffers, M. Rohde, M. Müsken, F. Kage, A. Steffen, J. Faix, B. Nieswandt, K. Rottner, T.E.B. Stradal, Current Biology 31 (2021) 2051–2064.e8. date_created: 2022-03-08T07:51:04Z date_published: 2021-05-24T00:00:00Z date_updated: 2023-08-17T07:01:14Z day: '24' department: - _id: MiSi doi: 10.1016/j.cub.2021.02.043 external_id: isi: - '000654652200002' pmid: - '33711252' intvolume: ' 31' isi: 1 issue: '10' keyword: - General Agricultural and Biological Sciences - General Biochemistry - Genetics and Molecular Biology language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1101/2020.03.24.005835 month: '05' oa: 1 oa_version: Preprint page: 2051-2064.e8 pmid: 1 publication: Current Biology publication_identifier: issn: - 0960-9822 publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: Loss of Hem1 disrupts macrophage function and impacts migration, phagocytosis, and integrin-mediated adhesion type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 31 year: '2021' ... --- _id: '9094' abstract: - lang: eng text: Dendritic cells (DCs) are crucial for the priming of naive T cells and the initiation of adaptive immunity. Priming is initiated at a heterologous cell–cell contact, the immunological synapse (IS). While it is established that F-actin dynamics regulates signaling at the T cell side of the contact, little is known about the cytoskeletal contribution on the DC side. Here, we show that the DC actin cytoskeleton is decisive for the formation of a multifocal synaptic structure, which correlates with T cell priming efficiency. DC actin at the IS appears in transient foci that are dynamized by the WAVE regulatory complex (WRC). The absence of the WRC in DCs leads to stabilized contacts with T cells, caused by an increase in ICAM1-integrin–mediated cell–cell adhesion. This results in lower numbers of activated and proliferating T cells, demonstrating an important role for DC actin in the regulation of immune synapse functionality. article_number: e202006081 article_processing_charge: No article_type: original author: - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: LM full_name: Altenburger, LM last_name: Altenburger - first_name: R full_name: Hauschild, R last_name: Hauschild - first_name: Frank P full_name: Assen, Frank P id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87 last_name: Assen orcid: 0000-0003-3470-6119 - first_name: K full_name: Rottner, K last_name: Rottner - first_name: Stradal full_name: TEB, Stradal last_name: TEB - first_name: A full_name: Diz-Muñoz, A last_name: Diz-Muñoz - first_name: JV full_name: Stein, JV last_name: Stein - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Leithner AF, Altenburger L, Hauschild R, et al. Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse. Journal of Cell Biology. 2021;220(4). doi:10.1083/jcb.202006081 apa: Leithner, A. F., Altenburger, L., Hauschild, R., Assen, F. P., Rottner, K., TEB, S., … Sixt, M. K. (2021). Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.202006081 chicago: Leithner, Alexander F, LM Altenburger, R Hauschild, Frank P Assen, K Rottner, Stradal TEB, A Diz-Muñoz, JV Stein, and Michael K Sixt. “Dendritic Cell Actin Dynamics Control Contact Duration and Priming Efficiency at the Immunological Synapse.” Journal of Cell Biology. Rockefeller University Press, 2021. https://doi.org/10.1083/jcb.202006081. ieee: A. F. Leithner et al., “Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse,” Journal of Cell Biology, vol. 220, no. 4. Rockefeller University Press, 2021. ista: Leithner AF, Altenburger L, Hauschild R, Assen FP, Rottner K, TEB S, Diz-Muñoz A, Stein J, Sixt MK. 2021. Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse. Journal of Cell Biology. 220(4), e202006081. mla: Leithner, Alexander F., et al. “Dendritic Cell Actin Dynamics Control Contact Duration and Priming Efficiency at the Immunological Synapse.” Journal of Cell Biology, vol. 220, no. 4, e202006081, Rockefeller University Press, 2021, doi:10.1083/jcb.202006081. short: A.F. Leithner, L. Altenburger, R. Hauschild, F.P. Assen, K. Rottner, S. TEB, A. Diz-Muñoz, J. Stein, M.K. Sixt, Journal of Cell Biology 220 (2021). date_created: 2021-02-05T10:08:04Z date_published: 2021-04-05T00:00:00Z date_updated: 2023-09-05T13:57:53Z day: '05' ddc: - '570' department: - _id: MiSi doi: 10.1083/jcb.202006081 external_id: isi: - '000626365700001' pmid: - '33533935' file: - access_level: open_access checksum: 843ebc153847c8626e13c9c5ce71d533 content_type: application/pdf creator: dernst date_created: 2022-05-12T14:16:21Z date_updated: 2022-05-12T14:16:21Z file_id: '11367' file_name: 2021_JournCellBiology_Leithner.pdf file_size: 5102328 relation: main_file success: 1 file_date_updated: 2022-05-12T14:16:21Z has_accepted_license: '1' intvolume: ' 220' isi: 1 issue: '4' language: - iso: eng month: '04' oa: 1 oa_version: Published Version pmid: 1 publication: Journal of Cell Biology publication_identifier: eissn: - 1540-8140 issn: - 0021-9525 publication_status: published publisher: Rockefeller University Press quality_controlled: '1' scopus_import: '1' status: public title: Dendritic cell actin dynamics control contact duration and priming efficiency at the immunological synapse tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 220 year: '2021' ... --- _id: '10316' abstract: - lang: eng text: A key attribute of persistent or recurring bacterial infections is the ability of the pathogen to evade the host’s immune response. Many Enterobacteriaceae express type 1 pili, a pre-adapted virulence trait, to invade host epithelial cells and establish persistent infections. However, the molecular mechanisms and strategies by which bacteria actively circumvent the immune response of the host remain poorly understood. Here, we identified CD14, the major co-receptor for lipopolysaccharide detection, on dendritic cells as a previously undescribed binding partner of FimH, the protein located at the tip of the type 1 pilus of Escherichia coli. The FimH amino acids involved in CD14 binding are highly conserved across pathogenic and non-pathogenic strains. Binding of pathogenic bacteria to CD14 lead to reduced dendritic cell migration and blunted expression of co-stimulatory molecules, both rate-limiting factors of T cell activation. While defining an active molecular mechanism of immune evasion by pathogens, the interaction between FimH and CD14 represents a potential target to interfere with persistent and recurrent infections, such as urinary tract infections or Crohn’s disease. acknowledged_ssus: - _id: Bio - _id: PreCl - _id: EM-Fac acknowledgement: We thank Ulrich Dobrindt for providing UPEC strain CFT073, Vlad Gavra and Maximilian Götz, Bor Kavčič, Jonna Alanko and Eva Kiermaier for help with experiments and Robert Hauschild, Julian Stopp and Saren Tasciyan for help with data analysis. We thank the IST Austria Scientific Service Units, especially the Bioimaging facility, the Preclinical facility and the Electron microscopy facility for technical support, Jakob Wallner and all members of the Guet and Sixt lab for fruitful discussions and Daria Siekhaus for critically reading the manuscript. This work was supported by grants from the Austrian Research Promotion Agency (FEMtech 868984) to I.G., the European Research Council (CoG 724373) and the Austrian Science Fund (FWF P29911) to M.S. article_processing_charge: No author: - first_name: Kathrin full_name: Tomasek, Kathrin id: 3AEC8556-F248-11E8-B48F-1D18A9856A87 last_name: Tomasek orcid: 0000-0003-3768-877X - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Ivana full_name: Glatzová, Ivana id: 727b3c7d-4939-11ec-89b3-b9b0750ab74d last_name: Glatzová - first_name: Michael S. full_name: Lukesch, Michael S. last_name: Lukesch - first_name: Calin C full_name: Guet, Calin C id: 47F8433E-F248-11E8-B48F-1D18A9856A87 last_name: Guet orcid: 0000-0001-6220-2052 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-4561-241X citation: ama: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. bioRxiv. doi:10.1101/2021.10.18.464770 apa: Tomasek, K., Leithner, A. F., Glatzová, I., Lukesch, M. S., Guet, C. C., & Sixt, M. K. (n.d.). Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. bioRxiv. Cold Spring Harbor Laboratory. https://doi.org/10.1101/2021.10.18.464770 chicago: Tomasek, Kathrin, Alexander F Leithner, Ivana Glatzová, Michael S. Lukesch, Calin C Guet, and Michael K Sixt. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack the Host Immune Response by Binding to CD14.” BioRxiv. Cold Spring Harbor Laboratory, n.d. https://doi.org/10.1101/2021.10.18.464770. ieee: K. Tomasek, A. F. Leithner, I. Glatzová, M. S. Lukesch, C. C. Guet, and M. K. Sixt, “Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14,” bioRxiv. Cold Spring Harbor Laboratory. ista: Tomasek K, Leithner AF, Glatzová I, Lukesch MS, Guet CC, Sixt MK. Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14. bioRxiv, 10.1101/2021.10.18.464770. mla: Tomasek, Kathrin, et al. “Type 1 Piliated Uropathogenic Escherichia Coli Hijack the Host Immune Response by Binding to CD14.” BioRxiv, Cold Spring Harbor Laboratory, doi:10.1101/2021.10.18.464770. short: K. Tomasek, A.F. Leithner, I. Glatzová, M.S. Lukesch, C.C. Guet, M.K. Sixt, BioRxiv (n.d.). date_created: 2021-11-19T12:24:16Z date_published: 2021-10-18T00:00:00Z date_updated: 2024-03-27T23:30:35Z day: '18' department: - _id: CaGu - _id: MiSi doi: 10.1101/2021.10.18.464770 ec_funded: 1 language: - iso: eng main_file_link: - open_access: '1' url: https://www.biorxiv.org/content/10.1101/2021.10.18.464770v1 month: '10' oa: 1 oa_version: Preprint project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 26018E70-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29911 name: Mechanical adaptation of lamellipodial actin publication: bioRxiv publication_status: submitted publisher: Cold Spring Harbor Laboratory related_material: record: - id: '11843' relation: later_version status: public - id: '10307' relation: dissertation_contains status: public status: public title: Type 1 piliated uropathogenic Escherichia coli hijack the host immune response by binding to CD14 type: preprint user_id: 8b945eb4-e2f2-11eb-945a-df72226e66a9 year: '2021' ... --- _id: '7234' abstract: - lang: eng text: T lymphocytes utilize amoeboid migration to navigate effectively within complex microenvironments. The precise rearrangement of the actin cytoskeleton required for cellular forward propulsion is mediated by actin regulators, including the actin‐related protein 2/3 (Arp2/3) complex, a macromolecular machine that nucleates branched actin filaments at the leading edge. The consequences of modulating Arp2/3 activity on the biophysical properties of the actomyosin cortex and downstream T cell function are incompletely understood. We report that even a moderate decrease of Arp3 levels in T cells profoundly affects actin cortex integrity. Reduction in total F‐actin content leads to reduced cortical tension and disrupted lamellipodia formation. Instead, in Arp3‐knockdown cells, the motility mode is dominated by blebbing migration characterized by transient, balloon‐like protrusions at the leading edge. Although this migration mode seems to be compatible with interstitial migration in three‐dimensional environments, diminished locomotion kinetics and impaired cytotoxicity interfere with optimal T cell function. These findings define the importance of finely tuned, Arp2/3‐dependent mechanophysical membrane integrity in cytotoxic effector T lymphocyte activities. article_processing_charge: No article_type: original author: - first_name: Peyman full_name: Obeidy, Peyman last_name: Obeidy - first_name: Lining A. full_name: Ju, Lining A. last_name: Ju - first_name: Stefan H. full_name: Oehlers, Stefan H. last_name: Oehlers - first_name: Nursafwana S. full_name: Zulkhernain, Nursafwana S. last_name: Zulkhernain - first_name: Quintin full_name: Lee, Quintin last_name: Lee - first_name: Jorge L. full_name: Galeano Niño, Jorge L. last_name: Galeano Niño - first_name: Rain Y.Q. full_name: Kwan, Rain Y.Q. last_name: Kwan - first_name: Shweta full_name: Tikoo, Shweta last_name: Tikoo - first_name: Lois L. full_name: Cavanagh, Lois L. last_name: Cavanagh - first_name: Paulus full_name: Mrass, Paulus last_name: Mrass - first_name: Adam J.L. full_name: Cook, Adam J.L. last_name: Cook - first_name: Shaun P. full_name: Jackson, Shaun P. last_name: Jackson - first_name: Maté full_name: Biro, Maté last_name: Biro - first_name: Ben full_name: Roediger, Ben last_name: Roediger - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Wolfgang full_name: Weninger, Wolfgang last_name: Weninger citation: ama: Obeidy P, Ju LA, Oehlers SH, et al. Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes. Immunology and Cell Biology. 2020;98(2):93-113. doi:10.1111/imcb.12304 apa: Obeidy, P., Ju, L. A., Oehlers, S. H., Zulkhernain, N. S., Lee, Q., Galeano Niño, J. L., … Weninger, W. (2020). Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes. Immunology and Cell Biology. Wiley. https://doi.org/10.1111/imcb.12304 chicago: Obeidy, Peyman, Lining A. Ju, Stefan H. Oehlers, Nursafwana S. Zulkhernain, Quintin Lee, Jorge L. Galeano Niño, Rain Y.Q. Kwan, et al. “Partial Loss of Actin Nucleator Actin-Related Protein 2/3 Activity Triggers Blebbing in Primary T Lymphocytes.” Immunology and Cell Biology. Wiley, 2020. https://doi.org/10.1111/imcb.12304. ieee: P. Obeidy et al., “Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes,” Immunology and Cell Biology, vol. 98, no. 2. Wiley, pp. 93–113, 2020. ista: Obeidy P, Ju LA, Oehlers SH, Zulkhernain NS, Lee Q, Galeano Niño JL, Kwan RYQ, Tikoo S, Cavanagh LL, Mrass P, Cook AJL, Jackson SP, Biro M, Roediger B, Sixt MK, Weninger W. 2020. Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes. Immunology and Cell Biology. 98(2), 93–113. mla: Obeidy, Peyman, et al. “Partial Loss of Actin Nucleator Actin-Related Protein 2/3 Activity Triggers Blebbing in Primary T Lymphocytes.” Immunology and Cell Biology, vol. 98, no. 2, Wiley, 2020, pp. 93–113, doi:10.1111/imcb.12304. short: P. Obeidy, L.A. Ju, S.H. Oehlers, N.S. Zulkhernain, Q. Lee, J.L. Galeano Niño, R.Y.Q. Kwan, S. Tikoo, L.L. Cavanagh, P. Mrass, A.J.L. Cook, S.P. Jackson, M. Biro, B. Roediger, M.K. Sixt, W. Weninger, Immunology and Cell Biology 98 (2020) 93–113. date_created: 2020-01-05T23:00:48Z date_published: 2020-02-01T00:00:00Z date_updated: 2023-08-17T14:21:12Z day: '01' ddc: - '570' department: - _id: MiSi doi: 10.1111/imcb.12304 external_id: isi: - '000503885600001' pmid: - '31698518' file: - access_level: open_access checksum: c389477b4b52172ef76afff8a06c6775 content_type: application/pdf creator: dernst date_created: 2020-11-19T11:22:33Z date_updated: 2020-11-19T11:22:33Z file_id: '8775' file_name: 2020_ImmunologyCellBio_Obeidy.pdf file_size: 8569945 relation: main_file success: 1 file_date_updated: 2020-11-19T11:22:33Z has_accepted_license: '1' intvolume: ' 98' isi: 1 issue: '2' language: - iso: eng month: '02' oa: 1 oa_version: Published Version page: 93-113 pmid: 1 publication: Immunology and Cell Biology publication_identifier: eissn: - '14401711' issn: - '08189641' publication_status: published publisher: Wiley quality_controlled: '1' scopus_import: '1' status: public title: Partial loss of actin nucleator actin-related protein 2/3 activity triggers blebbing in primary T lymphocytes tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 98 year: '2020' ... --- _id: '7623' abstract: - lang: eng text: A two-dimensional mathematical model for cells migrating without adhesion capabilities is presented and analyzed. Cells are represented by their cortex, which is modeled as an elastic curve, subject to an internal pressure force. Net polymerization or depolymerization in the cortex is modeled via local addition or removal of material, driving a cortical flow. The model takes the form of a fully nonlinear degenerate parabolic system. An existence analysis is carried out by adapting ideas from the theory of gradient flows. Numerical simulations show that these simple rules can account for the behavior observed in experiments, suggesting a possible mechanical mechanism for adhesion-independent motility. acknowledgement: This work has been supported by the Vienna Science and Technology Fund, Grant no. LS13-029. G.J. and C.S. also acknowledge support by the Austrian Science Fund, Grants no. W1245, F 65, and W1261, as well as by the Fondation Sciences Mathématiques de Paris, and by Paris-Sciences-et-Lettres. article_processing_charge: No article_type: original author: - first_name: Gaspard full_name: Jankowiak, Gaspard last_name: Jankowiak - first_name: Diane full_name: Peurichard, Diane last_name: Peurichard - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Christian full_name: Schmeiser, Christian last_name: Schmeiser - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Jankowiak G, Peurichard D, Reversat A, Schmeiser C, Sixt MK. Modeling adhesion-independent cell migration. Mathematical Models and Methods in Applied Sciences. 2020;30(3):513-537. doi:10.1142/S021820252050013X apa: Jankowiak, G., Peurichard, D., Reversat, A., Schmeiser, C., & Sixt, M. K. (2020). Modeling adhesion-independent cell migration. Mathematical Models and Methods in Applied Sciences. World Scientific. https://doi.org/10.1142/S021820252050013X chicago: Jankowiak, Gaspard, Diane Peurichard, Anne Reversat, Christian Schmeiser, and Michael K Sixt. “Modeling Adhesion-Independent Cell Migration.” Mathematical Models and Methods in Applied Sciences. World Scientific, 2020. https://doi.org/10.1142/S021820252050013X. ieee: G. Jankowiak, D. Peurichard, A. Reversat, C. Schmeiser, and M. K. Sixt, “Modeling adhesion-independent cell migration,” Mathematical Models and Methods in Applied Sciences, vol. 30, no. 3. World Scientific, pp. 513–537, 2020. ista: Jankowiak G, Peurichard D, Reversat A, Schmeiser C, Sixt MK. 2020. Modeling adhesion-independent cell migration. Mathematical Models and Methods in Applied Sciences. 30(3), 513–537. mla: Jankowiak, Gaspard, et al. “Modeling Adhesion-Independent Cell Migration.” Mathematical Models and Methods in Applied Sciences, vol. 30, no. 3, World Scientific, 2020, pp. 513–37, doi:10.1142/S021820252050013X. short: G. Jankowiak, D. Peurichard, A. Reversat, C. Schmeiser, M.K. Sixt, Mathematical Models and Methods in Applied Sciences 30 (2020) 513–537. date_created: 2020-03-31T11:25:05Z date_published: 2020-03-18T00:00:00Z date_updated: 2023-08-18T10:18:56Z day: '18' department: - _id: MiSi doi: 10.1142/S021820252050013X external_id: arxiv: - '1903.09426' isi: - '000525349900003' intvolume: ' 30' isi: 1 issue: '3' language: - iso: eng main_file_link: - open_access: '1' url: https://arxiv.org/abs/1903.09426 month: '03' oa: 1 oa_version: Preprint page: 513-537 project: - _id: 25AD6156-B435-11E9-9278-68D0E5697425 grant_number: LS13-029 name: Modeling of Polarization and Motility of Leukocytes in Three-Dimensional Environments publication: Mathematical Models and Methods in Applied Sciences publication_identifier: issn: - '02182025' publication_status: published publisher: World Scientific quality_controlled: '1' scopus_import: '1' status: public title: Modeling adhesion-independent cell migration type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 30 year: '2020' ... --- _id: '7875' abstract: - lang: eng text: 'Cells navigating through complex tissues face a fundamental challenge: while multiple protrusions explore different paths, the cell needs to avoid entanglement. How a cell surveys and then corrects its own shape is poorly understood. Here, we demonstrate that spatially distinct microtubule dynamics regulate amoeboid cell migration by locally promoting the retraction of protrusions. In migrating dendritic cells, local microtubule depolymerization within protrusions remote from the microtubule organizing center triggers actomyosin contractility controlled by RhoA and its exchange factor Lfc. Depletion of Lfc leads to aberrant myosin localization, thereby causing two effects that rate-limit locomotion: (1) impaired cell edge coordination during path finding and (2) defective adhesion resolution. Compromised shape control is particularly hindering in geometrically complex microenvironments, where it leads to entanglement and ultimately fragmentation of the cell body. We thus demonstrate that microtubules can act as a proprioceptive device: they sense cell shape and control actomyosin retraction to sustain cellular coherence.' acknowledged_ssus: - _id: LifeSc - _id: Bio - _id: PreCl acknowledgement: "The authors thank the Scientific Service Units (Life Sciences, Bioimaging, Preclinical) of the Institute of Science and Technology Austria for excellent support. This work was funded by the European Research Council (ERC StG 281556 and CoG 724373), two grants from the Austrian\r\nScience Fund (FWF; P29911 and DK Nanocell W1250-B20 to M. Sixt) and by the German Research Foundation (DFG SFB1032 project B09) to O. Thorn-Seshold and D. Trauner. J. Renkawitz was supported by ISTFELLOW funding from the People Program (Marie Curie Actions) of the European Union’s Seventh Framework Programme (FP7/2007-2013) under the Research Executive Agency grant agreement (291734) and a European Molecular Biology Organization long-term fellowship (ALTF 1396-2014) co-funded by the European Commission (LTFCOFUND2013, GA-2013-609409), E. Kiermaier by the Deutsche Forschungsgemeinschaft (DFG, German Research Foundation) under Germany’s Excellence Strategy—EXC 2151—390873048, and H. Hacker by the American Lebanese Syrian Associated ¨Charities. K.-D. Fischer was supported by the Analysis, Imaging and Modelling of Neuronal and Inflammatory Processes graduate school funded by the Ministry of Economics, Science, and Digitisation of the State Saxony-Anhalt and by the European Funds for Social and Regional Development." article_number: e201907154 article_processing_charge: No article_type: original author: - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Irute full_name: Girkontaite, Irute last_name: Girkontaite - first_name: Kerry full_name: Tedford, Kerry last_name: Tedford - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Oliver full_name: Thorn-Seshold, Oliver last_name: Thorn-Seshold - first_name: Dirk full_name: Trauner, Dirk id: E8F27F48-3EBA-11E9-92A1-B709E6697425 last_name: Trauner - first_name: Hans full_name: Häcker, Hans last_name: Häcker - first_name: Klaus Dieter full_name: Fischer, Klaus Dieter last_name: Fischer - first_name: Eva full_name: Kiermaier, Eva id: 3EB04B78-F248-11E8-B48F-1D18A9856A87 last_name: Kiermaier orcid: 0000-0001-6165-5738 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Kopf A, Renkawitz J, Hauschild R, et al. Microtubules control cellular shape and coherence in amoeboid migrating cells. The Journal of Cell Biology. 2020;219(6). doi:10.1083/jcb.201907154 apa: Kopf, A., Renkawitz, J., Hauschild, R., Girkontaite, I., Tedford, K., Merrin, J., … Sixt, M. K. (2020). Microtubules control cellular shape and coherence in amoeboid migrating cells. The Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201907154 chicago: Kopf, Aglaja, Jörg Renkawitz, Robert Hauschild, Irute Girkontaite, Kerry Tedford, Jack Merrin, Oliver Thorn-Seshold, et al. “Microtubules Control Cellular Shape and Coherence in Amoeboid Migrating Cells.” The Journal of Cell Biology. Rockefeller University Press, 2020. https://doi.org/10.1083/jcb.201907154. ieee: A. Kopf et al., “Microtubules control cellular shape and coherence in amoeboid migrating cells,” The Journal of Cell Biology, vol. 219, no. 6. Rockefeller University Press, 2020. ista: Kopf A, Renkawitz J, Hauschild R, Girkontaite I, Tedford K, Merrin J, Thorn-Seshold O, Trauner D, Häcker H, Fischer KD, Kiermaier E, Sixt MK. 2020. Microtubules control cellular shape and coherence in amoeboid migrating cells. The Journal of Cell Biology. 219(6), e201907154. mla: Kopf, Aglaja, et al. “Microtubules Control Cellular Shape and Coherence in Amoeboid Migrating Cells.” The Journal of Cell Biology, vol. 219, no. 6, e201907154, Rockefeller University Press, 2020, doi:10.1083/jcb.201907154. short: A. Kopf, J. Renkawitz, R. Hauschild, I. Girkontaite, K. Tedford, J. Merrin, O. Thorn-Seshold, D. Trauner, H. Häcker, K.D. Fischer, E. Kiermaier, M.K. Sixt, The Journal of Cell Biology 219 (2020). date_created: 2020-05-24T22:00:56Z date_published: 2020-06-01T00:00:00Z date_updated: 2023-08-21T06:28:17Z day: '01' ddc: - '570' department: - _id: MiSi - _id: Bio - _id: NanoFab doi: 10.1083/jcb.201907154 ec_funded: 1 external_id: isi: - '000538141100020' pmid: - '32379884' file: - access_level: open_access checksum: cb0b9c77842ae1214caade7b77e4d82d content_type: application/pdf creator: dernst date_created: 2020-11-24T13:25:13Z date_updated: 2020-11-24T13:25:13Z file_id: '8801' file_name: 2020_JCellBiol_Kopf.pdf file_size: 7536712 relation: main_file success: 1 file_date_updated: 2020-11-24T13:25:13Z has_accepted_license: '1' intvolume: ' 219' isi: 1 issue: '6' language: - iso: eng month: '06' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 26018E70-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29911 name: Mechanical adaptation of lamellipodial actin - _id: 252C3B08-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: W 1250-B20 name: Nano-Analytics of Cellular Systems - _id: 25681D80-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '291734' name: International IST Postdoc Fellowship Programme - _id: 25A48D24-B435-11E9-9278-68D0E5697425 grant_number: ALTF 1396-2014 name: Molecular and system level view of immune cell migration publication: The Journal of Cell Biology publication_identifier: eissn: - 1540-8140 publication_status: published publisher: Rockefeller University Press quality_controlled: '1' scopus_import: '1' status: public title: Microtubules control cellular shape and coherence in amoeboid migrating cells tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 219 year: '2020' ... --- _id: '7876' abstract: - lang: eng text: 'In contrast to lymph nodes, the lymphoid regions of the spleen—the white pulp—are located deep within the organ, yielding the trafficking paths of T cells in the white pulp largely invisible. In an intravital microscopy tour de force reported in this issue of Immunity, Chauveau et al. show that T cells perform unidirectional, perivascular migration through the enigmatic marginal zone bridging channels. ' article_processing_charge: No article_type: original author: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Tim full_name: Lämmermann, Tim last_name: Lämmermann citation: ama: 'Sixt MK, Lämmermann T. T cells: Bridge-and-channel commute to the white pulp. Immunity. 2020;52(5):721-723. doi:10.1016/j.immuni.2020.04.020' apa: 'Sixt, M. K., & Lämmermann, T. (2020). T cells: Bridge-and-channel commute to the white pulp. Immunity. Elsevier. https://doi.org/10.1016/j.immuni.2020.04.020' chicago: 'Sixt, Michael K, and Tim Lämmermann. “T Cells: Bridge-and-Channel Commute to the White Pulp.” Immunity. Elsevier, 2020. https://doi.org/10.1016/j.immuni.2020.04.020.' ieee: 'M. K. Sixt and T. Lämmermann, “T cells: Bridge-and-channel commute to the white pulp,” Immunity, vol. 52, no. 5. Elsevier, pp. 721–723, 2020.' ista: 'Sixt MK, Lämmermann T. 2020. T cells: Bridge-and-channel commute to the white pulp. Immunity. 52(5), 721–723.' mla: 'Sixt, Michael K., and Tim Lämmermann. “T Cells: Bridge-and-Channel Commute to the White Pulp.” Immunity, vol. 52, no. 5, Elsevier, 2020, pp. 721–23, doi:10.1016/j.immuni.2020.04.020.' short: M.K. Sixt, T. Lämmermann, Immunity 52 (2020) 721–723. date_created: 2020-05-24T22:00:57Z date_published: 2020-05-19T00:00:00Z date_updated: 2023-08-21T06:27:18Z day: '19' department: - _id: MiSi doi: 10.1016/j.immuni.2020.04.020 external_id: isi: - '000535371100002' intvolume: ' 52' isi: 1 issue: '5' language: - iso: eng main_file_link: - open_access: '1' url: https://pure.mpg.de/pubman/item/item_3265599_2/component/file_3265620/Sixt%20et%20al..pdf month: '05' oa: 1 oa_version: Published Version page: 721-723 publication: Immunity publication_identifier: eissn: - '10974180' issn: - '10747613' publication_status: published publisher: Elsevier quality_controlled: '1' scopus_import: '1' status: public title: 'T cells: Bridge-and-channel commute to the white pulp' type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 52 year: '2020' ... --- _id: '7909' abstract: - lang: eng text: Cell migration entails networks and bundles of actin filaments termed lamellipodia and microspikes or filopodia, respectively, as well as focal adhesions, all of which recruit Ena/VASP family members hitherto thought to antagonize efficient cell motility. However, we find these proteins to act as positive regulators of migration in different murine cell lines. CRISPR/Cas9-mediated loss of Ena/VASP proteins reduced lamellipodial actin assembly and perturbed lamellipodial architecture, as evidenced by changed network geometry as well as reduction of filament length and number that was accompanied by abnormal Arp2/3 complex and heterodimeric capping protein accumulation. Loss of Ena/VASP function also abolished the formation of microspikes normally embedded in lamellipodia, but not of filopodia capable of emanating without lamellipodia. Ena/VASP-deficiency also impaired integrin-mediated adhesion accompanied by reduced traction forces exerted through these structures. Our data thus uncover novel Ena/VASP functions of these actin polymerases that are fully consistent with their promotion of cell migration. article_number: e55351 article_processing_charge: No article_type: original author: - first_name: Julia full_name: Damiano-Guercio, Julia last_name: Damiano-Guercio - first_name: Laëtitia full_name: Kurzawa, Laëtitia last_name: Kurzawa - first_name: Jan full_name: Müller, Jan id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D last_name: Müller - first_name: Georgi A full_name: Dimchev, Georgi A id: 38C393BE-F248-11E8-B48F-1D18A9856A87 last_name: Dimchev orcid: 0000-0001-8370-6161 - first_name: Matthias full_name: Schaks, Matthias last_name: Schaks - first_name: Maria full_name: Nemethova, Maria id: 34E27F1C-F248-11E8-B48F-1D18A9856A87 last_name: Nemethova - first_name: Thomas full_name: Pokrant, Thomas last_name: Pokrant - first_name: Stefan full_name: Brühmann, Stefan last_name: Brühmann - first_name: Joern full_name: Linkner, Joern last_name: Linkner - first_name: Laurent full_name: Blanchoin, Laurent last_name: Blanchoin - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner - first_name: Jan full_name: Faix, Jan last_name: Faix citation: ama: Damiano-Guercio J, Kurzawa L, Müller J, et al. Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent adhesion. eLife. 2020;9. doi:10.7554/eLife.55351 apa: Damiano-Guercio, J., Kurzawa, L., Müller, J., Dimchev, G. A., Schaks, M., Nemethova, M., … Faix, J. (2020). Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent adhesion. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.55351 chicago: Damiano-Guercio, Julia, Laëtitia Kurzawa, Jan Müller, Georgi A Dimchev, Matthias Schaks, Maria Nemethova, Thomas Pokrant, et al. “Loss of Ena/VASP Interferes with Lamellipodium Architecture, Motility and Integrin-Dependent Adhesion.” ELife. eLife Sciences Publications, 2020. https://doi.org/10.7554/eLife.55351. ieee: J. Damiano-Guercio et al., “Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent adhesion,” eLife, vol. 9. eLife Sciences Publications, 2020. ista: Damiano-Guercio J, Kurzawa L, Müller J, Dimchev GA, Schaks M, Nemethova M, Pokrant T, Brühmann S, Linkner J, Blanchoin L, Sixt MK, Rottner K, Faix J. 2020. Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent adhesion. eLife. 9, e55351. mla: Damiano-Guercio, Julia, et al. “Loss of Ena/VASP Interferes with Lamellipodium Architecture, Motility and Integrin-Dependent Adhesion.” ELife, vol. 9, e55351, eLife Sciences Publications, 2020, doi:10.7554/eLife.55351. short: J. Damiano-Guercio, L. Kurzawa, J. Müller, G.A. Dimchev, M. Schaks, M. Nemethova, T. Pokrant, S. Brühmann, J. Linkner, L. Blanchoin, M.K. Sixt, K. Rottner, J. Faix, ELife 9 (2020). date_created: 2020-05-31T22:00:49Z date_published: 2020-05-11T00:00:00Z date_updated: 2023-08-21T06:32:25Z day: '11' ddc: - '570' department: - _id: MiSi doi: 10.7554/eLife.55351 ec_funded: 1 external_id: isi: - '000537208000001' file: - access_level: open_access checksum: d33bd4441b9a0195718ce1ba5d2c48a6 content_type: application/pdf creator: dernst date_created: 2020-06-02T10:35:37Z date_updated: 2020-07-14T12:48:05Z file_id: '7914' file_name: 2020_eLife_Damiano_Guercio.pdf file_size: 10535713 relation: main_file file_date_updated: 2020-07-14T12:48:05Z has_accepted_license: '1' intvolume: ' 9' isi: 1 language: - iso: eng month: '05' oa: 1 oa_version: Published Version project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients publication: eLife publication_identifier: eissn: - 2050084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Loss of Ena/VASP interferes with lamellipodium architecture, motility and integrin-dependent adhesion tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 9 year: '2020' ... --- _id: '8132' abstract: - lang: eng text: The WAVE regulatory complex (WRC) is crucial for assembly of the peripheral branched actin network constituting one of the main drivers of eukaryotic cell migration. Here, we uncover an essential role of the hematopoietic-specific WRC component HEM1 for immune cell development. Germline-encoded HEM1 deficiency underlies an inborn error of immunity with systemic autoimmunity, at cellular level marked by WRC destabilization, reduced filamentous actin, and failure to assemble lamellipodia. Hem1−/− mice display systemic autoimmunity, phenocopying the human disease. In the absence of Hem1, B cells become deprived of extracellular stimuli necessary to maintain the strength of B cell receptor signaling at a level permissive for survival of non-autoreactive B cells. This shifts the balance of B cell fate choices toward autoreactive B cells and thus autoimmunity. article_number: eabc3979 article_processing_charge: No article_type: original author: - first_name: Elisabeth full_name: Salzer, Elisabeth last_name: Salzer - first_name: Samaneh full_name: Zoghi, Samaneh last_name: Zoghi - first_name: Máté G. full_name: Kiss, Máté G. last_name: Kiss - first_name: Frieda full_name: Kage, Frieda last_name: Kage - first_name: Christina full_name: Rashkova, Christina last_name: Rashkova - first_name: Stephanie full_name: Stahnke, Stephanie last_name: Stahnke - first_name: Matthias full_name: Haimel, Matthias last_name: Haimel - first_name: René full_name: Platzer, René last_name: Platzer - first_name: Michael full_name: Caldera, Michael last_name: Caldera - first_name: Rico Chandra full_name: Ardy, Rico Chandra last_name: Ardy - first_name: Birgit full_name: Hoeger, Birgit last_name: Hoeger - first_name: Jana full_name: Block, Jana last_name: Block - first_name: David full_name: Medgyesi, David last_name: Medgyesi - first_name: Celine full_name: Sin, Celine last_name: Sin - first_name: Sepideh full_name: Shahkarami, Sepideh last_name: Shahkarami - first_name: Renate full_name: Kain, Renate last_name: Kain - first_name: Vahid full_name: Ziaee, Vahid last_name: Ziaee - first_name: Peter full_name: Hammerl, Peter last_name: Hammerl - first_name: Christoph full_name: Bock, Christoph last_name: Bock - first_name: Jörg full_name: Menche, Jörg last_name: Menche - first_name: Loïc full_name: Dupré, Loïc last_name: Dupré - first_name: Johannes B. full_name: Huppa, Johannes B. last_name: Huppa - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Alexis full_name: Lomakin, Alexis last_name: Lomakin - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner - first_name: Christoph J. full_name: Binder, Christoph J. last_name: Binder - first_name: Theresia E.B. full_name: Stradal, Theresia E.B. last_name: Stradal - first_name: Nima full_name: Rezaei, Nima last_name: Rezaei - first_name: Kaan full_name: Boztug, Kaan last_name: Boztug citation: ama: Salzer E, Zoghi S, Kiss MG, et al. The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity. Science Immunology. 2020;5(49). doi:10.1126/sciimmunol.abc3979 apa: Salzer, E., Zoghi, S., Kiss, M. G., Kage, F., Rashkova, C., Stahnke, S., … Boztug, K. (2020). The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity. Science Immunology. AAAS. https://doi.org/10.1126/sciimmunol.abc3979 chicago: Salzer, Elisabeth, Samaneh Zoghi, Máté G. Kiss, Frieda Kage, Christina Rashkova, Stephanie Stahnke, Matthias Haimel, et al. “The Cytoskeletal Regulator HEM1 Governs B Cell Development and Prevents Autoimmunity.” Science Immunology. AAAS, 2020. https://doi.org/10.1126/sciimmunol.abc3979. ieee: E. Salzer et al., “The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity,” Science Immunology, vol. 5, no. 49. AAAS, 2020. ista: Salzer E, Zoghi S, Kiss MG, Kage F, Rashkova C, Stahnke S, Haimel M, Platzer R, Caldera M, Ardy RC, Hoeger B, Block J, Medgyesi D, Sin C, Shahkarami S, Kain R, Ziaee V, Hammerl P, Bock C, Menche J, Dupré L, Huppa JB, Sixt MK, Lomakin A, Rottner K, Binder CJ, Stradal TEB, Rezaei N, Boztug K. 2020. The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity. Science Immunology. 5(49), eabc3979. mla: Salzer, Elisabeth, et al. “The Cytoskeletal Regulator HEM1 Governs B Cell Development and Prevents Autoimmunity.” Science Immunology, vol. 5, no. 49, eabc3979, AAAS, 2020, doi:10.1126/sciimmunol.abc3979. short: E. Salzer, S. Zoghi, M.G. Kiss, F. Kage, C. Rashkova, S. Stahnke, M. Haimel, R. Platzer, M. Caldera, R.C. Ardy, B. Hoeger, J. Block, D. Medgyesi, C. Sin, S. Shahkarami, R. Kain, V. Ziaee, P. Hammerl, C. Bock, J. Menche, L. Dupré, J.B. Huppa, M.K. Sixt, A. Lomakin, K. Rottner, C.J. Binder, T.E.B. Stradal, N. Rezaei, K. Boztug, Science Immunology 5 (2020). date_created: 2020-07-19T22:00:58Z date_published: 2020-07-10T00:00:00Z date_updated: 2023-08-22T07:56:04Z day: '10' department: - _id: MiSi doi: 10.1126/sciimmunol.abc3979 external_id: isi: - '000546994600004' pmid: - '32646852' intvolume: ' 5' isi: 1 issue: '49' language: - iso: eng month: '07' oa_version: None pmid: 1 publication: Science Immunology publication_identifier: eissn: - '24709468' publication_status: published publisher: AAAS quality_controlled: '1' scopus_import: '1' status: public title: The cytoskeletal regulator HEM1 governs B cell development and prevents autoimmunity type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 5 year: '2020' ... --- _id: '8142' abstract: - lang: eng text: Cell production and differentiation for the acquisition of specific functions are key features of living systems. The dynamic network of cellular microtubules provides the necessary platform to accommodate processes associated with the transition of cells through the individual phases of cytogenesis. Here, we show that the plant hormone cytokinin fine‐tunes the activity of the microtubular cytoskeleton during cell differentiation and counteracts microtubular rearrangements driven by the hormone auxin. The endogenous upward gradient of cytokinin activity along the longitudinal growth axis in Arabidopsis thaliana roots correlates with robust rearrangements of the microtubule cytoskeleton in epidermal cells progressing from the proliferative to the differentiation stage. Controlled increases in cytokinin activity result in premature re‐organization of the microtubule network from transversal to an oblique disposition in cells prior to their differentiation, whereas attenuated hormone perception delays cytoskeleton conversion into a configuration typical for differentiated cells. Intriguingly, cytokinin can interfere with microtubules also in animal cells, such as leukocytes, suggesting that a cytokinin‐sensitive control pathway for the microtubular cytoskeleton may be at least partially conserved between plant and animal cells. acknowledged_ssus: - _id: Bio - _id: LifeSc acknowledgement: We thank Takashi Aoyama, David Alabadi, and Bert De Rybel for sharing material, Jiří Friml, Maciek Adamowski, and Katerina Schwarzerová for inspiring discussions, and Martine De Cock for help in preparing the manuscript. This research was supported by the Scientific Service Units (SSUs) of IST Austria through resources provided by the Bioimaging Facility (BIF), especially to Robert Hauschild; and the Life Science Facility (LSF). J.C.M. is the recipient of a EMBO Long‐Term Fellowship (ALTF number 710‐2016). This work was supported with MEYS CR, project no.CZ.02.1.01/0.0/0.0/16_019/0000738 to J.P., and by the Austrian Science Fund (FWF01_I1774S) to E.B. article_number: e104238 article_processing_charge: Yes (via OA deal) article_type: original author: - first_name: Juan C full_name: Montesinos López, Juan C id: 310A8E3E-F248-11E8-B48F-1D18A9856A87 last_name: Montesinos López orcid: 0000-0001-9179-6099 - first_name: A full_name: Abuzeineh, A last_name: Abuzeineh - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 - first_name: Alba full_name: Juanes Garcia, Alba id: 40F05888-F248-11E8-B48F-1D18A9856A87 last_name: Juanes Garcia orcid: 0000-0002-1009-9652 - first_name: Krisztina full_name: Ötvös, Krisztina id: 29B901B0-F248-11E8-B48F-1D18A9856A87 last_name: Ötvös orcid: 0000-0002-5503-4983 - first_name: J full_name: Petrášek, J last_name: Petrášek - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Eva full_name: Benková, Eva id: 38F4F166-F248-11E8-B48F-1D18A9856A87 last_name: Benková orcid: 0000-0002-8510-9739 citation: ama: Montesinos López JC, Abuzeineh A, Kopf A, et al. Phytohormone cytokinin guides microtubule dynamics during cell progression from proliferative to differentiated stage. The Embo Journal. 2020;39(17). doi:10.15252/embj.2019104238 apa: Montesinos López, J. C., Abuzeineh, A., Kopf, A., Juanes Garcia, A., Ötvös, K., Petrášek, J., … Benková, E. (2020). Phytohormone cytokinin guides microtubule dynamics during cell progression from proliferative to differentiated stage. The Embo Journal. Embo Press. https://doi.org/10.15252/embj.2019104238 chicago: Montesinos López, Juan C, A Abuzeineh, Aglaja Kopf, Alba Juanes Garcia, Krisztina Ötvös, J Petrášek, Michael K Sixt, and Eva Benková. “Phytohormone Cytokinin Guides Microtubule Dynamics during Cell Progression from Proliferative to Differentiated Stage.” The Embo Journal. Embo Press, 2020. https://doi.org/10.15252/embj.2019104238. ieee: J. C. Montesinos López et al., “Phytohormone cytokinin guides microtubule dynamics during cell progression from proliferative to differentiated stage,” The Embo Journal, vol. 39, no. 17. Embo Press, 2020. ista: Montesinos López JC, Abuzeineh A, Kopf A, Juanes Garcia A, Ötvös K, Petrášek J, Sixt MK, Benková E. 2020. Phytohormone cytokinin guides microtubule dynamics during cell progression from proliferative to differentiated stage. The Embo Journal. 39(17), e104238. mla: Montesinos López, Juan C., et al. “Phytohormone Cytokinin Guides Microtubule Dynamics during Cell Progression from Proliferative to Differentiated Stage.” The Embo Journal, vol. 39, no. 17, e104238, Embo Press, 2020, doi:10.15252/embj.2019104238. short: J.C. Montesinos López, A. Abuzeineh, A. Kopf, A. Juanes Garcia, K. Ötvös, J. Petrášek, M.K. Sixt, E. Benková, The Embo Journal 39 (2020). date_created: 2020-07-21T09:08:38Z date_published: 2020-09-01T00:00:00Z date_updated: 2023-09-05T13:05:47Z day: '01' ddc: - '580' department: - _id: MiSi - _id: EvBe doi: 10.15252/embj.2019104238 external_id: isi: - '000548311800001' pmid: - '32667089' file: - access_level: open_access checksum: 43d2b36598708e6ab05c69074e191d57 content_type: application/pdf creator: dernst date_created: 2020-12-02T09:13:23Z date_updated: 2020-12-02T09:13:23Z file_id: '8827' file_name: 2020_EMBO_Montesinos.pdf file_size: 3497156 relation: main_file success: 1 file_date_updated: 2020-12-02T09:13:23Z has_accepted_license: '1' intvolume: ' 39' isi: 1 issue: '17' language: - iso: eng month: '09' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 253E54C8-B435-11E9-9278-68D0E5697425 grant_number: ALTF710-2016 name: Molecular mechanism of auxindriven formative divisions delineating lateral root organogenesis in plants - _id: 2542D156-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: I 1774-B16 name: Hormone cross-talk drives nutrient dependent plant development publication: The Embo Journal publication_identifier: eissn: - 1460-2075 issn: - 0261-4189 publication_status: published publisher: Embo Press quality_controlled: '1' scopus_import: '1' status: public title: Phytohormone cytokinin guides microtubule dynamics during cell progression from proliferative to differentiated stage tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 39 year: '2020' ... --- _id: '7885' abstract: - lang: eng text: Eukaryotic cells migrate by coupling the intracellular force of the actin cytoskeleton to the environment. While force coupling is usually mediated by transmembrane adhesion receptors, especially those of the integrin family, amoeboid cells such as leukocytes can migrate extremely fast despite very low adhesive forces1. Here we show that leukocytes cannot only migrate under low adhesion but can also transmit forces in the complete absence of transmembrane force coupling. When confined within three-dimensional environments, they use the topographical features of the substrate to propel themselves. Here the retrograde flow of the actin cytoskeleton follows the texture of the substrate, creating retrograde shear forces that are sufficient to drive the cell body forwards. Notably, adhesion-dependent and adhesion-independent migration are not mutually exclusive, but rather are variants of the same principle of coupling retrograde actin flow to the environment and thus can potentially operate interchangeably and simultaneously. As adhesion-free migration is independent of the chemical composition of the environment, it renders cells completely autonomous in their locomotive behaviour. acknowledged_ssus: - _id: Bio - _id: LifeSc - _id: M-Shop acknowledgement: We thank A. Leithner and J. Renkawitz for discussion and critical reading of the manuscript; J. Schwarz and M. Mehling for establishing the microfluidic setups; the Bioimaging Facility of IST Austria for excellent support, as well as the Life Science Facility and the Miba Machine Shop of IST Austria; and F. N. Arslan, L. E. Burnett and L. Li for their work during their rotation in the IST PhD programme. This work was supported by the European Research Council (ERC StG 281556 and CoG 724373) to M.S. and grants from the Austrian Science Fund (FWF P29911) and the WWTF to M.S. M.H. was supported by the European Regional Development Fund Project (CZ.02.1.01/0.0/0.0/15_003/0000476). F.G. received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 747687. article_processing_charge: No article_type: original author: - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Florian R full_name: Gärtner, Florian R id: 397A88EE-F248-11E8-B48F-1D18A9856A87 last_name: Gärtner orcid: 0000-0001-6120-3723 - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Julian A full_name: Stopp, Julian A id: 489E3F00-F248-11E8-B48F-1D18A9856A87 last_name: Stopp - first_name: Saren full_name: Tasciyan, Saren id: 4323B49C-F248-11E8-B48F-1D18A9856A87 last_name: Tasciyan orcid: 0000-0003-1671-393X - first_name: Juan L full_name: Aguilera Servin, Juan L id: 2A67C376-F248-11E8-B48F-1D18A9856A87 last_name: Aguilera Servin orcid: 0000-0002-2862-8372 - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Matthieu full_name: Piel, Matthieu last_name: Piel - first_name: Andrew full_name: Callan-Jones, Andrew last_name: Callan-Jones - first_name: Raphael full_name: Voituriez, Raphael last_name: Voituriez - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Reversat A, Gärtner FR, Merrin J, et al. Cellular locomotion using environmental topography. Nature. 2020;582:582–585. doi:10.1038/s41586-020-2283-z apa: Reversat, A., Gärtner, F. R., Merrin, J., Stopp, J. A., Tasciyan, S., Aguilera Servin, J. L., … Sixt, M. K. (2020). Cellular locomotion using environmental topography. Nature. Springer Nature. https://doi.org/10.1038/s41586-020-2283-z chicago: Reversat, Anne, Florian R Gärtner, Jack Merrin, Julian A Stopp, Saren Tasciyan, Juan L Aguilera Servin, Ingrid de Vries, et al. “Cellular Locomotion Using Environmental Topography.” Nature. Springer Nature, 2020. https://doi.org/10.1038/s41586-020-2283-z. ieee: A. Reversat et al., “Cellular locomotion using environmental topography,” Nature, vol. 582. Springer Nature, pp. 582–585, 2020. ista: Reversat A, Gärtner FR, Merrin J, Stopp JA, Tasciyan S, Aguilera Servin JL, de Vries I, Hauschild R, Hons M, Piel M, Callan-Jones A, Voituriez R, Sixt MK. 2020. Cellular locomotion using environmental topography. Nature. 582, 582–585. mla: Reversat, Anne, et al. “Cellular Locomotion Using Environmental Topography.” Nature, vol. 582, Springer Nature, 2020, pp. 582–585, doi:10.1038/s41586-020-2283-z. short: A. Reversat, F.R. Gärtner, J. Merrin, J.A. Stopp, S. Tasciyan, J.L. Aguilera Servin, I. de Vries, R. Hauschild, M. Hons, M. Piel, A. Callan-Jones, R. Voituriez, M.K. Sixt, Nature 582 (2020) 582–585. date_created: 2020-05-24T22:01:01Z date_published: 2020-06-25T00:00:00Z date_updated: 2024-03-27T23:30:23Z day: '25' department: - _id: NanoFab - _id: Bio - _id: MiSi doi: 10.1038/s41586-020-2283-z ec_funded: 1 external_id: isi: - '000532688300008' intvolume: ' 582' isi: 1 language: - iso: eng month: '06' oa_version: None page: 582–585 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 26018E70-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29911 name: Mechanical adaptation of lamellipodial actin - _id: 260AA4E2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '747687' name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells publication: Nature publication_identifier: eissn: - '14764687' issn: - '00280836' publication_status: published publisher: Springer Nature quality_controlled: '1' related_material: link: - description: News on IST Homepage relation: press_release url: https://ist.ac.at/en/news/off-road-mode-enables-mobile-cells-to-move-freely/ record: - id: '14697' relation: dissertation_contains status: public - id: '12401' relation: dissertation_contains status: public scopus_import: '1' status: public title: Cellular locomotion using environmental topography type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 582 year: '2020' ... --- _id: '8190' article_number: e202007029 article_processing_charge: No article_type: letter_note author: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Anna full_name: Huttenlocher, Anna last_name: Huttenlocher citation: ama: 'Sixt MK, Huttenlocher A. Zena Werb (1945-2020): Cell biology in context. The Journal of Cell Biology. 2020;219(8). doi:10.1083/jcb.202007029' apa: 'Sixt, M. K., & Huttenlocher, A. (2020). Zena Werb (1945-2020): Cell biology in context. The Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.202007029' chicago: 'Sixt, Michael K, and Anna Huttenlocher. “Zena Werb (1945-2020): Cell Biology in Context.” The Journal of Cell Biology. Rockefeller University Press, 2020. https://doi.org/10.1083/jcb.202007029.' ieee: 'M. K. Sixt and A. Huttenlocher, “Zena Werb (1945-2020): Cell biology in context,” The Journal of Cell Biology, vol. 219, no. 8. Rockefeller University Press, 2020.' ista: 'Sixt MK, Huttenlocher A. 2020. Zena Werb (1945-2020): Cell biology in context. The Journal of Cell Biology. 219(8), e202007029.' mla: 'Sixt, Michael K., and Anna Huttenlocher. “Zena Werb (1945-2020): Cell Biology in Context.” The Journal of Cell Biology, vol. 219, no. 8, e202007029, Rockefeller University Press, 2020, doi:10.1083/jcb.202007029.' short: M.K. Sixt, A. Huttenlocher, The Journal of Cell Biology 219 (2020). date_created: 2020-08-02T22:00:57Z date_published: 2020-07-22T00:00:00Z date_updated: 2023-10-17T10:04:49Z day: '22' ddc: - '570' department: - _id: MiSi doi: 10.1083/jcb.202007029 external_id: isi: - '000573631000004' file: - access_level: open_access checksum: 30016d778d266b8e17d01094917873b8 content_type: application/pdf creator: dernst date_created: 2020-08-04T13:11:52Z date_updated: 2021-02-02T23:30:03Z embargo: 2021-02-01 file_id: '8200' file_name: 2020_JCB_Sixt.pdf file_size: 830725 relation: main_file file_date_updated: 2021-02-02T23:30:03Z has_accepted_license: '1' intvolume: ' 219' isi: 1 issue: '8' language: - iso: eng month: '07' oa: 1 oa_version: Published Version publication: The Journal of Cell Biology publication_identifier: eissn: - 1540-8140 publication_status: published publisher: Rockefeller University Press scopus_import: '1' status: public title: 'Zena Werb (1945-2020): Cell biology in context' tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 219 year: '2020' ... --- _id: '7009' abstract: - lang: eng text: Cell migration is essential for physiological processes as diverse as development, immune defence and wound healing. It is also a hallmark of cancer malignancy. Thousands of publications have elucidated detailed molecular and biophysical mechanisms of cultured cells migrating on flat, 2D substrates of glass and plastic. However, much less is known about how cells successfully navigate the complex 3D environments of living tissues. In these more complex, native environments, cells use multiple modes of migration, including mesenchymal, amoeboid, lobopodial and collective, and these are governed by the local extracellular microenvironment, specific modalities of Rho GTPase signalling and non- muscle myosin contractility. Migration through 3D environments is challenging because it requires the cell to squeeze through complex or dense extracellular structures. Doing so requires specific cellular adaptations to mechanical features of the extracellular matrix (ECM) or its remodelling. In addition, besides navigating through diverse ECM environments and overcoming extracellular barriers, cells often interact with neighbouring cells and tissues through physical and signalling interactions. Accordingly, cells need to call on an impressively wide diversity of mechanisms to meet these challenges. This Review examines how cells use both classical and novel mechanisms of locomotion as they traverse challenging 3D matrices and cellular environments. It focuses on principles rather than details of migratory mechanisms and draws comparisons between 1D, 2D and 3D migration. article_processing_charge: No article_type: review author: - first_name: KM full_name: Yamada, KM last_name: Yamada - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Yamada K, Sixt MK. Mechanisms of 3D cell migration. Nature Reviews Molecular Cell Biology. 2019;20(12):738–752. doi:10.1038/s41580-019-0172-9 apa: Yamada, K., & Sixt, M. K. (2019). Mechanisms of 3D cell migration. Nature Reviews Molecular Cell Biology. Springer Nature. https://doi.org/10.1038/s41580-019-0172-9 chicago: Yamada, KM, and Michael K Sixt. “Mechanisms of 3D Cell Migration.” Nature Reviews Molecular Cell Biology. Springer Nature, 2019. https://doi.org/10.1038/s41580-019-0172-9. ieee: K. Yamada and M. K. Sixt, “Mechanisms of 3D cell migration,” Nature Reviews Molecular Cell Biology, vol. 20, no. 12. Springer Nature, pp. 738–752, 2019. ista: Yamada K, Sixt MK. 2019. Mechanisms of 3D cell migration. Nature Reviews Molecular Cell Biology. 20(12), 738–752. mla: Yamada, KM, and Michael K. Sixt. “Mechanisms of 3D Cell Migration.” Nature Reviews Molecular Cell Biology, vol. 20, no. 12, Springer Nature, 2019, pp. 738–752, doi:10.1038/s41580-019-0172-9. short: K. Yamada, M.K. Sixt, Nature Reviews Molecular Cell Biology 20 (2019) 738–752. date_created: 2019-11-12T14:54:42Z date_published: 2019-12-01T00:00:00Z date_updated: 2023-08-30T07:22:20Z day: '01' department: - _id: MiSi doi: 10.1038/s41580-019-0172-9 external_id: isi: - '000497966900007' pmid: - '31582855' intvolume: ' 20' isi: 1 issue: '12' language: - iso: eng month: '12' oa_version: None page: 738–752 pmid: 1 publication: Nature Reviews Molecular Cell Biology publication_identifier: eissn: - 1471-0080 issn: - 1471-0072 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Mechanisms of 3D cell migration type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 20 year: '2019' ... --- _id: '6979' article_processing_charge: No article_type: original author: - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Kopf A, Sixt MK. Gut homeostasis: Active migration of intestinal epithelial cells in tissue renewal. Current Biology. 2019;29(20):R1091-R1093. doi:10.1016/j.cub.2019.08.068' apa: 'Kopf, A., & Sixt, M. K. (2019). Gut homeostasis: Active migration of intestinal epithelial cells in tissue renewal. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2019.08.068' chicago: 'Kopf, Aglaja, and Michael K Sixt. “Gut Homeostasis: Active Migration of Intestinal Epithelial Cells in Tissue Renewal.” Current Biology. Cell Press, 2019. https://doi.org/10.1016/j.cub.2019.08.068.' ieee: 'A. Kopf and M. K. Sixt, “Gut homeostasis: Active migration of intestinal epithelial cells in tissue renewal,” Current Biology, vol. 29, no. 20. Cell Press, pp. R1091–R1093, 2019.' ista: 'Kopf A, Sixt MK. 2019. Gut homeostasis: Active migration of intestinal epithelial cells in tissue renewal. Current Biology. 29(20), R1091–R1093.' mla: 'Kopf, Aglaja, and Michael K. Sixt. “Gut Homeostasis: Active Migration of Intestinal Epithelial Cells in Tissue Renewal.” Current Biology, vol. 29, no. 20, Cell Press, 2019, pp. R1091–93, doi:10.1016/j.cub.2019.08.068.' short: A. Kopf, M.K. Sixt, Current Biology 29 (2019) R1091–R1093. date_created: 2019-11-04T15:18:29Z date_published: 2019-10-21T00:00:00Z date_updated: 2023-09-05T12:43:43Z day: '21' department: - _id: MiSi doi: 10.1016/j.cub.2019.08.068 external_id: isi: - '000491286200016' pmid: - '31639357' intvolume: ' 29' isi: 1 issue: '20' language: - iso: eng month: '10' oa_version: None page: R1091-R1093 pmid: 1 publication: Current Biology publication_identifier: eissn: - 1879-0445 issn: - 0960-9822 publication_status: published publisher: Cell Press quality_controlled: '1' scopus_import: '1' status: public title: 'Gut homeostasis: Active migration of intestinal epithelial cells in tissue renewal' type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 29 year: '2019' ... --- _id: '7105' abstract: - lang: eng text: Cell migration is hypothesized to involve a cycle of behaviours beginning with leading edge extension. However, recent evidence suggests that the leading edge may be dispensable for migration, raising the question of what actually controls cell directionality. Here, we exploit the embryonic migration of Drosophila macrophages to bridge the different temporal scales of the behaviours controlling motility. This approach reveals that edge fluctuations during random motility are not persistent and are weakly correlated with motion. In contrast, flow of the actin network behind the leading edge is highly persistent. Quantification of actin flow structure during migration reveals a stable organization and asymmetry in the cell-wide flowfield that strongly correlates with cell directionality. This organization is regulated by a gradient of actin network compression and destruction, which is controlled by myosin contraction and cofilin-mediated disassembly. It is this stable actin-flow polarity, which integrates rapid fluctuations of the leading edge, that controls inherent cellular persistence. article_processing_charge: No article_type: original author: - first_name: Lawrence full_name: Yolland, Lawrence last_name: Yolland - first_name: Mubarik full_name: Burki, Mubarik last_name: Burki - first_name: Stefania full_name: Marcotti, Stefania last_name: Marcotti - first_name: Andrei full_name: Luchici, Andrei last_name: Luchici - first_name: Fiona N. full_name: Kenny, Fiona N. last_name: Kenny - first_name: John Robert full_name: Davis, John Robert last_name: Davis - first_name: Eduardo full_name: Serna-Morales, Eduardo last_name: Serna-Morales - first_name: Jan full_name: Müller, Jan id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D last_name: Müller - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Andrew full_name: Davidson, Andrew last_name: Davidson - first_name: Will full_name: Wood, Will last_name: Wood - first_name: Linus J. full_name: Schumacher, Linus J. last_name: Schumacher - first_name: Robert G. full_name: Endres, Robert G. last_name: Endres - first_name: Mark full_name: Miodownik, Mark last_name: Miodownik - first_name: Brian M. full_name: Stramer, Brian M. last_name: Stramer citation: ama: Yolland L, Burki M, Marcotti S, et al. Persistent and polarized global actin flow is essential for directionality during cell migration. Nature Cell Biology. 2019;21(11):1370-1381. doi:10.1038/s41556-019-0411-5 apa: Yolland, L., Burki, M., Marcotti, S., Luchici, A., Kenny, F. N., Davis, J. R., … Stramer, B. M. (2019). Persistent and polarized global actin flow is essential for directionality during cell migration. Nature Cell Biology. Springer Nature. https://doi.org/10.1038/s41556-019-0411-5 chicago: Yolland, Lawrence, Mubarik Burki, Stefania Marcotti, Andrei Luchici, Fiona N. Kenny, John Robert Davis, Eduardo Serna-Morales, et al. “Persistent and Polarized Global Actin Flow Is Essential for Directionality during Cell Migration.” Nature Cell Biology. Springer Nature, 2019. https://doi.org/10.1038/s41556-019-0411-5. ieee: L. Yolland et al., “Persistent and polarized global actin flow is essential for directionality during cell migration,” Nature Cell Biology, vol. 21, no. 11. Springer Nature, pp. 1370–1381, 2019. ista: Yolland L, Burki M, Marcotti S, Luchici A, Kenny FN, Davis JR, Serna-Morales E, Müller J, Sixt MK, Davidson A, Wood W, Schumacher LJ, Endres RG, Miodownik M, Stramer BM. 2019. Persistent and polarized global actin flow is essential for directionality during cell migration. Nature Cell Biology. 21(11), 1370–1381. mla: Yolland, Lawrence, et al. “Persistent and Polarized Global Actin Flow Is Essential for Directionality during Cell Migration.” Nature Cell Biology, vol. 21, no. 11, Springer Nature, 2019, pp. 1370–81, doi:10.1038/s41556-019-0411-5. short: L. Yolland, M. Burki, S. Marcotti, A. Luchici, F.N. Kenny, J.R. Davis, E. Serna-Morales, J. Müller, M.K. Sixt, A. Davidson, W. Wood, L.J. Schumacher, R.G. Endres, M. Miodownik, B.M. Stramer, Nature Cell Biology 21 (2019) 1370–1381. date_created: 2019-11-25T08:55:00Z date_published: 2019-11-01T00:00:00Z date_updated: 2023-09-06T11:08:52Z day: '01' department: - _id: MiSi doi: 10.1038/s41556-019-0411-5 external_id: isi: - '000495888300009' pmid: - '31685997' intvolume: ' 21' isi: 1 issue: '11' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7025891 month: '11' oa: 1 oa_version: Submitted Version page: 1370-1381 pmid: 1 publication: Nature Cell Biology publication_identifier: eissn: - 1476-4679 issn: - 1465-7392 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Persistent and polarized global actin flow is essential for directionality during cell migration type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 21 year: '2019' ... --- _id: '6328' abstract: - lang: eng text: During metazoan development, immune surveillance and cancer dissemination, cells migrate in complex three-dimensional microenvironments1,2,3. These spaces are crowded by cells and extracellular matrix, generating mazes with differently sized gaps that are typically smaller than the diameter of the migrating cell4,5. Most mesenchymal and epithelial cells and some—but not all—cancer cells actively generate their migratory path using pericellular tissue proteolysis6. By contrast, amoeboid cells such as leukocytes use non-destructive strategies of locomotion7, raising the question how these extremely fast cells navigate through dense tissues. Here we reveal that leukocytes sample their immediate vicinity for large pore sizes, and are thereby able to choose the path of least resistance. This allows them to circumnavigate local obstacles while effectively following global directional cues such as chemotactic gradients. Pore-size discrimination is facilitated by frontward positioning of the nucleus, which enables the cells to use their bulkiest compartment as a mechanical gauge. Once the nucleus and the closely associated microtubule organizing centre pass the largest pore, cytoplasmic protrusions still lingering in smaller pores are retracted. These retractions are coordinated by dynamic microtubules; when microtubules are disrupted, migrating cells lose coherence and frequently fragment into migratory cytoplasmic pieces. As nuclear positioning in front of the microtubule organizing centre is a typical feature of amoeboid migration, our findings link the fundamental organization of cellular polarity to the strategy of locomotion. acknowledged_ssus: - _id: SSU article_processing_charge: No article_type: letter_note author: - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 - first_name: Julian A full_name: Stopp, Julian A id: 489E3F00-F248-11E8-B48F-1D18A9856A87 last_name: Stopp - first_name: Ingrid full_name: de Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: de Vries - first_name: Meghan K. full_name: Driscoll, Meghan K. last_name: Driscoll - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Erik S. full_name: Welf, Erik S. last_name: Welf - first_name: Gaudenz full_name: Danuser, Gaudenz last_name: Danuser - first_name: Reto full_name: Fiolka, Reto last_name: Fiolka - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Renkawitz J, Kopf A, Stopp JA, et al. Nuclear positioning facilitates amoeboid migration along the path of least resistance. Nature. 2019;568:546-550. doi:10.1038/s41586-019-1087-5 apa: Renkawitz, J., Kopf, A., Stopp, J. A., de Vries, I., Driscoll, M. K., Merrin, J., … Sixt, M. K. (2019). Nuclear positioning facilitates amoeboid migration along the path of least resistance. Nature. Springer Nature. https://doi.org/10.1038/s41586-019-1087-5 chicago: Renkawitz, Jörg, Aglaja Kopf, Julian A Stopp, Ingrid de Vries, Meghan K. Driscoll, Jack Merrin, Robert Hauschild, et al. “Nuclear Positioning Facilitates Amoeboid Migration along the Path of Least Resistance.” Nature. Springer Nature, 2019. https://doi.org/10.1038/s41586-019-1087-5. ieee: J. Renkawitz et al., “Nuclear positioning facilitates amoeboid migration along the path of least resistance,” Nature, vol. 568. Springer Nature, pp. 546–550, 2019. ista: Renkawitz J, Kopf A, Stopp JA, de Vries I, Driscoll MK, Merrin J, Hauschild R, Welf ES, Danuser G, Fiolka R, Sixt MK. 2019. Nuclear positioning facilitates amoeboid migration along the path of least resistance. Nature. 568, 546–550. mla: Renkawitz, Jörg, et al. “Nuclear Positioning Facilitates Amoeboid Migration along the Path of Least Resistance.” Nature, vol. 568, Springer Nature, 2019, pp. 546–50, doi:10.1038/s41586-019-1087-5. short: J. Renkawitz, A. Kopf, J.A. Stopp, I. de Vries, M.K. Driscoll, J. Merrin, R. Hauschild, E.S. Welf, G. Danuser, R. Fiolka, M.K. Sixt, Nature 568 (2019) 546–550. date_created: 2019-04-17T06:52:28Z date_published: 2019-04-25T00:00:00Z date_updated: 2024-03-27T23:30:39Z day: '25' department: - _id: MiSi - _id: NanoFab - _id: Bio doi: 10.1038/s41586-019-1087-5 ec_funded: 1 external_id: isi: - '000465594200050' pmid: - '30944468' intvolume: ' 568' isi: 1 language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC7217284/ month: '04' oa: 1 oa_version: Submitted Version page: 546-550 pmid: 1 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 265FAEBA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: W01250-B20 name: Nano-Analytics of Cellular Systems - _id: 25681D80-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '291734' name: International IST Postdoc Fellowship Programme - _id: 25A48D24-B435-11E9-9278-68D0E5697425 grant_number: ALTF 1396-2014 name: Molecular and system level view of immune cell migration publication: Nature publication_status: published publisher: Springer Nature quality_controlled: '1' related_material: link: - description: News on IST Homepage relation: press_release url: https://ist.ac.at/en/news/leukocytes-use-their-nucleus-as-a-ruler-to-choose-path-of-least-resistance/ record: - id: '14697' relation: dissertation_contains status: public - id: '6891' relation: dissertation_contains status: public scopus_import: '1' status: public title: Nuclear positioning facilitates amoeboid migration along the path of least resistance type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 568 year: '2019' ... --- _id: '6877' article_processing_charge: No article_type: original author: - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Kopf A, Sixt MK. The neural crest pitches in to remove apoptotic debris. Cell. 2019;179(1):51-53. doi:10.1016/j.cell.2019.08.047 apa: Kopf, A., & Sixt, M. K. (2019). The neural crest pitches in to remove apoptotic debris. Cell. Elsevier. https://doi.org/10.1016/j.cell.2019.08.047 chicago: Kopf, Aglaja, and Michael K Sixt. “The Neural Crest Pitches in to Remove Apoptotic Debris.” Cell. Elsevier, 2019. https://doi.org/10.1016/j.cell.2019.08.047. ieee: A. Kopf and M. K. Sixt, “The neural crest pitches in to remove apoptotic debris,” Cell, vol. 179, no. 1. Elsevier, pp. 51–53, 2019. ista: Kopf A, Sixt MK. 2019. The neural crest pitches in to remove apoptotic debris. Cell. 179(1), 51–53. mla: Kopf, Aglaja, and Michael K. Sixt. “The Neural Crest Pitches in to Remove Apoptotic Debris.” Cell, vol. 179, no. 1, Elsevier, 2019, pp. 51–53, doi:10.1016/j.cell.2019.08.047. short: A. Kopf, M.K. Sixt, Cell 179 (2019) 51–53. date_created: 2019-09-15T22:00:46Z date_published: 2019-09-19T00:00:00Z date_updated: 2024-03-27T23:30:40Z day: '19' department: - _id: MiSi doi: 10.1016/j.cell.2019.08.047 external_id: isi: - '000486618500011' pmid: - '31539498' intvolume: ' 179' isi: 1 issue: '1' language: - iso: eng month: '09' oa_version: None page: 51-53 pmid: 1 publication: Cell publication_identifier: eissn: - 1097-4172 issn: - 0092-8674 publication_status: published publisher: Elsevier quality_controlled: '1' related_material: record: - id: '6891' relation: dissertation_contains status: public scopus_import: '1' status: public title: The neural crest pitches in to remove apoptotic debris type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 179 year: '2019' ... --- _id: '318' abstract: - lang: eng text: The insect’s fat body combines metabolic and immunological functions. In this issue of Developmental Cell, Franz et al. (2018) show that in Drosophila, cells of the fat body are not static, but can actively “swim” toward sites of epithelial injury, where they physically clog the wound and locally secrete antimicrobial peptides. acknowledgement: Short Survey article_processing_charge: No author: - first_name: Alessandra M full_name: Casano, Alessandra M id: 3DBA3F4E-F248-11E8-B48F-1D18A9856A87 last_name: Casano orcid: 0000-0002-6009-6804 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Casano AM, Sixt MK. A fat lot of good for wound healing. Developmental Cell. 2018;44(4):405-406. doi:10.1016/j.devcel.2018.02.009 apa: Casano, A. M., & Sixt, M. K. (2018). A fat lot of good for wound healing. Developmental Cell. Cell Press. https://doi.org/10.1016/j.devcel.2018.02.009 chicago: Casano, Alessandra M, and Michael K Sixt. “A Fat Lot of Good for Wound Healing.” Developmental Cell. Cell Press, 2018. https://doi.org/10.1016/j.devcel.2018.02.009. ieee: A. M. Casano and M. K. Sixt, “A fat lot of good for wound healing,” Developmental Cell, vol. 44, no. 4. Cell Press, pp. 405–406, 2018. ista: Casano AM, Sixt MK. 2018. A fat lot of good for wound healing. Developmental Cell. 44(4), 405–406. mla: Casano, Alessandra M., and Michael K. Sixt. “A Fat Lot of Good for Wound Healing.” Developmental Cell, vol. 44, no. 4, Cell Press, 2018, pp. 405–06, doi:10.1016/j.devcel.2018.02.009. short: A.M. Casano, M.K. Sixt, Developmental Cell 44 (2018) 405–406. date_created: 2018-12-11T11:45:47Z date_published: 2018-02-26T00:00:00Z date_updated: 2023-09-08T11:42:28Z day: '26' department: - _id: MiSi doi: 10.1016/j.devcel.2018.02.009 external_id: isi: - '000426150700002' pmid: - '29486189' intvolume: ' 44' isi: 1 issue: '4' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pubmed/29486189 month: '02' oa: 1 oa_version: Published Version page: 405 - 406 pmid: 1 publication: Developmental Cell publication_status: published publisher: Cell Press publist_id: '7547' quality_controlled: '1' scopus_import: '1' status: public title: A fat lot of good for wound healing type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 44 year: '2018' ... --- _id: '437' abstract: - lang: eng text: Dendritic cells (DCs) are sentinels of the adaptive immune system that reside in peripheral organs of mammals. Upon pathogen encounter, they undergo maturation and up-regulate the chemokine receptor CCR7 that guides them along gradients of its chemokine ligands CCL19 and 21 to the next draining lymph node. There, DCs present peripherally acquired antigen to naïve T cells, thereby triggering adaptive immunity. acknowledged_ssus: - _id: SSU acknowledgement: "This work was supported by grants of the European Research Council (ERC CoG 724373) and the Austrian Science Fund (FWF) to M.S. We thank the scientific support units at IST Austria for excellent technical support.\r\nWe thank the scientific \ support units at IST Austria for excellent technical support. " article_processing_charge: Yes (via OA deal) author: - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Hans full_name: Haecker, Hans last_name: Haecker - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Leithner AF, Renkawitz J, de Vries I, Hauschild R, Haecker H, Sixt MK. Fast and efficient genetic engineering of hematopoietic precursor cells for the study of dendritic cell migration. European Journal of Immunology. 2018;48(6):1074-1077. doi:10.1002/eji.201747358 apa: Leithner, A. F., Renkawitz, J., de Vries, I., Hauschild, R., Haecker, H., & Sixt, M. K. (2018). Fast and efficient genetic engineering of hematopoietic precursor cells for the study of dendritic cell migration. European Journal of Immunology. Wiley-Blackwell. https://doi.org/10.1002/eji.201747358 chicago: Leithner, Alexander F, Jörg Renkawitz, Ingrid de Vries, Robert Hauschild, Hans Haecker, and Michael K Sixt. “Fast and Efficient Genetic Engineering of Hematopoietic Precursor Cells for the Study of Dendritic Cell Migration.” European Journal of Immunology. Wiley-Blackwell, 2018. https://doi.org/10.1002/eji.201747358. ieee: A. F. Leithner, J. Renkawitz, I. de Vries, R. Hauschild, H. Haecker, and M. K. Sixt, “Fast and efficient genetic engineering of hematopoietic precursor cells for the study of dendritic cell migration,” European Journal of Immunology, vol. 48, no. 6. Wiley-Blackwell, pp. 1074–1077, 2018. ista: Leithner AF, Renkawitz J, de Vries I, Hauschild R, Haecker H, Sixt MK. 2018. Fast and efficient genetic engineering of hematopoietic precursor cells for the study of dendritic cell migration. European Journal of Immunology. 48(6), 1074–1077. mla: Leithner, Alexander F., et al. “Fast and Efficient Genetic Engineering of Hematopoietic Precursor Cells for the Study of Dendritic Cell Migration.” European Journal of Immunology, vol. 48, no. 6, Wiley-Blackwell, 2018, pp. 1074–77, doi:10.1002/eji.201747358. short: A.F. Leithner, J. Renkawitz, I. de Vries, R. Hauschild, H. Haecker, M.K. Sixt, European Journal of Immunology 48 (2018) 1074–1077. date_created: 2018-12-11T11:46:28Z date_published: 2018-02-13T00:00:00Z date_updated: 2023-09-11T14:01:18Z day: '13' ddc: - '570' department: - _id: MiSi - _id: Bio doi: 10.1002/eji.201747358 ec_funded: 1 external_id: isi: - '000434963700016' file: - access_level: open_access checksum: 9d5b74cd016505aeb9a4c2d33bbedaeb content_type: application/pdf creator: system date_created: 2018-12-12T10:13:56Z date_updated: 2020-07-14T12:46:27Z file_id: '5044' file_name: IST-2018-1067-v1+2_Leithner_et_al-2018-European_Journal_of_Immunology.pdf file_size: 590106 relation: main_file file_date_updated: 2020-07-14T12:46:27Z has_accepted_license: '1' intvolume: ' 48' isi: 1 issue: '6' language: - iso: eng license: https://creativecommons.org/licenses/by-nc/4.0/ month: '02' oa: 1 oa_version: Published Version page: 1074 - 1077 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients publication: European Journal of Immunology publication_status: published publisher: Wiley-Blackwell publist_id: '7386' pubrep_id: '1067' quality_controlled: '1' scopus_import: '1' status: public title: Fast and efficient genetic engineering of hematopoietic precursor cells for the study of dendritic cell migration tmp: image: /images/cc_by_nc.png legal_code_url: https://creativecommons.org/licenses/by-nc/4.0/legalcode name: Creative Commons Attribution-NonCommercial 4.0 International (CC BY-NC 4.0) short: CC BY-NC (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 48 year: '2018' ... --- _id: '5672' abstract: - lang: eng text: The release of IgM is the first line of an antibody response and precedes the generation of high affinity IgG in germinal centers. Once secreted by freshly activated plasmablasts, IgM is released into the efferent lymph of reactive lymph nodes as early as 3 d after immunization. As pentameric IgM has an enormous size of 1,000 kD, its diffusibility is low, and one might wonder how it can pass through the densely lymphocyte-packed environment of a lymph node parenchyma in order to reach its exit. In this issue of JEM, Thierry et al. show that, in order to reach the blood stream, IgM molecules take a specific micro-anatomical route via lymph node conduits. article_processing_charge: No author: - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Reversat A, Sixt MK. IgM’s exit route. Journal of Experimental Medicine. 2018;215(12):2959-2961. doi:10.1084/jem.20181934 apa: Reversat, A., & Sixt, M. K. (2018). IgM’s exit route. Journal of Experimental Medicine. Rockefeller University Press. https://doi.org/10.1084/jem.20181934 chicago: Reversat, Anne, and Michael K Sixt. “IgM’s Exit Route.” Journal of Experimental Medicine. Rockefeller University Press, 2018. https://doi.org/10.1084/jem.20181934. ieee: A. Reversat and M. K. Sixt, “IgM’s exit route,” Journal of Experimental Medicine, vol. 215, no. 12. Rockefeller University Press, pp. 2959–2961, 2018. ista: Reversat A, Sixt MK. 2018. IgM’s exit route. Journal of Experimental Medicine. 215(12), 2959–2961. mla: Reversat, Anne, and Michael K. Sixt. “IgM’s Exit Route.” Journal of Experimental Medicine, vol. 215, no. 12, Rockefeller University Press, 2018, pp. 2959–61, doi:10.1084/jem.20181934. short: A. Reversat, M.K. Sixt, Journal of Experimental Medicine 215 (2018) 2959–2961. date_created: 2018-12-16T22:59:18Z date_published: 2018-11-20T00:00:00Z date_updated: 2023-09-11T14:12:06Z day: '20' ddc: - '570' department: - _id: MiSi doi: 10.1084/jem.20181934 external_id: isi: - '000451920600002' file: - access_level: open_access checksum: 687beea1d64c213f4cb9e3c29ec11a14 content_type: application/pdf creator: dernst date_created: 2019-02-06T08:49:52Z date_updated: 2020-07-14T12:47:09Z file_id: '5931' file_name: 2018_JournalExperMed_Reversat.pdf file_size: 1216437 relation: main_file file_date_updated: 2020-07-14T12:47:09Z has_accepted_license: '1' intvolume: ' 215' isi: 1 issue: '12' language: - iso: eng month: '11' oa: 1 oa_version: Published Version page: 2959-2961 publication: Journal of Experimental Medicine publication_identifier: issn: - '00221007' publication_status: published publisher: Rockefeller University Press quality_controlled: '1' scopus_import: '1' status: public title: IgM's exit route tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 215 year: '2018' ... --- _id: '275' abstract: - lang: eng text: Lymphatic endothelial cells (LECs) release extracellular chemokines to guide the migration of dendritic cells. In this study, we report that LECs also release basolateral exosome-rich endothelial vesicles (EEVs) that are secreted in greater numbers in the presence of inflammatory cytokines and accumulate in the perivascular stroma of small lymphatic vessels in human chronic inflammatory diseases. Proteomic analyses of EEV fractions identified > 1,700 cargo proteins and revealed a dominant motility-promoting protein signature. In vitro and ex vivo EEV fractions augmented cellular protrusion formation in a CX3CL1/fractalkine-dependent fashion and enhanced the directional migratory response of human dendritic cells along guidance cues. We conclude that perilymphatic LEC exosomes enhance exploratory behavior and thus promote directional migration of CX3CR1-expressing cells in complex tissue environments. acknowledgement: M. Brown was supported by the Cell Communication in Health and Disease Graduate Study Program of the Austrian Science Fund and Medizinische Universität Wien, M. Sixt by the European Research Council (ERC GA 281556) and an Austrian Science Fund START award, K.L. Bennett by the Austrian Academy of Sciences, D.G. Jackson and L.A. Johnson by Unit Funding (MC_UU_12010/2) and project grants from the Medical Research Council (G1100134 and MR/L008610/1), and M. Detmar by the Schweizerischer Nationalfonds zur Förderung der Wissenschaftlichen Forschung and Advanced European Research Council grant LYVICAM. K. Vaahtomeri was supported by an Academy of Finland postdoctoral research grant (287853). This project has received funding from the European Union’s Horizon 2020 research and innovation program under grant agreement No. 668036 (RELENT). article_processing_charge: No author: - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Louise full_name: Johnson, Louise last_name: Johnson - first_name: Dario full_name: Leone, Dario last_name: Leone - first_name: Peter full_name: Májek, Peter last_name: Májek - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Daniel full_name: Senfter, Daniel last_name: Senfter - first_name: Nora full_name: Bukosza, Nora last_name: Bukosza - first_name: Helga full_name: Schachner, Helga last_name: Schachner - first_name: Gabriele full_name: Asfour, Gabriele last_name: Asfour - first_name: Brigitte full_name: Langer, Brigitte last_name: Langer - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Katja full_name: Parapatics, Katja last_name: Parapatics - first_name: Young full_name: Hong, Young last_name: Hong - first_name: Keiryn full_name: Bennett, Keiryn last_name: Bennett - first_name: Renate full_name: Kain, Renate last_name: Kain - first_name: Michael full_name: Detmar, Michael last_name: Detmar - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: David full_name: Jackson, David last_name: Jackson - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki citation: ama: Brown M, Johnson L, Leone D, et al. Lymphatic exosomes promote dendritic cell migration along guidance cues. Journal of Cell Biology. 2018;217(6):2205-2221. doi:10.1083/jcb.201612051 apa: Brown, M., Johnson, L., Leone, D., Májek, P., Vaahtomeri, K., Senfter, D., … Kerjaschki, D. (2018). Lymphatic exosomes promote dendritic cell migration along guidance cues. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201612051 chicago: Brown, Markus, Louise Johnson, Dario Leone, Peter Májek, Kari Vaahtomeri, Daniel Senfter, Nora Bukosza, et al. “Lymphatic Exosomes Promote Dendritic Cell Migration along Guidance Cues.” Journal of Cell Biology. Rockefeller University Press, 2018. https://doi.org/10.1083/jcb.201612051. ieee: M. Brown et al., “Lymphatic exosomes promote dendritic cell migration along guidance cues,” Journal of Cell Biology, vol. 217, no. 6. Rockefeller University Press, pp. 2205–2221, 2018. ista: Brown M, Johnson L, Leone D, Májek P, Vaahtomeri K, Senfter D, Bukosza N, Schachner H, Asfour G, Langer B, Hauschild R, Parapatics K, Hong Y, Bennett K, Kain R, Detmar M, Sixt MK, Jackson D, Kerjaschki D. 2018. Lymphatic exosomes promote dendritic cell migration along guidance cues. Journal of Cell Biology. 217(6), 2205–2221. mla: Brown, Markus, et al. “Lymphatic Exosomes Promote Dendritic Cell Migration along Guidance Cues.” Journal of Cell Biology, vol. 217, no. 6, Rockefeller University Press, 2018, pp. 2205–21, doi:10.1083/jcb.201612051. short: M. Brown, L. Johnson, D. Leone, P. Májek, K. Vaahtomeri, D. Senfter, N. Bukosza, H. Schachner, G. Asfour, B. Langer, R. Hauschild, K. Parapatics, Y. Hong, K. Bennett, R. Kain, M. Detmar, M.K. Sixt, D. Jackson, D. Kerjaschki, Journal of Cell Biology 217 (2018) 2205–2221. date_created: 2018-12-11T11:45:33Z date_published: 2018-04-12T00:00:00Z date_updated: 2023-09-13T08:51:29Z day: '12' ddc: - '570' department: - _id: MiSi - _id: Bio doi: 10.1083/jcb.201612051 ec_funded: 1 external_id: isi: - '000438077800026' pmid: - '29650776' file: - access_level: open_access checksum: 9c7eba51a35c62da8c13f98120b64df4 content_type: application/pdf creator: dernst date_created: 2018-12-17T12:50:07Z date_updated: 2020-07-14T12:45:45Z file_id: '5704' file_name: 2018_JournalCellBiology_Brown.pdf file_size: 2252043 relation: main_file file_date_updated: 2020-07-14T12:45:45Z has_accepted_license: '1' intvolume: ' 217' isi: 1 issue: '6' language: - iso: eng month: '04' oa: 1 oa_version: Published Version page: 2205 - 2221 pmid: 1 project: - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Journal of Cell Biology publication_status: published publisher: Rockefeller University Press publist_id: '7627' quality_controlled: '1' scopus_import: '1' status: public title: Lymphatic exosomes promote dendritic cell migration along guidance cues tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 217 year: '2018' ... --- _id: '5858' abstract: - lang: eng text: Spatial patterns are ubiquitous on the subcellular, cellular and tissue level, and can be studied using imaging techniques such as light and fluorescence microscopy. Imaging data provide quantitative information about biological systems; however, mechanisms causing spatial patterning often remain elusive. In recent years, spatio-temporal mathematical modelling has helped to overcome this problem. Yet, outliers and structured noise limit modelling of whole imaging data, and models often consider spatial summary statistics. Here, we introduce an integrated data-driven modelling approach that can cope with measurement artefacts and whole imaging data. Our approach combines mechanistic models of the biological processes with robust statistical models of the measurement process. The parameters of the integrated model are calibrated using a maximum-likelihood approach. We used this integrated modelling approach to study in vivo gradients of the chemokine (C-C motif) ligand 21 (CCL21). CCL21 gradients guide dendritic cells and are important in the adaptive immune response. Using artificial data, we verified that the integrated modelling approach provides reliable parameter estimates in the presence of measurement noise and that bias and variance of these estimates are reduced compared to conventional approaches. The application to experimental data allowed the parametrization and subsequent refinement of the model using additional mechanisms. Among other results, model-based hypothesis testing predicted lymphatic vessel-dependent concentration of heparan sulfate, the binding partner of CCL21. The selected model provided an accurate description of the experimental data and was partially validated using published data. Our findings demonstrate that integrated statistical modelling of whole imaging data is computationally feasible and can provide novel biological insights. article_number: '20180600' article_processing_charge: No author: - first_name: Sabrina full_name: Hross, Sabrina last_name: Hross - first_name: Fabian J. full_name: Theis, Fabian J. last_name: Theis - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Jan full_name: Hasenauer, Jan last_name: Hasenauer citation: ama: Hross S, Theis FJ, Sixt MK, Hasenauer J. Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data. Journal of the Royal Society Interface. 2018;15(149). doi:10.1098/rsif.2018.0600 apa: Hross, S., Theis, F. J., Sixt, M. K., & Hasenauer, J. (2018). Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data. Journal of the Royal Society Interface. Royal Society Publishing. https://doi.org/10.1098/rsif.2018.0600 chicago: Hross, Sabrina, Fabian J. Theis, Michael K Sixt, and Jan Hasenauer. “Mechanistic Description of Spatial Processes Using Integrative Modelling of Noise-Corrupted Imaging Data.” Journal of the Royal Society Interface. Royal Society Publishing, 2018. https://doi.org/10.1098/rsif.2018.0600. ieee: S. Hross, F. J. Theis, M. K. Sixt, and J. Hasenauer, “Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data,” Journal of the Royal Society Interface, vol. 15, no. 149. Royal Society Publishing, 2018. ista: Hross S, Theis FJ, Sixt MK, Hasenauer J. 2018. Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data. Journal of the Royal Society Interface. 15(149), 20180600. mla: Hross, Sabrina, et al. “Mechanistic Description of Spatial Processes Using Integrative Modelling of Noise-Corrupted Imaging Data.” Journal of the Royal Society Interface, vol. 15, no. 149, 20180600, Royal Society Publishing, 2018, doi:10.1098/rsif.2018.0600. short: S. Hross, F.J. Theis, M.K. Sixt, J. Hasenauer, Journal of the Royal Society Interface 15 (2018). date_created: 2019-01-20T22:59:18Z date_published: 2018-12-05T00:00:00Z date_updated: 2023-09-13T08:55:05Z day: '05' ddc: - '570' department: - _id: MiSi doi: 10.1098/rsif.2018.0600 external_id: isi: - '000456783800011' file: - access_level: open_access checksum: 56eb4308a15b7190bff938fab1f780e8 content_type: application/pdf creator: dernst date_created: 2019-02-05T14:46:44Z date_updated: 2020-07-14T12:47:13Z file_id: '5925' file_name: 2018_Interface_Hross.pdf file_size: 1464288 relation: main_file file_date_updated: 2020-07-14T12:47:13Z has_accepted_license: '1' intvolume: ' 15' isi: 1 issue: '149' language: - iso: eng month: '12' oa: 1 oa_version: Published Version publication: Journal of the Royal Society Interface publication_identifier: issn: - '17425689' publication_status: published publisher: Royal Society Publishing quality_controlled: '1' scopus_import: '1' status: public title: Mechanistic description of spatial processes using integrative modelling of noise-corrupted imaging data tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 15 year: '2018' ... --- _id: '153' abstract: - lang: eng text: Cells migrating in multicellular organisms steadily traverse complex three-dimensional (3D) environments. To decipher the underlying cell biology, current experimental setups either use simplified 2D, tissue-mimetic 3D (e.g., collagen matrices) or in vivo environments. While only in vivo experiments are truly physiological, they do not allow for precise manipulation of environmental parameters. 2D in vitro experiments do allow mechanical and chemical manipulations, but increasing evidence demonstrates substantial differences of migratory mechanisms in 2D and 3D. Here, we describe simple, robust, and versatile “pillar forests” to investigate cell migration in complex but fully controllable 3D environments. Pillar forests are polydimethylsiloxane-based setups, in which two closely adjacent surfaces are interconnected by arrays of micrometer-sized pillars. Changing the pillar shape, size, height and the inter-pillar distance precisely manipulates microenvironmental parameters (e.g., pore sizes, micro-geometry, micro-topology), while being easily combined with chemotactic cues, surface coatings, diverse cell types and advanced imaging techniques. Thus, pillar forests combine the advantages of 2D cell migration assays with the precise definition of 3D environmental parameters. article_processing_charge: No author: - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Renkawitz J, Reversat A, Leithner AF, Merrin J, Sixt MK. Micro-engineered “pillar forests” to study cell migration in complex but controlled 3D environments. In: Methods in Cell Biology. Vol 147. Academic Press; 2018:79-91. doi:10.1016/bs.mcb.2018.07.004' apa: Renkawitz, J., Reversat, A., Leithner, A. F., Merrin, J., & Sixt, M. K. (2018). Micro-engineered “pillar forests” to study cell migration in complex but controlled 3D environments. In Methods in Cell Biology (Vol. 147, pp. 79–91). Academic Press. https://doi.org/10.1016/bs.mcb.2018.07.004 chicago: Renkawitz, Jörg, Anne Reversat, Alexander F Leithner, Jack Merrin, and Michael K Sixt. “Micro-Engineered ‘Pillar Forests’ to Study Cell Migration in Complex but Controlled 3D Environments.” In Methods in Cell Biology, 147:79–91. Academic Press, 2018. https://doi.org/10.1016/bs.mcb.2018.07.004. ieee: J. Renkawitz, A. Reversat, A. F. Leithner, J. Merrin, and M. K. Sixt, “Micro-engineered ‘pillar forests’ to study cell migration in complex but controlled 3D environments,” in Methods in Cell Biology, vol. 147, Academic Press, 2018, pp. 79–91. ista: 'Renkawitz J, Reversat A, Leithner AF, Merrin J, Sixt MK. 2018.Micro-engineered “pillar forests” to study cell migration in complex but controlled 3D environments. In: Methods in Cell Biology. vol. 147, 79–91.' mla: Renkawitz, Jörg, et al. “Micro-Engineered ‘Pillar Forests’ to Study Cell Migration in Complex but Controlled 3D Environments.” Methods in Cell Biology, vol. 147, Academic Press, 2018, pp. 79–91, doi:10.1016/bs.mcb.2018.07.004. short: J. Renkawitz, A. Reversat, A.F. Leithner, J. Merrin, M.K. Sixt, in:, Methods in Cell Biology, Academic Press, 2018, pp. 79–91. date_created: 2018-12-11T11:44:54Z date_published: 2018-07-27T00:00:00Z date_updated: 2023-09-13T08:56:35Z day: '27' department: - _id: MiSi - _id: NanoFab doi: 10.1016/bs.mcb.2018.07.004 external_id: isi: - '000452412300006' pmid: - '30165964' intvolume: ' 147' isi: 1 language: - iso: eng month: '07' oa_version: None page: 79 - 91 pmid: 1 publication: Methods in Cell Biology publication_identifier: issn: - 0091679X publication_status: published publisher: Academic Press publist_id: '7768' quality_controlled: '1' scopus_import: '1' status: public title: Micro-engineered “pillar forests” to study cell migration in complex but controlled 3D environments type: book_chapter user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 147 year: '2018' ... --- _id: '5861' abstract: - lang: eng text: In zebrafish larvae, it is the cell type that determines how the cell responds to a chemokine signal. article_number: e37888 article_processing_charge: No article_type: original author: - first_name: Jonna H full_name: Alanko, Jonna H id: 2CC12E8C-F248-11E8-B48F-1D18A9856A87 last_name: Alanko orcid: 0000-0002-7698-3061 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Alanko JH, Sixt MK. The cell sets the tone. eLife. 2018;7. doi:10.7554/eLife.37888 apa: Alanko, J. H., & Sixt, M. K. (2018). The cell sets the tone. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.37888 chicago: Alanko, Jonna H, and Michael K Sixt. “The Cell Sets the Tone.” ELife. eLife Sciences Publications, 2018. https://doi.org/10.7554/eLife.37888. ieee: J. H. Alanko and M. K. Sixt, “The cell sets the tone,” eLife, vol. 7. eLife Sciences Publications, 2018. ista: Alanko JH, Sixt MK. 2018. The cell sets the tone. eLife. 7, e37888. mla: Alanko, Jonna H., and Michael K. Sixt. “The Cell Sets the Tone.” ELife, vol. 7, e37888, eLife Sciences Publications, 2018, doi:10.7554/eLife.37888. short: J.H. Alanko, M.K. Sixt, ELife 7 (2018). date_created: 2019-01-20T22:59:19Z date_published: 2018-06-06T00:00:00Z date_updated: 2023-09-19T10:01:39Z day: '06' ddc: - '570' department: - _id: MiSi doi: 10.7554/eLife.37888 external_id: isi: - '000434375000001' file: - access_level: open_access checksum: f1c7ec2a809408d763c4b529a98f9a3b content_type: application/pdf creator: dernst date_created: 2019-02-13T10:52:11Z date_updated: 2020-07-14T12:47:13Z file_id: '5973' file_name: 2018_eLife_Alanko.pdf file_size: 358141 relation: main_file file_date_updated: 2020-07-14T12:47:13Z has_accepted_license: '1' intvolume: ' 7' isi: 1 language: - iso: eng month: '06' oa: 1 oa_version: Published Version publication: eLife publication_identifier: issn: - 2050084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: The cell sets the tone tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 7 year: '2018' ... --- _id: '5992' abstract: - lang: eng text: Lamellipodia are flat membrane protrusions formed during mesenchymal motion. Polymerization at the leading edge assembles the actin filament network and generates protrusion force. How this force is supported by the network and how the assembly rate is shared between protrusion and network retrograde flow determines the protrusion rate. We use mathematical modeling to understand experiments changing the F-actin density in lamellipodia of B16-F1 melanoma cells by modulation of Arp2/3 complex activity or knockout of the formins FMNL2 and FMNL3. Cells respond to a reduction of density with a decrease of protrusion velocity, an increase in the ratio of force to filament number, but constant network assembly rate. The relation between protrusion force and tension gradient in the F-actin network and the density dependency of friction, elasticity, and viscosity of the network explain the experimental observations. The formins act as filament nucleators and elongators with differential rates. Modulation of their activity suggests an effect on network assembly rate. Contrary to these expectations, the effect of changes in elongator composition is much weaker than the consequences of the density change. We conclude that the force acting on the leading edge membrane is the force required to drive F-actin network retrograde flow. article_processing_charge: No author: - first_name: Setareh full_name: Dolati, Setareh last_name: Dolati - first_name: Frieda full_name: Kage, Frieda last_name: Kage - first_name: Jan full_name: Mueller, Jan last_name: Mueller - first_name: Mathias full_name: Müsken, Mathias last_name: Müsken - first_name: Marieluise full_name: Kirchner, Marieluise last_name: Kirchner - first_name: Gunnar full_name: Dittmar, Gunnar last_name: Dittmar - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner - first_name: Martin full_name: Falcke, Martin last_name: Falcke citation: ama: Dolati S, Kage F, Mueller J, et al. On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility. Molecular Biology of the Cell. 2018;29(22):2674-2686. doi:10.1091/mbc.e18-02-0082 apa: Dolati, S., Kage, F., Mueller, J., Müsken, M., Kirchner, M., Dittmar, G., … Falcke, M. (2018). On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility. Molecular Biology of the Cell. American Society for Cell Biology . https://doi.org/10.1091/mbc.e18-02-0082 chicago: Dolati, Setareh, Frieda Kage, Jan Mueller, Mathias Müsken, Marieluise Kirchner, Gunnar Dittmar, Michael K Sixt, Klemens Rottner, and Martin Falcke. “On the Relation between Filament Density, Force Generation, and Protrusion Rate in Mesenchymal Cell Motility.” Molecular Biology of the Cell. American Society for Cell Biology , 2018. https://doi.org/10.1091/mbc.e18-02-0082. ieee: S. Dolati et al., “On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility,” Molecular Biology of the Cell, vol. 29, no. 22. American Society for Cell Biology , pp. 2674–2686, 2018. ista: Dolati S, Kage F, Mueller J, Müsken M, Kirchner M, Dittmar G, Sixt MK, Rottner K, Falcke M. 2018. On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility. Molecular Biology of the Cell. 29(22), 2674–2686. mla: Dolati, Setareh, et al. “On the Relation between Filament Density, Force Generation, and Protrusion Rate in Mesenchymal Cell Motility.” Molecular Biology of the Cell, vol. 29, no. 22, American Society for Cell Biology , 2018, pp. 2674–86, doi:10.1091/mbc.e18-02-0082. short: S. Dolati, F. Kage, J. Mueller, M. Müsken, M. Kirchner, G. Dittmar, M.K. Sixt, K. Rottner, M. Falcke, Molecular Biology of the Cell 29 (2018) 2674–2686. date_created: 2019-02-14T12:25:47Z date_published: 2018-11-01T00:00:00Z date_updated: 2023-09-19T14:30:23Z day: '01' ddc: - '570' department: - _id: MiSi doi: 10.1091/mbc.e18-02-0082 external_id: isi: - '000455641000011' pmid: - '30156465' file: - access_level: open_access checksum: e98465b4416b3e804c47f40086932af2 content_type: application/pdf creator: kschuh date_created: 2019-02-14T12:34:29Z date_updated: 2020-07-14T12:47:15Z file_id: '5994' file_name: 2018_ASCB_Dolati.pdf file_size: 6668971 relation: main_file file_date_updated: 2020-07-14T12:47:15Z has_accepted_license: '1' intvolume: ' 29' isi: 1 issue: '22' language: - iso: eng month: '11' oa: 1 oa_version: Published Version page: 2674-2686 pmid: 1 publication: Molecular Biology of the Cell publication_identifier: eissn: - 1939-4586 publication_status: published publisher: 'American Society for Cell Biology ' quality_controlled: '1' scopus_import: '1' status: public title: On the relation between filament density, force generation, and protrusion rate in mesenchymal cell motility tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 29 year: '2018' ... --- _id: '6497' abstract: - lang: eng text: T cells are actively scanning pMHC-presenting cells in lymphoid organs and nonlymphoid tissues (NLTs) with divergent topologies and confinement. How the T cell actomyosin cytoskeleton facilitates this task in distinct environments is incompletely understood. Here, we show that lack of Myosin IXb (Myo9b), a negative regulator of the small GTPase Rho, led to increased Rho-GTP levels and cell surface stiffness in primary T cells. Nonetheless, intravital imaging revealed robust motility of Myo9b−/− CD8+ T cells in lymphoid tissue and similar expansion and differentiation during immune responses. In contrast, accumulation of Myo9b−/− CD8+ T cells in NLTs was strongly impaired. Specifically, Myo9b was required for T cell crossing of basement membranes, such as those which are present between dermis and epidermis. As consequence, Myo9b−/− CD8+ T cells showed impaired control of skin infections. In sum, we show that Myo9b is critical for the CD8+ T cell adaptation from lymphoid to NLT surveillance and the establishment of protective tissue–resident T cell populations. article_processing_charge: No author: - first_name: Federica full_name: Moalli, Federica last_name: Moalli - first_name: Xenia full_name: Ficht, Xenia last_name: Ficht - first_name: Philipp full_name: Germann, Philipp last_name: Germann - first_name: Mykhailo full_name: Vladymyrov, Mykhailo last_name: Vladymyrov - first_name: Bettina full_name: Stolp, Bettina last_name: Stolp - first_name: Ingrid full_name: de Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: de Vries - first_name: Ruth full_name: Lyck, Ruth last_name: Lyck - first_name: Jasmin full_name: Balmer, Jasmin last_name: Balmer - first_name: Amleto full_name: Fiocchi, Amleto last_name: Fiocchi - first_name: Mario full_name: Kreutzfeldt, Mario last_name: Kreutzfeldt - first_name: Doron full_name: Merkler, Doron last_name: Merkler - first_name: Matteo full_name: Iannacone, Matteo last_name: Iannacone - first_name: Akitaka full_name: Ariga, Akitaka last_name: Ariga - first_name: Michael H. full_name: Stoffel, Michael H. last_name: Stoffel - first_name: James full_name: Sharpe, James last_name: Sharpe - first_name: Martin full_name: Bähler, Martin last_name: Bähler - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Alba full_name: Diz-Muñoz, Alba last_name: Diz-Muñoz - first_name: Jens V. full_name: Stein, Jens V. last_name: Stein citation: ama: Moalli F, Ficht X, Germann P, et al. The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells. The Journal of Experimental Medicine. 2018;2015(7):1869–1890. doi:10.1084/jem.20170896 apa: Moalli, F., Ficht, X., Germann, P., Vladymyrov, M., Stolp, B., de Vries, I., … Stein, J. V. (2018). The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells. The Journal of Experimental Medicine. Rockefeller University Press. https://doi.org/10.1084/jem.20170896 chicago: Moalli, Federica, Xenia Ficht, Philipp Germann, Mykhailo Vladymyrov, Bettina Stolp, Ingrid de Vries, Ruth Lyck, et al. “The Rho Regulator Myosin IXb Enables Nonlymphoid Tissue Seeding of Protective CD8+T Cells.” The Journal of Experimental Medicine. Rockefeller University Press, 2018. https://doi.org/10.1084/jem.20170896. ieee: F. Moalli et al., “The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells,” The Journal of Experimental Medicine, vol. 2015, no. 7. Rockefeller University Press, pp. 1869–1890, 2018. ista: Moalli F, Ficht X, Germann P, Vladymyrov M, Stolp B, de Vries I, Lyck R, Balmer J, Fiocchi A, Kreutzfeldt M, Merkler D, Iannacone M, Ariga A, Stoffel MH, Sharpe J, Bähler M, Sixt MK, Diz-Muñoz A, Stein JV. 2018. The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells. The Journal of Experimental Medicine. 2015(7), 1869–1890. mla: Moalli, Federica, et al. “The Rho Regulator Myosin IXb Enables Nonlymphoid Tissue Seeding of Protective CD8+T Cells.” The Journal of Experimental Medicine, vol. 2015, no. 7, Rockefeller University Press, 2018, pp. 1869–1890, doi:10.1084/jem.20170896. short: F. Moalli, X. Ficht, P. Germann, M. Vladymyrov, B. Stolp, I. de Vries, R. Lyck, J. Balmer, A. Fiocchi, M. Kreutzfeldt, D. Merkler, M. Iannacone, A. Ariga, M.H. Stoffel, J. Sharpe, M. Bähler, M.K. Sixt, A. Diz-Muñoz, J.V. Stein, The Journal of Experimental Medicine 2015 (2018) 1869–1890. date_created: 2019-05-28T12:36:47Z date_published: 2018-06-06T00:00:00Z date_updated: 2023-09-19T14:52:08Z day: '06' ddc: - '570' department: - _id: MiSi doi: 10.1084/jem.20170896 external_id: isi: - '000440822900011' file: - access_level: open_access checksum: 86ae5331f9bfced9a6358a790a04bef4 content_type: application/pdf creator: kschuh date_created: 2019-05-28T12:40:05Z date_updated: 2020-07-14T12:47:32Z file_id: '6498' file_name: 2018_rupress_Moalli.pdf file_size: 3841660 relation: main_file file_date_updated: 2020-07-14T12:47:32Z has_accepted_license: '1' intvolume: ' 2015' isi: 1 issue: '7' language: - iso: eng month: '06' oa: 1 oa_version: Published Version page: 1869–1890 publication: The Journal of Experimental Medicine publication_identifier: eissn: - 1540-9538 issn: - 0022-1007 publication_status: published publisher: Rockefeller University Press quality_controlled: '1' scopus_import: '1' status: public title: The Rho regulator Myosin IXb enables nonlymphoid tissue seeding of protective CD8+T cells tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 2015 year: '2018' ... --- _id: '402' abstract: - lang: eng text: During metastasis, malignant cells escape the primary tumor, intravasate lymphatic vessels, and reach draining sentinel lymph nodes before they colonize distant organs via the blood circulation. Although lymph node metastasis in cancer patients correlates with poor prognosis, evidence is lacking as to whether and how tumor cells enter the bloodstream via lymph nodes. To investigate this question, we delivered carcinoma cells into the lymph nodes of mice by microinfusing the cells into afferent lymphatic vessels. We found that tumor cells rapidly infiltrated the lymph node parenchyma, invaded blood vessels, and seeded lung metastases without involvement of the thoracic duct. These results suggest that the lymph node blood vessels can serve as an exit route for systemic dissemination of cancer cells in experimental mouse models. Whether this form of tumor cell spreading occurs in cancer patients remains to be determined. acknowledged_ssus: - _id: Bio acknowledgement: "M.B. was supported by the Cell Communication in Health and Disease graduate study program of the Austrian Science Fund (FWF) and the Medical University of Vienna. M.S. was supported by the European Research Council (grant ERC GA 281556) and an FWF START award.\r\nWe thank C. Moussion for establishing the intralymphatic injection at IST Austria and for providing anti-PNAd hybridoma supernatant, R. Förster and A. Braun for sharing the intralymphatic injection technology, K. Vaahtomeri for the lentiviral constructs, M. Hons for establishing in vivo multiphoton imaging, the Sixt lab for intellectual input, M. Schunn for help with the design of the in vivo experiments, F. Langer for technical assistance with the in vivo experiments, the bioimaging facility of IST Austria for support, and R. Efferl for providing the CT26 cell line." article_processing_charge: No article_type: original author: - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Frank P full_name: Assen, Frank P id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87 last_name: Assen orcid: 0000-0003-3470-6119 - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Jun full_name: Abe, Jun last_name: Abe - first_name: Helga full_name: Schachner, Helga last_name: Schachner - first_name: Gabriele full_name: Asfour, Gabriele last_name: Asfour - first_name: Zsuzsanna full_name: Bagó Horváth, Zsuzsanna last_name: Bagó Horváth - first_name: Jens full_name: Stein, Jens last_name: Stein - first_name: Pavel full_name: Uhrin, Pavel last_name: Uhrin - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki citation: ama: Brown M, Assen FP, Leithner AF, et al. Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice. Science. 2018;359(6382):1408-1411. doi:10.1126/science.aal3662 apa: Brown, M., Assen, F. P., Leithner, A. F., Abe, J., Schachner, H., Asfour, G., … Kerjaschki, D. (2018). Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.aal3662 chicago: Brown, Markus, Frank P Assen, Alexander F Leithner, Jun Abe, Helga Schachner, Gabriele Asfour, Zsuzsanna Bagó Horváth, et al. “Lymph Node Blood Vessels Provide Exit Routes for Metastatic Tumor Cell Dissemination in Mice.” Science. American Association for the Advancement of Science, 2018. https://doi.org/10.1126/science.aal3662. ieee: M. Brown et al., “Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice,” Science, vol. 359, no. 6382. American Association for the Advancement of Science, pp. 1408–1411, 2018. ista: Brown M, Assen FP, Leithner AF, Abe J, Schachner H, Asfour G, Bagó Horváth Z, Stein J, Uhrin P, Sixt MK, Kerjaschki D. 2018. Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice. Science. 359(6382), 1408–1411. mla: Brown, Markus, et al. “Lymph Node Blood Vessels Provide Exit Routes for Metastatic Tumor Cell Dissemination in Mice.” Science, vol. 359, no. 6382, American Association for the Advancement of Science, 2018, pp. 1408–11, doi:10.1126/science.aal3662. short: M. Brown, F.P. Assen, A.F. Leithner, J. Abe, H. Schachner, G. Asfour, Z. Bagó Horváth, J. Stein, P. Uhrin, M.K. Sixt, D. Kerjaschki, Science 359 (2018) 1408–1411. date_created: 2018-12-11T11:46:16Z date_published: 2018-03-23T00:00:00Z date_updated: 2024-03-27T23:30:09Z day: '23' department: - _id: MiSi doi: 10.1126/science.aal3662 ec_funded: 1 external_id: isi: - '000428043600047' pmid: - '29567714' intvolume: ' 359' isi: 1 issue: '6382' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1126/science.aal3662 month: '03' oa: 1 oa_version: Published Version page: 1408 - 1411 pmid: 1 project: - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Science publication_status: published publisher: American Association for the Advancement of Science publist_id: '7428' quality_controlled: '1' related_material: record: - id: '6947' relation: dissertation_contains status: public scopus_import: '1' status: public title: Lymph node blood vessels provide exit routes for metastatic tumor cell dissemination in mice type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 359 year: '2018' ... --- _id: '15' abstract: - lang: eng text: Although much is known about the physiological framework of T cell motility, and numerous rate-limiting molecules have been identified through loss-of-function approaches, an integrated functional concept of T cell motility is lacking. Here, we used in vivo precision morphometry together with analysis of cytoskeletal dynamics in vitro to deconstruct the basic mechanisms of T cell migration within lymphatic organs. We show that the contributions of the integrin LFA-1 and the chemokine receptor CCR7 are complementary rather than positioned in a linear pathway, as they are during leukocyte extravasation from the blood vasculature. Our data demonstrate that CCR7 controls cortical actin flows, whereas integrins mediate substrate friction that is sufficient to drive locomotion in the absence of considerable surface adhesions and plasma membrane flux. acknowledged_ssus: - _id: SSU acknowledgement: This work was funded by grants from the European Research Council (ERC StG 281556 and CoG 724373) and the Austrian Science Foundation (FWF) to M.S. and by Swiss National Foundation (SNF) project grants 31003A_135649, 31003A_153457 and CR23I3_156234 to J.V.S. F.G. received funding from the European Union’s Horizon 2020 research and innovation programme under the Marie Skłodowska-Curie grant agreement no. 747687, and J.R. was funded by an EMBO long-term fellowship (ALTF 1396-2014). article_processing_charge: No author: - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Aglaja full_name: Kopf, Aglaja id: 31DAC7B6-F248-11E8-B48F-1D18A9856A87 last_name: Kopf orcid: 0000-0002-2187-6656 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Florian R full_name: Gärtner, Florian R id: 397A88EE-F248-11E8-B48F-1D18A9856A87 last_name: Gärtner orcid: 0000-0001-6120-3723 - first_name: Jun full_name: Abe, Jun last_name: Abe - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Jens full_name: Stein, Jens last_name: Stein - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Hons M, Kopf A, Hauschild R, et al. Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. Nature Immunology. 2018;19(6):606-616. doi:10.1038/s41590-018-0109-z apa: Hons, M., Kopf, A., Hauschild, R., Leithner, A. F., Gärtner, F. R., Abe, J., … Sixt, M. K. (2018). Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/s41590-018-0109-z chicago: Hons, Miroslav, Aglaja Kopf, Robert Hauschild, Alexander F Leithner, Florian R Gärtner, Jun Abe, Jörg Renkawitz, Jens Stein, and Michael K Sixt. “Chemokines and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal Migration of T Cells.” Nature Immunology. Nature Publishing Group, 2018. https://doi.org/10.1038/s41590-018-0109-z. ieee: M. Hons et al., “Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells,” Nature Immunology, vol. 19, no. 6. Nature Publishing Group, pp. 606–616, 2018. ista: Hons M, Kopf A, Hauschild R, Leithner AF, Gärtner FR, Abe J, Renkawitz J, Stein J, Sixt MK. 2018. Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells. Nature Immunology. 19(6), 606–616. mla: Hons, Miroslav, et al. “Chemokines and Integrins Independently Tune Actin Flow and Substrate Friction during Intranodal Migration of T Cells.” Nature Immunology, vol. 19, no. 6, Nature Publishing Group, 2018, pp. 606–16, doi:10.1038/s41590-018-0109-z. short: M. Hons, A. Kopf, R. Hauschild, A.F. Leithner, F.R. Gärtner, J. Abe, J. Renkawitz, J. Stein, M.K. Sixt, Nature Immunology 19 (2018) 606–616. date_created: 2018-12-11T11:44:10Z date_published: 2018-05-18T00:00:00Z date_updated: 2024-03-27T23:30:39Z day: '18' department: - _id: MiSi - _id: Bio doi: 10.1038/s41590-018-0109-z ec_funded: 1 external_id: isi: - '000433041500026' pmid: - '29777221' intvolume: ' 19' isi: 1 issue: '6' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pubmed/29777221 month: '05' oa: 1 oa_version: Published Version page: 606 - 616 pmid: 1 project: - _id: 25FE9508-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '724373' name: Cellular navigation along spatial gradients - _id: 260AA4E2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '747687' name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells - _id: 25A48D24-B435-11E9-9278-68D0E5697425 grant_number: ALTF 1396-2014 name: Molecular and system level view of immune cell migration - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Nature Immunology publication_status: published publisher: Nature Publishing Group publist_id: '8040' quality_controlled: '1' related_material: record: - id: '6891' relation: dissertation_contains status: public scopus_import: '1' status: public title: Chemokines and integrins independently tune actin flow and substrate friction during intranodal migration of T cells type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 19 year: '2018' ... --- _id: '569' abstract: - lang: eng text: The actomyosin ring generates force to ingress the cytokinetic cleavage furrow in animal cells, yet its filament organization and the mechanism of contractility is not well understood. We quantified actin filament order in human cells using fluorescence polarization microscopy and found that cleavage furrow ingression initiates by contraction of an equatorial actin network with randomly oriented filaments. The network subsequently gradually reoriented actin filaments along the cell equator. This strictly depended on myosin II activity, suggesting local network reorganization by mechanical forces. Cortical laser microsurgery revealed that during cytokinesis progression, mechanical tension increased substantially along the direction of the cell equator, while the network contracted laterally along the pole-to-pole axis without a detectable increase in tension. Our data suggest that an asymmetric increase in cortical tension promotes filament reorientation along the cytokinetic cleavage furrow, which might have implications for diverse other biological processes involving actomyosin rings. article_number: e30867 author: - first_name: Felix full_name: Spira, Felix last_name: Spira - first_name: Sara full_name: Cuylen Haering, Sara last_name: Cuylen Haering - first_name: Shalin full_name: Mehta, Shalin last_name: Mehta - first_name: Matthias full_name: Samwer, Matthias last_name: Samwer - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Amitabh full_name: Verma, Amitabh last_name: Verma - first_name: Rudolf full_name: Oldenbourg, Rudolf last_name: Oldenbourg - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Daniel full_name: Gerlich, Daniel last_name: Gerlich citation: ama: Spira F, Cuylen Haering S, Mehta S, et al. Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments. eLife. 2017;6. doi:10.7554/eLife.30867 apa: Spira, F., Cuylen Haering, S., Mehta, S., Samwer, M., Reversat, A., Verma, A., … Gerlich, D. (2017). Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.30867 chicago: Spira, Felix, Sara Cuylen Haering, Shalin Mehta, Matthias Samwer, Anne Reversat, Amitabh Verma, Rudolf Oldenbourg, Michael K Sixt, and Daniel Gerlich. “Cytokinesis in Vertebrate Cells Initiates by Contraction of an Equatorial Actomyosin Network Composed of Randomly Oriented Filaments.” ELife. eLife Sciences Publications, 2017. https://doi.org/10.7554/eLife.30867. ieee: F. Spira et al., “Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments,” eLife, vol. 6. eLife Sciences Publications, 2017. ista: Spira F, Cuylen Haering S, Mehta S, Samwer M, Reversat A, Verma A, Oldenbourg R, Sixt MK, Gerlich D. 2017. Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments. eLife. 6, e30867. mla: Spira, Felix, et al. “Cytokinesis in Vertebrate Cells Initiates by Contraction of an Equatorial Actomyosin Network Composed of Randomly Oriented Filaments.” ELife, vol. 6, e30867, eLife Sciences Publications, 2017, doi:10.7554/eLife.30867. short: F. Spira, S. Cuylen Haering, S. Mehta, M. Samwer, A. Reversat, A. Verma, R. Oldenbourg, M.K. Sixt, D. Gerlich, ELife 6 (2017). date_created: 2018-12-11T11:47:14Z date_published: 2017-11-06T00:00:00Z date_updated: 2023-02-23T12:30:29Z day: '06' ddc: - '570' department: - _id: MiSi doi: 10.7554/eLife.30867 file: - access_level: open_access checksum: ba09c1451153d39e4f4b7cee013e314c content_type: application/pdf creator: system date_created: 2018-12-12T10:10:40Z date_updated: 2020-07-14T12:47:10Z file_id: '4829' file_name: IST-2017-919-v1+1_elife-30867-figures-v1.pdf file_size: 9666973 relation: main_file - access_level: open_access checksum: 01eb51f1d6ad679947415a51c988e137 content_type: application/pdf creator: system date_created: 2018-12-12T10:10:41Z date_updated: 2020-07-14T12:47:10Z file_id: '4830' file_name: IST-2017-919-v1+2_elife-30867-v1.pdf file_size: 5951246 relation: main_file file_date_updated: 2020-07-14T12:47:10Z has_accepted_license: '1' intvolume: ' 6' language: - iso: eng month: '11' oa: 1 oa_version: Published Version publication: eLife publication_identifier: issn: - 2050084X publication_status: published publisher: eLife Sciences Publications publist_id: '7245' pubrep_id: '919' quality_controlled: '1' scopus_import: 1 status: public title: Cytokinesis in vertebrate cells initiates by contraction of an equatorial actomyosin network composed of randomly oriented filaments tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 6 year: '2017' ... --- _id: '571' abstract: - lang: eng text: Blood platelets are critical for hemostasis and thrombosis and play diverse roles during immune responses. Despite these versatile tasks in mammalian biology, their skills on a cellular level are deemed limited, mainly consisting in rolling, adhesion, and aggregate formation. Here, we identify an unappreciated asset of platelets and show that adherent platelets use adhesion receptors to mechanically probe the adhesive substrate in their local microenvironment. When actomyosin-dependent traction forces overcome substrate resistance, platelets migrate and pile up the adhesive substrate together with any bound particulate material. They use this ability to act as cellular scavengers, scanning the vascular surface for potential invaders and collecting deposited bacteria. Microbe collection by migrating platelets boosts the activity of professional phagocytes, exacerbating inflammatory tissue injury in sepsis. This assigns platelets a central role in innate immune responses and identifies them as potential targets to dampen inflammatory tissue damage in clinical scenarios of severe systemic infection. In addition to their role in thrombosis and hemostasis, platelets can also migrate to sites of infection to help trap bacteria and clear the vascular surface. author: - first_name: Florian R full_name: Gärtner, Florian R id: 397A88EE-F248-11E8-B48F-1D18A9856A87 last_name: Gärtner orcid: 0000-0001-6120-3723 - first_name: Zerkah full_name: Ahmad, Zerkah last_name: Ahmad - first_name: Gerhild full_name: Rosenberger, Gerhild last_name: Rosenberger - first_name: Shuxia full_name: Fan, Shuxia last_name: Fan - first_name: Leo full_name: Nicolai, Leo last_name: Nicolai - first_name: Benjamin full_name: Busch, Benjamin last_name: Busch - first_name: Gökce full_name: Yavuz, Gökce last_name: Yavuz - first_name: Manja full_name: Luckner, Manja last_name: Luckner - first_name: Hellen full_name: Ishikawa Ankerhold, Hellen last_name: Ishikawa Ankerhold - first_name: Roman full_name: Hennel, Roman last_name: Hennel - first_name: Alexandre full_name: Benechet, Alexandre last_name: Benechet - first_name: Michael full_name: Lorenz, Michael last_name: Lorenz - first_name: Sue full_name: Chandraratne, Sue last_name: Chandraratne - first_name: Irene full_name: Schubert, Irene last_name: Schubert - first_name: Sebastian full_name: Helmer, Sebastian last_name: Helmer - first_name: Bianca full_name: Striednig, Bianca last_name: Striednig - first_name: Konstantin full_name: Stark, Konstantin last_name: Stark - first_name: Marek full_name: Janko, Marek last_name: Janko - first_name: Ralph full_name: Böttcher, Ralph last_name: Böttcher - first_name: Admar full_name: Verschoor, Admar last_name: Verschoor - first_name: Catherine full_name: Leon, Catherine last_name: Leon - first_name: Christian full_name: Gachet, Christian last_name: Gachet - first_name: Thomas full_name: Gudermann, Thomas last_name: Gudermann - first_name: Michael full_name: Mederos Y Schnitzler, Michael last_name: Mederos Y Schnitzler - first_name: Zachary full_name: Pincus, Zachary last_name: Pincus - first_name: Matteo full_name: Iannacone, Matteo last_name: Iannacone - first_name: Rainer full_name: Haas, Rainer last_name: Haas - first_name: Gerhard full_name: Wanner, Gerhard last_name: Wanner - first_name: Kirsten full_name: Lauber, Kirsten last_name: Lauber - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Steffen full_name: Massberg, Steffen last_name: Massberg citation: ama: Gärtner FR, Ahmad Z, Rosenberger G, et al. Migrating platelets are mechano scavengers that collect and bundle bacteria. Cell Press. 2017;171(6):1368-1382. doi:10.1016/j.cell.2017.11.001 apa: Gärtner, F. R., Ahmad, Z., Rosenberger, G., Fan, S., Nicolai, L., Busch, B., … Massberg, S. (2017). Migrating platelets are mechano scavengers that collect and bundle bacteria. Cell Press. Cell Press. https://doi.org/10.1016/j.cell.2017.11.001 chicago: Gärtner, Florian R, Zerkah Ahmad, Gerhild Rosenberger, Shuxia Fan, Leo Nicolai, Benjamin Busch, Gökce Yavuz, et al. “Migrating Platelets Are Mechano Scavengers That Collect and Bundle Bacteria.” Cell Press. Cell Press, 2017. https://doi.org/10.1016/j.cell.2017.11.001. ieee: F. R. Gärtner et al., “Migrating platelets are mechano scavengers that collect and bundle bacteria,” Cell Press, vol. 171, no. 6. Cell Press, pp. 1368–1382, 2017. ista: Gärtner FR, Ahmad Z, Rosenberger G, Fan S, Nicolai L, Busch B, Yavuz G, Luckner M, Ishikawa Ankerhold H, Hennel R, Benechet A, Lorenz M, Chandraratne S, Schubert I, Helmer S, Striednig B, Stark K, Janko M, Böttcher R, Verschoor A, Leon C, Gachet C, Gudermann T, Mederos Y Schnitzler M, Pincus Z, Iannacone M, Haas R, Wanner G, Lauber K, Sixt MK, Massberg S. 2017. Migrating platelets are mechano scavengers that collect and bundle bacteria. Cell Press. 171(6), 1368–1382. mla: Gärtner, Florian R., et al. “Migrating Platelets Are Mechano Scavengers That Collect and Bundle Bacteria.” Cell Press, vol. 171, no. 6, Cell Press, 2017, pp. 1368–82, doi:10.1016/j.cell.2017.11.001. short: F.R. Gärtner, Z. Ahmad, G. Rosenberger, S. Fan, L. Nicolai, B. Busch, G. Yavuz, M. Luckner, H. Ishikawa Ankerhold, R. Hennel, A. Benechet, M. Lorenz, S. Chandraratne, I. Schubert, S. Helmer, B. Striednig, K. Stark, M. Janko, R. Böttcher, A. Verschoor, C. Leon, C. Gachet, T. Gudermann, M. Mederos Y Schnitzler, Z. Pincus, M. Iannacone, R. Haas, G. Wanner, K. Lauber, M.K. Sixt, S. Massberg, Cell Press 171 (2017) 1368–1382. date_created: 2018-12-11T11:47:15Z date_published: 2017-11-30T00:00:00Z date_updated: 2021-01-12T08:03:15Z day: '30' department: - _id: MiSi doi: 10.1016/j.cell.2017.11.001 ec_funded: 1 intvolume: ' 171' issue: '6' language: - iso: eng month: '11' oa_version: None page: 1368 - 1382 project: - _id: 260AA4E2-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '747687' name: Mechanical Adaptation of Lamellipodial Actin Networks in Migrating Cells publication: Cell Press publication_identifier: issn: - '00928674' publication_status: published publisher: Cell Press publist_id: '7243' quality_controlled: '1' scopus_import: 1 status: public title: Migrating platelets are mechano scavengers that collect and bundle bacteria type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 171 year: '2017' ... --- _id: '659' abstract: - lang: eng text: Migration frequently involves Rac-mediated protrusion of lamellipodia, formed by Arp2/3 complex-dependent branching thought to be crucial for force generation and stability of these networks. The formins FMNL2 and FMNL3 are Cdc42 effectors targeting to the lamellipodium tip and shown here to nucleate and elongate actin filaments with complementary activities in vitro. In migrating B16-F1 melanoma cells, both formins contribute to the velocity of lamellipodium protrusion. Loss of FMNL2/3 function in melanoma cells and fibroblasts reduces lamellipodial width, actin filament density and -bundling, without changing patterns of Arp2/3 complex incorporation. Strikingly, in melanoma cells, FMNL2/3 gene inactivation almost completely abolishes protrusion forces exerted by lamellipodia and modifies their ultrastructural organization. Consistently, CRISPR/Cas-mediated depletion of FMNL2/3 in fibroblasts reduces both migration and capability of cells to move against viscous media. Together, we conclude that force generation in lamellipodia strongly depends on FMNL formin activity, operating in addition to Arp2/3 complex-dependent filament branching. article_number: '14832' article_processing_charge: No author: - first_name: Frieda full_name: Kage, Frieda last_name: Kage - first_name: Moritz full_name: Winterhoff, Moritz last_name: Winterhoff - first_name: Vanessa full_name: Dimchev, Vanessa last_name: Dimchev - first_name: Jan full_name: Müller, Jan id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D last_name: Müller - first_name: Tobias full_name: Thalheim, Tobias last_name: Thalheim - first_name: Anika full_name: Freise, Anika last_name: Freise - first_name: Stefan full_name: Brühmann, Stefan last_name: Brühmann - first_name: Jana full_name: Kollasser, Jana last_name: Kollasser - first_name: Jennifer full_name: Block, Jennifer last_name: Block - first_name: Georgi A full_name: Dimchev, Georgi A last_name: Dimchev - first_name: Matthias full_name: Geyer, Matthias last_name: Geyer - first_name: Hams full_name: Schnittler, Hams last_name: Schnittler - first_name: Cord full_name: Brakebusch, Cord last_name: Brakebusch - first_name: Theresia full_name: Stradal, Theresia last_name: Stradal - first_name: Marie full_name: Carlier, Marie last_name: Carlier - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Josef full_name: Käs, Josef last_name: Käs - first_name: Jan full_name: Faix, Jan last_name: Faix - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner citation: ama: Kage F, Winterhoff M, Dimchev V, et al. FMNL formins boost lamellipodial force generation. Nature Communications. 2017;8. doi:10.1038/ncomms14832 apa: Kage, F., Winterhoff, M., Dimchev, V., Müller, J., Thalheim, T., Freise, A., … Rottner, K. (2017). FMNL formins boost lamellipodial force generation. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms14832 chicago: Kage, Frieda, Moritz Winterhoff, Vanessa Dimchev, Jan Müller, Tobias Thalheim, Anika Freise, Stefan Brühmann, et al. “FMNL Formins Boost Lamellipodial Force Generation.” Nature Communications. Nature Publishing Group, 2017. https://doi.org/10.1038/ncomms14832. ieee: F. Kage et al., “FMNL formins boost lamellipodial force generation,” Nature Communications, vol. 8. Nature Publishing Group, 2017. ista: Kage F, Winterhoff M, Dimchev V, Müller J, Thalheim T, Freise A, Brühmann S, Kollasser J, Block J, Dimchev GA, Geyer M, Schnittler H, Brakebusch C, Stradal T, Carlier M, Sixt MK, Käs J, Faix J, Rottner K. 2017. FMNL formins boost lamellipodial force generation. Nature Communications. 8, 14832. mla: Kage, Frieda, et al. “FMNL Formins Boost Lamellipodial Force Generation.” Nature Communications, vol. 8, 14832, Nature Publishing Group, 2017, doi:10.1038/ncomms14832. short: F. Kage, M. Winterhoff, V. Dimchev, J. Müller, T. Thalheim, A. Freise, S. Brühmann, J. Kollasser, J. Block, G.A. Dimchev, M. Geyer, H. Schnittler, C. Brakebusch, T. Stradal, M. Carlier, M.K. Sixt, J. Käs, J. Faix, K. Rottner, Nature Communications 8 (2017). date_created: 2018-12-11T11:47:46Z date_published: 2017-03-22T00:00:00Z date_updated: 2021-01-12T08:08:06Z day: '22' ddc: - '570' department: - _id: MiSi doi: 10.1038/ncomms14832 file: - access_level: open_access checksum: dae30190291c3630e8102d8714a8d23e content_type: application/pdf creator: system date_created: 2018-12-12T10:14:21Z date_updated: 2020-07-14T12:47:34Z file_id: '5072' file_name: IST-2017-902-v1+1_Kage_et_al-2017-Nature_Communications.pdf file_size: 9523746 relation: main_file file_date_updated: 2020-07-14T12:47:34Z has_accepted_license: '1' intvolume: ' 8' language: - iso: eng month: '03' oa: 1 oa_version: Published Version publication: Nature Communications publication_identifier: issn: - '20411723' publication_status: published publisher: Nature Publishing Group publist_id: '7075' pubrep_id: '902' quality_controlled: '1' scopus_import: 1 status: public title: FMNL formins boost lamellipodial force generation tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 8 year: '2017' ... --- _id: '668' abstract: - lang: eng text: Macrophage filopodia, finger-like membrane protrusions, were first implicated in phagocytosis more than 100 years ago, but little is still known about the involvement of these actin-dependent structures in particle clearance. Using spinning disk confocal microscopy to image filopodial dynamics in mouse resident Lifeact-EGFP macrophages, we show that filopodia, or filopodia-like structures, support pathogen clearance by multiple means. Filopodia supported the phagocytic uptake of bacterial (Escherichia coli) particles by (i) capturing along the filopodial shaft and surfing toward the cell body, the most common mode of capture; (ii) capturing via the tip followed by retraction; (iii) combinations of surfing and retraction; or (iv) sweeping actions. In addition, filopodia supported the uptake of zymosan (Saccharomyces cerevisiae) particles by (i) providing fixation, (ii) capturing at the tip and filopodia-guided actin anterograde flow with phagocytic cup formation, and (iii) the rapid growth of new protrusions. To explore the role of filopodia-inducing Cdc42, we generated myeloid-restricted Cdc42 knock-out mice. Cdc42-deficient macrophages exhibited rapid phagocytic cup kinetics, but reduced particle clearance, which could be explained by the marked rounded-up morphology of these cells. Macrophages lacking Myo10, thought to act downstream of Cdc42, had normal morphology, motility, and phagocytic cup formation, but displayed markedly reduced filopodia formation. In conclusion, live-cell imaging revealed multiple mechanisms involving macrophage filopodia in particle capture and engulfment. Cdc42 is not critical for filopodia or phagocytic cup formation, but plays a key role in driving macrophage lamellipodial spreading. article_type: original author: - first_name: Markus full_name: Horsthemke, Markus last_name: Horsthemke - first_name: Anne full_name: Bachg, Anne last_name: Bachg - first_name: Katharina full_name: Groll, Katharina last_name: Groll - first_name: Sven full_name: Moyzio, Sven last_name: Moyzio - first_name: Barbara full_name: Müther, Barbara last_name: Müther - first_name: Sandra full_name: Hemkemeyer, Sandra last_name: Hemkemeyer - first_name: Roland full_name: Wedlich Söldner, Roland last_name: Wedlich Söldner - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Sebastian full_name: Tacke, Sebastian last_name: Tacke - first_name: Martin full_name: Bähler, Martin last_name: Bähler - first_name: Peter full_name: Hanley, Peter last_name: Hanley citation: ama: Horsthemke M, Bachg A, Groll K, et al. Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. 2017;292(17):7258-7273. doi:10.1074/jbc.M116.766923 apa: Horsthemke, M., Bachg, A., Groll, K., Moyzio, S., Müther, B., Hemkemeyer, S., … Hanley, P. (2017). Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. American Society for Biochemistry and Molecular Biology. https://doi.org/10.1074/jbc.M116.766923 chicago: Horsthemke, Markus, Anne Bachg, Katharina Groll, Sven Moyzio, Barbara Müther, Sandra Hemkemeyer, Roland Wedlich Söldner, et al. “Multiple Roles of Filopodial Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” Journal of Biological Chemistry. American Society for Biochemistry and Molecular Biology, 2017. https://doi.org/10.1074/jbc.M116.766923. ieee: M. Horsthemke et al., “Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion,” Journal of Biological Chemistry, vol. 292, no. 17. American Society for Biochemistry and Molecular Biology, pp. 7258–7273, 2017. ista: Horsthemke M, Bachg A, Groll K, Moyzio S, Müther B, Hemkemeyer S, Wedlich Söldner R, Sixt MK, Tacke S, Bähler M, Hanley P. 2017. Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion. Journal of Biological Chemistry. 292(17), 7258–7273. mla: Horsthemke, Markus, et al. “Multiple Roles of Filopodial Dynamics in Particle Capture and Phagocytosis and Phenotypes of Cdc42 and Myo10 Deletion.” Journal of Biological Chemistry, vol. 292, no. 17, American Society for Biochemistry and Molecular Biology, 2017, pp. 7258–73, doi:10.1074/jbc.M116.766923. short: M. Horsthemke, A. Bachg, K. Groll, S. Moyzio, B. Müther, S. Hemkemeyer, R. Wedlich Söldner, M.K. Sixt, S. Tacke, M. Bähler, P. Hanley, Journal of Biological Chemistry 292 (2017) 7258–7273. date_created: 2018-12-11T11:47:49Z date_published: 2017-04-28T00:00:00Z date_updated: 2021-01-12T08:08:34Z day: '28' ddc: - '570' department: - _id: MiSi doi: 10.1074/jbc.M116.766923 file: - access_level: open_access checksum: d488162874326a4bb056065fa549dc4a content_type: application/pdf creator: dernst date_created: 2019-10-24T15:25:42Z date_updated: 2020-07-14T12:47:37Z file_id: '6971' file_name: 2017_JBC_Horsthemke.pdf file_size: 5647880 relation: main_file file_date_updated: 2020-07-14T12:47:37Z has_accepted_license: '1' intvolume: ' 292' issue: '17' language: - iso: eng month: '04' oa: 1 oa_version: Published Version page: 7258 - 7273 publication: Journal of Biological Chemistry publication_identifier: issn: - '00219258' publication_status: published publisher: American Society for Biochemistry and Molecular Biology publist_id: '7059' quality_controlled: '1' scopus_import: 1 status: public title: Multiple roles of filopodial dynamics in particle capture and phagocytosis and phenotypes of Cdc42 and Myo10 deletion type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 292 year: '2017' ... --- _id: '672' abstract: - lang: eng text: Trafficking cells frequently transmigrate through epithelial and endothelial monolayers. How monolayers cooperate with the penetrating cells to support their transit is poorly understood. We studied dendritic cell (DC) entry into lymphatic capillaries as a model system for transendothelial migration. We find that the chemokine CCL21, which is the decisive guidance cue for intravasation, mainly localizes in the trans-Golgi network and intracellular vesicles of lymphatic endothelial cells. Upon DC transmigration, these Golgi deposits disperse and CCL21 becomes extracellularly enriched at the sites of endothelial cell-cell junctions. When we reconstitute the transmigration process in vitro, we find that secretion of CCL21-positive vesicles is triggered by a DC contact-induced calcium signal, and selective calcium chelation in lymphatic endothelium attenuates transmigration. Altogether, our data demonstrate a chemokine-mediated feedback between DCs and lymphatic endothelium, which facilitates transendothelial migration. article_processing_charge: Yes author: - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner - first_name: Matthias full_name: Mehling, Matthias id: 3C23B994-F248-11E8-B48F-1D18A9856A87 last_name: Mehling orcid: 0000-0001-8599-1226 - first_name: Walter full_name: Kaufmann, Walter id: 3F99E422-F248-11E8-B48F-1D18A9856A87 last_name: Kaufmann orcid: 0000-0001-9735-5315 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Vaahtomeri K, Brown M, Hauschild R, et al. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. 2017;19(5):902-909. doi:10.1016/j.celrep.2017.04.027 apa: Vaahtomeri, K., Brown, M., Hauschild, R., de Vries, I., Leithner, A. F., Mehling, M., … Sixt, M. K. (2017). Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2017.04.027 chicago: Vaahtomeri, Kari, Markus Brown, Robert Hauschild, Ingrid de Vries, Alexander F Leithner, Matthias Mehling, Walter Kaufmann, and Michael K Sixt. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports. Cell Press, 2017. https://doi.org/10.1016/j.celrep.2017.04.027. ieee: K. Vaahtomeri et al., “Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia,” Cell Reports, vol. 19, no. 5. Cell Press, pp. 902–909, 2017. ista: Vaahtomeri K, Brown M, Hauschild R, de Vries I, Leithner AF, Mehling M, Kaufmann W, Sixt MK. 2017. Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia. Cell Reports. 19(5), 902–909. mla: Vaahtomeri, Kari, et al. “Locally Triggered Release of the Chemokine CCL21 Promotes Dendritic Cell Transmigration across Lymphatic Endothelia.” Cell Reports, vol. 19, no. 5, Cell Press, 2017, pp. 902–09, doi:10.1016/j.celrep.2017.04.027. short: K. Vaahtomeri, M. Brown, R. Hauschild, I. de Vries, A.F. Leithner, M. Mehling, W. Kaufmann, M.K. Sixt, Cell Reports 19 (2017) 902–909. date_created: 2018-12-11T11:47:50Z date_published: 2017-05-02T00:00:00Z date_updated: 2023-02-23T12:50:09Z day: '02' ddc: - '570' department: - _id: MiSi - _id: Bio - _id: EM-Fac doi: 10.1016/j.celrep.2017.04.027 ec_funded: 1 file: - access_level: open_access checksum: 8fdddaab1f1d76a6ec9ca94dcb6b07a2 content_type: application/pdf creator: system date_created: 2018-12-12T10:14:54Z date_updated: 2020-07-14T12:47:38Z file_id: '5109' file_name: IST-2017-900-v1+1_1-s2.0-S2211124717305211-main.pdf file_size: 2248814 relation: main_file file_date_updated: 2020-07-14T12:47:38Z has_accepted_license: '1' intvolume: ' 19' issue: '5' language: - iso: eng month: '05' oa: 1 oa_version: Published Version page: 902 - 909 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Cell Reports publication_identifier: issn: - '22111247' publication_status: published publisher: Cell Press publist_id: '7052' pubrep_id: '900' quality_controlled: '1' scopus_import: 1 status: public title: Locally triggered release of the chemokine CCL21 promotes dendritic cell transmigration across lymphatic endothelia tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 19 year: '2017' ... --- _id: '674' abstract: - lang: eng text: Navigation of cells along gradients of guidance cues is a determining step in many developmental and immunological processes. Gradients can either be soluble or immobilized to tissues as demonstrated for the haptotactic migration of dendritic cells (DCs) toward higher concentrations of immobilized chemokine CCL21. To elucidate how gradient characteristics govern cellular response patterns, we here introduce an in vitro system allowing to track migratory responses of DCs to precisely controlled immobilized gradients of CCL21. We find that haptotactic sensing depends on the absolute CCL21 concentration and local steepness of the gradient, consistent with a scenario where DC directionality is governed by the signal-to-noise ratio of CCL21 binding to the receptor CCR7. We find that the conditions for optimal DC guidance are perfectly provided by the CCL21 gradients we measure in vivo. Furthermore, we find that CCR7 signal termination by the G-protein-coupled receptor kinase 6 (GRK6) is crucial for haptotactic but dispensable for chemotactic CCL21 gradient sensing in vitro and confirm those observations in vivo. These findings suggest that stable, tissue-bound CCL21 gradients as sustainable “roads” ensure optimal guidance in vivo. author: - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Veronika full_name: Bierbaum, Veronika id: 3FD04378-F248-11E8-B48F-1D18A9856A87 last_name: Bierbaum - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Teresa full_name: Tarrant, Teresa last_name: Tarrant - first_name: Tobias full_name: Bollenbach, Tobias id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87 last_name: Bollenbach orcid: 0000-0003-4398-476X - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Schwarz J, Bierbaum V, Vaahtomeri K, et al. Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. 2017;27(9):1314-1325. doi:10.1016/j.cub.2017.04.004 apa: Schwarz, J., Bierbaum, V., Vaahtomeri, K., Hauschild, R., Brown, M., de Vries, I., … Sixt, M. K. (2017). Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2017.04.004 chicago: Schwarz, Jan, Veronika Bierbaum, Kari Vaahtomeri, Robert Hauschild, Markus Brown, Ingrid de Vries, Alexander F Leithner, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2017.04.004. ieee: J. Schwarz et al., “Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6,” Current Biology, vol. 27, no. 9. Cell Press, pp. 1314–1325, 2017. ista: Schwarz J, Bierbaum V, Vaahtomeri K, Hauschild R, Brown M, de Vries I, Leithner AF, Reversat A, Merrin J, Tarrant T, Bollenbach MT, Sixt MK. 2017. Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6. Current Biology. 27(9), 1314–1325. mla: Schwarz, Jan, et al. “Dendritic Cells Interpret Haptotactic Chemokine Gradients in a Manner Governed by Signal to Noise Ratio and Dependent on GRK6.” Current Biology, vol. 27, no. 9, Cell Press, 2017, pp. 1314–25, doi:10.1016/j.cub.2017.04.004. short: J. Schwarz, V. Bierbaum, K. Vaahtomeri, R. Hauschild, M. Brown, I. de Vries, A.F. Leithner, A. Reversat, J. Merrin, T. Tarrant, M.T. Bollenbach, M.K. Sixt, Current Biology 27 (2017) 1314–1325. date_created: 2018-12-11T11:47:51Z date_published: 2017-05-09T00:00:00Z date_updated: 2023-02-23T12:50:44Z day: '09' department: - _id: MiSi - _id: Bio - _id: NanoFab doi: 10.1016/j.cub.2017.04.004 ec_funded: 1 intvolume: ' 27' issue: '9' language: - iso: eng month: '05' oa_version: None page: 1314 - 1325 project: - _id: 25681D80-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '291734' name: International IST Postdoc Fellowship Programme - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Current Biology publication_identifier: issn: - '09609822' publication_status: published publisher: Cell Press publist_id: '7050' quality_controlled: '1' scopus_import: 1 status: public title: Dendritic cells interpret haptotactic chemokine gradients in a manner governed by signal to noise ratio and dependent on GRK6 type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 27 year: '2017' ... --- _id: '694' abstract: - lang: eng text: A change regarding the extent of adhesion - hereafter referred to as adhesion plasticity - between adhesive and less-adhesive states of mammalian cells is important for their behavior. To investigate adhesion plasticity, we have selected a stable isogenic subpopulation of human MDA-MB-468 breast carcinoma cells growing in suspension. These suspension cells are unable to re-adhere to various matrices or to contract three-dimensional collagen lattices. By using transcriptome analysis, we identified the focal adhesion protein tensin3 (Tns3) as a determinant of adhesion plasticity. Tns3 is strongly reduced at mRNA and protein levels in suspension cells. Furthermore, by transiently challenging breast cancer cells to grow under non-adherent conditions markedly reduces Tns3 protein expression, which is regained upon re-adhesion. Stable knockdown of Tns3 in parental MDA-MB-468 cells results in defective adhesion, spreading and migration. Tns3-knockdown cells display impaired structure and dynamics of focal adhesion complexes as determined by immunostaining. Restoration of Tns3 protein expression in suspension cells partially rescues adhesion and focal contact composition. Our work identifies Tns3 as a crucial focal adhesion component regulated by, and functionally contributing to, the switch between adhesive and non-adhesive states in MDA-MB-468 cancer cells. article_type: original author: - first_name: Astrid full_name: Veß, Astrid last_name: Veß - first_name: Ulrich full_name: Blache, Ulrich last_name: Blache - first_name: Laura full_name: Leitner, Laura last_name: Leitner - first_name: Angela full_name: Kurz, Angela last_name: Kurz - first_name: Anja full_name: Ehrenpfordt, Anja last_name: Ehrenpfordt - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Guido full_name: Posern, Guido last_name: Posern citation: ama: Veß A, Blache U, Leitner L, et al. A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell Science. 2017;130(13):2172-2184. doi:10.1242/jcs.200899 apa: Veß, A., Blache, U., Leitner, L., Kurz, A., Ehrenpfordt, A., Sixt, M. K., & Posern, G. (2017). A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.200899 chicago: Veß, Astrid, Ulrich Blache, Laura Leitner, Angela Kurz, Anja Ehrenpfordt, Michael K Sixt, and Guido Posern. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell Science. Company of Biologists, 2017. https://doi.org/10.1242/jcs.200899. ieee: A. Veß et al., “A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity,” Journal of Cell Science, vol. 130, no. 13. Company of Biologists, pp. 2172–2184, 2017. ista: Veß A, Blache U, Leitner L, Kurz A, Ehrenpfordt A, Sixt MK, Posern G. 2017. A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity. Journal of Cell Science. 130(13), 2172–2184. mla: Veß, Astrid, et al. “A Dual Phenotype of MDA MB 468 Cancer Cells Reveals Mutual Regulation of Tensin3 and Adhesion Plasticity.” Journal of Cell Science, vol. 130, no. 13, Company of Biologists, 2017, pp. 2172–84, doi:10.1242/jcs.200899. short: A. Veß, U. Blache, L. Leitner, A. Kurz, A. Ehrenpfordt, M.K. Sixt, G. Posern, Journal of Cell Science 130 (2017) 2172–2184. date_created: 2018-12-11T11:47:58Z date_published: 2017-07-01T00:00:00Z date_updated: 2021-01-12T08:09:41Z day: '01' ddc: - '570' department: - _id: MiSi doi: 10.1242/jcs.200899 external_id: pmid: - '28515231' file: - access_level: open_access checksum: 42c81a0a4fc3128883b391c3af3f74bc content_type: application/pdf creator: dernst date_created: 2019-10-24T09:43:56Z date_updated: 2020-07-14T12:47:45Z file_id: '6966' file_name: 2017_CellScience_Vess.pdf file_size: 10847596 relation: main_file file_date_updated: 2020-07-14T12:47:45Z has_accepted_license: '1' intvolume: ' 130' issue: '13' language: - iso: eng month: '07' oa: 1 oa_version: Published Version page: 2172 - 2184 pmid: 1 publication: Journal of Cell Science publication_identifier: issn: - '00219533' publication_status: published publisher: Company of Biologists publist_id: '7008' quality_controlled: '1' scopus_import: 1 status: public title: A dual phenotype of MDA MB 468 cancer cells reveals mutual regulation of tensin3 and adhesion plasticity type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 130 year: '2017' ... --- _id: '1161' abstract: - lang: eng text: Coordinated changes of cell shape are often the result of the excitable, wave-like dynamics of the actin cytoskeleton. New work shows that, in migrating cells, protrusion waves arise from mechanochemical crosstalk between adhesion sites, membrane tension and the actin protrusive machinery. article_processing_charge: No author: - first_name: Jan full_name: Müller, Jan id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D last_name: Müller - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Müller J, Sixt MK. Cell migration: Making the waves. Current Biology. 2017;27(1):R24-R25. doi:10.1016/j.cub.2016.11.035' apa: 'Müller, J., & Sixt, M. K. (2017). Cell migration: Making the waves. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2016.11.035' chicago: 'Müller, Jan, and Michael K Sixt. “Cell Migration: Making the Waves.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2016.11.035.' ieee: 'J. Müller and M. K. Sixt, “Cell migration: Making the waves,” Current Biology, vol. 27, no. 1. Cell Press, pp. R24–R25, 2017.' ista: 'Müller J, Sixt MK. 2017. Cell migration: Making the waves. Current Biology. 27(1), R24–R25.' mla: 'Müller, Jan, and Michael K. Sixt. “Cell Migration: Making the Waves.” Current Biology, vol. 27, no. 1, Cell Press, 2017, pp. R24–25, doi:10.1016/j.cub.2016.11.035.' short: J. Müller, M.K. Sixt, Current Biology 27 (2017) R24–R25. date_created: 2018-12-11T11:50:29Z date_published: 2017-01-09T00:00:00Z date_updated: 2023-09-20T11:28:19Z day: '09' department: - _id: MiSi doi: 10.1016/j.cub.2016.11.035 external_id: isi: - '000391902500010' intvolume: ' 27' isi: 1 issue: '1' language: - iso: eng month: '01' oa_version: None page: R24 - R25 publication: Current Biology publication_identifier: issn: - '09609822' publication_status: published publisher: Cell Press publist_id: '6197' quality_controlled: '1' scopus_import: '1' status: public title: 'Cell migration: Making the waves' type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 27 year: '2017' ... --- _id: '727' abstract: - lang: eng text: 'Actin filaments polymerizing against membranes power endocytosis, vesicular traffic, and cell motility. In vitro reconstitution studies suggest that the structure and the dynamics of actin networks respond to mechanical forces. We demonstrate that lamellipodial actin of migrating cells responds to mechanical load when membrane tension is modulated. In a steady state, migrating cell filaments assume the canonical dendritic geometry, defined by Arp2/3-generated 70° branch points. Increased tension triggers a dense network with a broadened range of angles, whereas decreased tension causes a shift to a sparse configuration dominated by filaments growing perpendicularly to the plasma membrane. We show that these responses emerge from the geometry of branched actin: when load per filament decreases, elongation speed increases and perpendicular filaments gradually outcompete others because they polymerize the shortest distance to the membrane, where they are protected from capping. This network-intrinsic geometrical adaptation mechanism tunes protrusive force in response to mechanical load.' acknowledged_ssus: - _id: ScienComp article_processing_charge: No author: - first_name: Jan full_name: Mueller, Jan last_name: Mueller - first_name: Gregory full_name: Szep, Gregory id: 4BFB7762-F248-11E8-B48F-1D18A9856A87 last_name: Szep - first_name: Maria full_name: Nemethova, Maria id: 34E27F1C-F248-11E8-B48F-1D18A9856A87 last_name: Nemethova - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Arnon full_name: Lieber, Arnon last_name: Lieber - first_name: Christoph full_name: Winkler, Christoph last_name: Winkler - first_name: Karsten full_name: Kruse, Karsten last_name: Kruse - first_name: John full_name: Small, John last_name: Small - first_name: Christian full_name: Schmeiser, Christian last_name: Schmeiser - first_name: Kinneret full_name: Keren, Kinneret last_name: Keren - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Mueller J, Szep G, Nemethova M, et al. Load adaptation of lamellipodial actin networks. Cell. 2017;171(1):188-200. doi:10.1016/j.cell.2017.07.051 apa: Mueller, J., Szep, G., Nemethova, M., de Vries, I., Lieber, A., Winkler, C., … Sixt, M. K. (2017). Load adaptation of lamellipodial actin networks. Cell. Cell Press. https://doi.org/10.1016/j.cell.2017.07.051 chicago: Mueller, Jan, Gregory Szep, Maria Nemethova, Ingrid de Vries, Arnon Lieber, Christoph Winkler, Karsten Kruse, et al. “Load Adaptation of Lamellipodial Actin Networks.” Cell. Cell Press, 2017. https://doi.org/10.1016/j.cell.2017.07.051. ieee: J. Mueller et al., “Load adaptation of lamellipodial actin networks,” Cell, vol. 171, no. 1. Cell Press, pp. 188–200, 2017. ista: Mueller J, Szep G, Nemethova M, de Vries I, Lieber A, Winkler C, Kruse K, Small J, Schmeiser C, Keren K, Hauschild R, Sixt MK. 2017. Load adaptation of lamellipodial actin networks. Cell. 171(1), 188–200. mla: Mueller, Jan, et al. “Load Adaptation of Lamellipodial Actin Networks.” Cell, vol. 171, no. 1, Cell Press, 2017, pp. 188–200, doi:10.1016/j.cell.2017.07.051. short: J. Mueller, G. Szep, M. Nemethova, I. de Vries, A. Lieber, C. Winkler, K. Kruse, J. Small, C. Schmeiser, K. Keren, R. Hauschild, M.K. Sixt, Cell 171 (2017) 188–200. date_created: 2018-12-11T11:48:10Z date_published: 2017-09-21T00:00:00Z date_updated: 2023-09-28T11:33:49Z day: '21' department: - _id: MiSi - _id: Bio doi: 10.1016/j.cell.2017.07.051 ec_funded: 1 external_id: isi: - '000411331800020' intvolume: ' 171' isi: 1 issue: '1' language: - iso: eng month: '09' oa_version: None page: 188 - 200 project: - _id: 25AD6156-B435-11E9-9278-68D0E5697425 grant_number: LS13-029 name: Modeling of Polarization and Motility of Leukocytes in Three-Dimensional Environments - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Cell publication_identifier: issn: - '00928674' publication_status: published publisher: Cell Press publist_id: '6951' quality_controlled: '1' scopus_import: '1' status: public title: Load adaptation of lamellipodial actin networks type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 171 year: '2017' ... --- _id: '664' abstract: - lang: eng text: Immune cells communicate using cytokine signals, but the quantitative rules of this communication aren't clear. In this issue of Immunity, Oyler-Yaniv et al. (2017) suggest that the distribution of a cytokine within a lymphatic organ is primarily governed by the local density of cells consuming it. author: - first_name: Frank P full_name: Assen, Frank P id: 3A8E7F24-F248-11E8-B48F-1D18A9856A87 last_name: Assen orcid: 0000-0003-3470-6119 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Assen FP, Sixt MK. The dynamic cytokine niche. Immunity. 2017;46(4):519-520. doi:10.1016/j.immuni.2017.04.006 apa: Assen, F. P., & Sixt, M. K. (2017). The dynamic cytokine niche. Immunity. Cell Press. https://doi.org/10.1016/j.immuni.2017.04.006 chicago: Assen, Frank P, and Michael K Sixt. “The Dynamic Cytokine Niche.” Immunity. Cell Press, 2017. https://doi.org/10.1016/j.immuni.2017.04.006. ieee: F. P. Assen and M. K. Sixt, “The dynamic cytokine niche,” Immunity, vol. 46, no. 4. Cell Press, pp. 519–520, 2017. ista: Assen FP, Sixt MK. 2017. The dynamic cytokine niche. Immunity. 46(4), 519–520. mla: Assen, Frank P., and Michael K. Sixt. “The Dynamic Cytokine Niche.” Immunity, vol. 46, no. 4, Cell Press, 2017, pp. 519–20, doi:10.1016/j.immuni.2017.04.006. short: F.P. Assen, M.K. Sixt, Immunity 46 (2017) 519–520. date_created: 2018-12-11T11:47:47Z date_published: 2017-04-18T00:00:00Z date_updated: 2024-03-27T23:30:09Z day: '18' department: - _id: MiSi doi: 10.1016/j.immuni.2017.04.006 intvolume: ' 46' issue: '4' language: - iso: eng month: '04' oa_version: None page: 519 - 520 publication: Immunity publication_identifier: issn: - '10747613' publication_status: published publisher: Cell Press publist_id: '7065' quality_controlled: '1' related_material: record: - id: '6947' relation: dissertation_contains status: public scopus_import: 1 status: public title: The dynamic cytokine niche type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 46 year: '2017' ... --- _id: '679' abstract: - lang: eng text: Protective responses against pathogens require a rapid mobilization of resting neutrophils and the timely removal of activated ones. Neutrophils are exceptionally short-lived leukocytes, yet it remains unclear whether the lifespan of pathogen-engaged neutrophils is regulated differently from that in the circulating steady-state pool. Here, we have found that under homeostatic conditions, the mRNA-destabilizing protein tristetraprolin (TTP) regulates apoptosis and the numbers of activated infiltrating murine neutrophils but not neutrophil cellularity. Activated TTP-deficient neutrophils exhibited decreased apoptosis and enhanced accumulation at the infection site. In the context of myeloid-specific deletion of Ttp, the potentiation of neutrophil deployment protected mice against lethal soft tissue infection with Streptococcus pyogenes and prevented bacterial dissemination. Neutrophil transcriptome analysis revealed that decreased apoptosis of TTP-deficient neutrophils was specifically associated with elevated expression of myeloid cell leukemia 1 (Mcl1) but not other antiapoptotic B cell leukemia/ lymphoma 2 (Bcl2) family members. Higher Mcl1 expression resulted from stabilization of Mcl1 mRNA in the absence of TTP. The low apoptosis rate of infiltrating TTP-deficient neutrophils was comparable to that of transgenic Mcl1-overexpressing neutrophils. Our study demonstrates that posttranscriptional gene regulation by TTP schedules the termination of the antimicrobial engagement of neutrophils. The balancing role of TTP comes at the cost of an increased risk of bacterial infections. acknowledgement: This work was supported by grants from the Austrian Science Fund (FWF) (P27538-B21, I1621-B22, and SFB 43, to PK); by funding from the European Union Seventh Framework Programme Marie Curie Initial Training Networks (FP7-PEOPLE-2012-ITN) for the project INBIONET (INfection BIOlogy Training NETwork under grant agreement PITN-GA-2012-316682; and by a joint research cluster initiative of the University of Vienna and the Medical University of Vienna. author: - first_name: Florian full_name: Ebner, Florian last_name: Ebner - first_name: Vitaly full_name: Sedlyarov, Vitaly last_name: Sedlyarov - first_name: Saren full_name: Tasciyan, Saren id: 4323B49C-F248-11E8-B48F-1D18A9856A87 last_name: Tasciyan orcid: 0000-0003-1671-393X - first_name: Masa full_name: Ivin, Masa last_name: Ivin - first_name: Franz full_name: Kratochvill, Franz last_name: Kratochvill - first_name: Nina full_name: Gratz, Nina last_name: Gratz - first_name: Lukas full_name: Kenner, Lukas last_name: Kenner - first_name: Andreas full_name: Villunger, Andreas last_name: Villunger - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Pavel full_name: Kovarik, Pavel last_name: Kovarik citation: ama: Ebner F, Sedlyarov V, Tasciyan S, et al. The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. 2017;127(6):2051-2065. doi:10.1172/JCI80631 apa: Ebner, F., Sedlyarov, V., Tasciyan, S., Ivin, M., Kratochvill, F., Gratz, N., … Kovarik, P. (2017). The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. American Society for Clinical Investigation. https://doi.org/10.1172/JCI80631 chicago: Ebner, Florian, Vitaly Sedlyarov, Saren Tasciyan, Masa Ivin, Franz Kratochvill, Nina Gratz, Lukas Kenner, Andreas Villunger, Michael K Sixt, and Pavel Kovarik. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged Neutrophils during Bacterial Infection.” The Journal of Clinical Investigation. American Society for Clinical Investigation, 2017. https://doi.org/10.1172/JCI80631. ieee: F. Ebner et al., “The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection,” The Journal of Clinical Investigation, vol. 127, no. 6. American Society for Clinical Investigation, pp. 2051–2065, 2017. ista: Ebner F, Sedlyarov V, Tasciyan S, Ivin M, Kratochvill F, Gratz N, Kenner L, Villunger A, Sixt MK, Kovarik P. 2017. The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection. The Journal of Clinical Investigation. 127(6), 2051–2065. mla: Ebner, Florian, et al. “The RNA-Binding Protein Tristetraprolin Schedules Apoptosis of Pathogen-Engaged Neutrophils during Bacterial Infection.” The Journal of Clinical Investigation, vol. 127, no. 6, American Society for Clinical Investigation, 2017, pp. 2051–65, doi:10.1172/JCI80631. short: F. Ebner, V. Sedlyarov, S. Tasciyan, M. Ivin, F. Kratochvill, N. Gratz, L. Kenner, A. Villunger, M.K. Sixt, P. Kovarik, The Journal of Clinical Investigation 127 (2017) 2051–2065. date_created: 2018-12-11T11:47:53Z date_published: 2017-06-01T00:00:00Z date_updated: 2024-03-27T23:30:23Z day: '01' department: - _id: MiSi doi: 10.1172/JCI80631 external_id: pmid: - '28504646' intvolume: ' 127' issue: '6' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5451238/ month: '06' oa: 1 oa_version: Submitted Version page: 2051 - 2065 pmid: 1 project: - _id: 25985A36-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: T00817-B21 name: The biochemical basis of PAR polarization - _id: 25E9AF9E-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P27201-B22 name: Revealing the mechanisms underlying drug interactions publication: The Journal of Clinical Investigation publication_identifier: issn: - '00219738' publication_status: published publisher: American Society for Clinical Investigation publist_id: '7038' quality_controlled: '1' related_material: record: - id: '12401' relation: dissertation_contains status: public scopus_import: 1 status: public title: The RNA-binding protein tristetraprolin schedules apoptosis of pathogen-engaged neutrophils during bacterial infection type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 127 year: '2017' ... --- _id: '1137' abstract: - lang: eng text: RASGRP1 is an important guanine nucleotide exchange factor and activator of the RAS-MAPK pathway following T cell antigen receptor (TCR) signaling. The consequences of RASGRP1 mutations in humans are unknown. In a patient with recurrent bacterial and viral infections, born to healthy consanguineous parents, we used homozygosity mapping and exome sequencing to identify a biallelic stop-gain variant in RASGRP1. This variant segregated perfectly with the disease and has not been reported in genetic databases. RASGRP1 deficiency was associated in T cells and B cells with decreased phosphorylation of the extracellular-signal-regulated serine kinase ERK, which was restored following expression of wild-type RASGRP1. RASGRP1 deficiency also resulted in defective proliferation, activation and motility of T cells and B cells. RASGRP1-deficient natural killer (NK) cells exhibited impaired cytotoxicity with defective granule convergence and actin accumulation. Interaction proteomics identified the dynein light chain DYNLL1 as interacting with RASGRP1, which links RASGRP1 to cytoskeletal dynamics. RASGRP1-deficient cells showed decreased activation of the GTPase RhoA. Treatment with lenalidomide increased RhoA activity and reversed the migration and activation defects of RASGRP1-deficient lymphocytes. article_processing_charge: No article_type: original author: - first_name: Elisabeth full_name: Salzer, Elisabeth last_name: Salzer - first_name: Deniz full_name: Çaǧdaş, Deniz last_name: Çaǧdaş - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Emily full_name: Mace, Emily last_name: Mace - first_name: Wojciech full_name: Garncarz, Wojciech last_name: Garncarz - first_name: Oezlem full_name: Petronczki, Oezlem last_name: Petronczki - first_name: René full_name: Platzer, René last_name: Platzer - first_name: Laurène full_name: Pfajfer, Laurène last_name: Pfajfer - first_name: Ivan full_name: Bilic, Ivan last_name: Bilic - first_name: Sol full_name: Ban, Sol last_name: Ban - first_name: Katharina full_name: Willmann, Katharina last_name: Willmann - first_name: Malini full_name: Mukherjee, Malini last_name: Mukherjee - first_name: Verena full_name: Supper, Verena last_name: Supper - first_name: Hsiangting full_name: Hsu, Hsiangting last_name: Hsu - first_name: Pinaki full_name: Banerjee, Pinaki last_name: Banerjee - first_name: Papiya full_name: Sinha, Papiya last_name: Sinha - first_name: Fabienne full_name: Mcclanahan, Fabienne last_name: Mcclanahan - first_name: Gerhard full_name: Zlabinger, Gerhard last_name: Zlabinger - first_name: Winfried full_name: Pickl, Winfried last_name: Pickl - first_name: John full_name: Gribben, John last_name: Gribben - first_name: Hannes full_name: Stockinger, Hannes last_name: Stockinger - first_name: Keiryn full_name: Bennett, Keiryn last_name: Bennett - first_name: Johannes full_name: Huppa, Johannes last_name: Huppa - first_name: Loï̈C full_name: Dupré, Loï̈C last_name: Dupré - first_name: Özden full_name: Sanal, Özden last_name: Sanal - first_name: Ulrich full_name: Jäger, Ulrich last_name: Jäger - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Ilhan full_name: Tezcan, Ilhan last_name: Tezcan - first_name: Jordan full_name: Orange, Jordan last_name: Orange - first_name: Kaan full_name: Boztug, Kaan last_name: Boztug citation: ama: Salzer E, Çaǧdaş D, Hons M, et al. RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics. Nature Immunology. 2016;17(12):1352-1360. doi:10.1038/ni.3575 apa: Salzer, E., Çaǧdaş, D., Hons, M., Mace, E., Garncarz, W., Petronczki, O., … Boztug, K. (2016). RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3575 chicago: Salzer, Elisabeth, Deniz Çaǧdaş, Miroslav Hons, Emily Mace, Wojciech Garncarz, Oezlem Petronczki, René Platzer, et al. “RASGRP1 Deficiency Causes Immunodeficiency with Impaired Cytoskeletal Dynamics.” Nature Immunology. Nature Publishing Group, 2016. https://doi.org/10.1038/ni.3575. ieee: E. Salzer et al., “RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics,” Nature Immunology, vol. 17, no. 12. Nature Publishing Group, pp. 1352–1360, 2016. ista: Salzer E, Çaǧdaş D, Hons M, Mace E, Garncarz W, Petronczki O, Platzer R, Pfajfer L, Bilic I, Ban S, Willmann K, Mukherjee M, Supper V, Hsu H, Banerjee P, Sinha P, Mcclanahan F, Zlabinger G, Pickl W, Gribben J, Stockinger H, Bennett K, Huppa J, Dupré L, Sanal Ö, Jäger U, Sixt MK, Tezcan I, Orange J, Boztug K. 2016. RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics. Nature Immunology. 17(12), 1352–1360. mla: Salzer, Elisabeth, et al. “RASGRP1 Deficiency Causes Immunodeficiency with Impaired Cytoskeletal Dynamics.” Nature Immunology, vol. 17, no. 12, Nature Publishing Group, 2016, pp. 1352–60, doi:10.1038/ni.3575. short: E. Salzer, D. Çaǧdaş, M. Hons, E. Mace, W. Garncarz, O. Petronczki, R. Platzer, L. Pfajfer, I. Bilic, S. Ban, K. Willmann, M. Mukherjee, V. Supper, H. Hsu, P. Banerjee, P. Sinha, F. Mcclanahan, G. Zlabinger, W. Pickl, J. Gribben, H. Stockinger, K. Bennett, J. Huppa, L. Dupré, Ö. Sanal, U. Jäger, M.K. Sixt, I. Tezcan, J. Orange, K. Boztug, Nature Immunology 17 (2016) 1352–1360. date_created: 2018-12-11T11:50:21Z date_published: 2016-12-01T00:00:00Z date_updated: 2021-01-12T06:48:33Z day: '01' department: - _id: MiSi doi: 10.1038/ni.3575 external_id: pmid: - '27776107' intvolume: ' 17' issue: '12' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6400263 month: '12' oa: 1 oa_version: Submitted Version page: 1352 - 1360 pmid: 1 publication: Nature Immunology publication_status: published publisher: Nature Publishing Group publist_id: '6221' quality_controlled: '1' scopus_import: 1 status: public title: RASGRP1 deficiency causes immunodeficiency with impaired cytoskeletal dynamics type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 17 year: '2016' ... --- _id: '1142' abstract: - lang: eng text: Hemolysis drives susceptibility to bacterial infections and predicts poor outcome from sepsis. These detrimental effects are commonly considered to be a consequence of heme-iron serving as a nutrient for bacteria. We employed a Gram-negative sepsis model and found that elevated heme levels impaired the control of bacterial proliferation independently of heme-iron acquisition by pathogens. Heme strongly inhibited phagocytosis and the migration of human and mouse phagocytes by disrupting actin cytoskeletal dynamics via activation of the GTP-binding Rho family protein Cdc42 by the guanine nucleotide exchange factor DOCK8. A chemical screening approach revealed that quinine effectively prevented heme effects on the cytoskeleton, restored phagocytosis and improved survival in sepsis. These mechanistic insights provide potential therapeutic targets for patients with sepsis or hemolytic disorders. acknowledgement: 'Y. Fukui (Medical Institute of Bioregulation, Kyushu University) and J. Stein (Theodor Kocher Institute, University of Bern) are acknowledged for providing the DOCK8 deficient bone marrow. and H. Häcker (St. Judes Children''s Research Hospital) for providing the ERHBD-HoxB8-encoding retroviral construct. pSpCas9(BB)-2a-Puro (PX459) was a gift from F. Zhang (Massachusetts Institute of Technology) (Addgene plasmid # 48139) and pGRG36 was a gift from N. Craig (Johns Hopkins University School of Medicine) (Addgene plasmid # 16666). LifeAct-GFP-encoding retrovirus was kindly provided by A. Leithner (Institute of Science and Technology Austria). pSIM8 and TKC E. coli were gifts from D.L. Court (Center for Cancer Research, National Cancer Institute). We acknowledge M. Gröger and S. Rauscher for excellent technical support (Core imaging facility, Medical University of Vienna). We thank D.P. Barlow and L.R. Cheever for critical reading of the manuscript. This work was supported by the Austrian Academy of Sciences, the Science Fund of the Austrian National Bank (14107) and the Austrian Science Fund FWF (I1620-B22) in the Infect-ERA framework (to S.Knapp).' author: - first_name: Rui full_name: Martins, Rui last_name: Martins - first_name: Julia full_name: Maier, Julia last_name: Maier - first_name: Anna full_name: Gorki, Anna last_name: Gorki - first_name: Kilian full_name: Huber, Kilian last_name: Huber - first_name: Omar full_name: Sharif, Omar last_name: Sharif - first_name: Philipp full_name: Starkl, Philipp last_name: Starkl - first_name: Simona full_name: Saluzzo, Simona last_name: Saluzzo - first_name: Federica full_name: Quattrone, Federica last_name: Quattrone - first_name: Riem full_name: Gawish, Riem last_name: Gawish - first_name: Karin full_name: Lakovits, Karin last_name: Lakovits - first_name: Michael full_name: Aichinger, Michael last_name: Aichinger - first_name: Branka full_name: Radic Sarikas, Branka last_name: Radic Sarikas - first_name: Charles full_name: Lardeau, Charles last_name: Lardeau - first_name: Anastasiya full_name: Hladik, Anastasiya last_name: Hladik - first_name: Ana full_name: Korosec, Ana last_name: Korosec - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Michelle full_name: Duggan, Michelle id: 2EDEA62C-F248-11E8-B48F-1D18A9856A87 last_name: Duggan - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki - first_name: Harald full_name: Esterbauer, Harald last_name: Esterbauer - first_name: Jacques full_name: Colinge, Jacques last_name: Colinge - first_name: Stephanie full_name: Eisenbarth, Stephanie last_name: Eisenbarth - first_name: Thomas full_name: Decker, Thomas last_name: Decker - first_name: Keiryn full_name: Bennett, Keiryn last_name: Bennett - first_name: Stefan full_name: Kubicek, Stefan last_name: Kubicek - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Giulio full_name: Superti Furga, Giulio last_name: Superti Furga - first_name: Sylvia full_name: Knapp, Sylvia last_name: Knapp citation: ama: Martins R, Maier J, Gorki A, et al. Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. Nature Immunology. 2016;17(12):1361-1372. doi:10.1038/ni.3590 apa: Martins, R., Maier, J., Gorki, A., Huber, K., Sharif, O., Starkl, P., … Knapp, S. (2016). Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3590 chicago: Martins, Rui, Julia Maier, Anna Gorki, Kilian Huber, Omar Sharif, Philipp Starkl, Simona Saluzzo, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection via Disruption of Phagocyte Functions.” Nature Immunology. Nature Publishing Group, 2016. https://doi.org/10.1038/ni.3590. ieee: R. Martins et al., “Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions,” Nature Immunology, vol. 17, no. 12. Nature Publishing Group, pp. 1361–1372, 2016. ista: Martins R, Maier J, Gorki A, Huber K, Sharif O, Starkl P, Saluzzo S, Quattrone F, Gawish R, Lakovits K, Aichinger M, Radic Sarikas B, Lardeau C, Hladik A, Korosec A, Brown M, Vaahtomeri K, Duggan M, Kerjaschki D, Esterbauer H, Colinge J, Eisenbarth S, Decker T, Bennett K, Kubicek S, Sixt MK, Superti Furga G, Knapp S. 2016. Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions. Nature Immunology. 17(12), 1361–1372. mla: Martins, Rui, et al. “Heme Drives Hemolysis-Induced Susceptibility to Infection via Disruption of Phagocyte Functions.” Nature Immunology, vol. 17, no. 12, Nature Publishing Group, 2016, pp. 1361–72, doi:10.1038/ni.3590. short: R. Martins, J. Maier, A. Gorki, K. Huber, O. Sharif, P. Starkl, S. Saluzzo, F. Quattrone, R. Gawish, K. Lakovits, M. Aichinger, B. Radic Sarikas, C. Lardeau, A. Hladik, A. Korosec, M. Brown, K. Vaahtomeri, M. Duggan, D. Kerjaschki, H. Esterbauer, J. Colinge, S. Eisenbarth, T. Decker, K. Bennett, S. Kubicek, M.K. Sixt, G. Superti Furga, S. Knapp, Nature Immunology 17 (2016) 1361–1372. date_created: 2018-12-11T11:50:22Z date_published: 2016-12-01T00:00:00Z date_updated: 2021-01-12T06:48:36Z day: '01' department: - _id: MiSi - _id: PeJo doi: 10.1038/ni.3590 intvolume: ' 17' issue: '12' language: - iso: eng main_file_link: - open_access: '1' url: https://ora.ox.ac.uk/objects/uuid:f53a464e-1e5b-4f08-a7d8-b6749b852b9d month: '12' oa: 1 oa_version: Submitted Version page: 1361 - 1372 publication: Nature Immunology publication_status: published publisher: Nature Publishing Group publist_id: '6216' quality_controlled: '1' scopus_import: 1 status: public title: Heme drives hemolysis-induced susceptibility to infection via disruption of phagocyte functions type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 17 year: '2016' ... --- _id: '1150' abstract: - lang: eng text: When neutrophils infiltrate a site of inflammation, they have to stop at the right place to exert their effector function. In this issue of Developmental Cell, Wang et al. (2016) show that neutrophils sense reactive oxygen species via the TRPM2 channel to arrest migration at their target site. © 2016 Elsevier Inc. author: - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Renkawitz J, Sixt MK. A Radical Break Restraining Neutrophil Migration. Developmental Cell. 2016;38(5):448-450. doi:10.1016/j.devcel.2016.08.017 apa: Renkawitz, J., & Sixt, M. K. (2016). A Radical Break Restraining Neutrophil Migration. Developmental Cell. Cell Press. https://doi.org/10.1016/j.devcel.2016.08.017 chicago: Renkawitz, Jörg, and Michael K Sixt. “A Radical Break Restraining Neutrophil Migration.” Developmental Cell. Cell Press, 2016. https://doi.org/10.1016/j.devcel.2016.08.017. ieee: J. Renkawitz and M. K. Sixt, “A Radical Break Restraining Neutrophil Migration,” Developmental Cell, vol. 38, no. 5. Cell Press, pp. 448–450, 2016. ista: Renkawitz J, Sixt MK. 2016. A Radical Break Restraining Neutrophil Migration. Developmental Cell. 38(5), 448–450. mla: Renkawitz, Jörg, and Michael K. Sixt. “A Radical Break Restraining Neutrophil Migration.” Developmental Cell, vol. 38, no. 5, Cell Press, 2016, pp. 448–50, doi:10.1016/j.devcel.2016.08.017. short: J. Renkawitz, M.K. Sixt, Developmental Cell 38 (2016) 448–450. date_created: 2018-12-11T11:50:25Z date_published: 2016-09-12T00:00:00Z date_updated: 2021-01-12T06:48:39Z day: '12' department: - _id: MiSi doi: 10.1016/j.devcel.2016.08.017 intvolume: ' 38' issue: '5' language: - iso: eng month: '09' oa_version: None page: 448 - 450 publication: Developmental Cell publication_status: published publisher: Cell Press publist_id: '6208' quality_controlled: '1' scopus_import: 1 status: public title: A Radical Break Restraining Neutrophil Migration type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 38 year: '2016' ... --- _id: '1154' abstract: - lang: eng text: "Cellular locomotion is a central hallmark of eukaryotic life. It is governed by cell-extrinsic molecular factors, which can either emerge in the soluble phase or as immobilized, often adhesive ligands. To encode for direction, every cue must be present as a spatial or temporal gradient. Here, we developed a microfluidic chamber that allows measurement of cell migration in combined response to surface immobilized and soluble molecular gradients. As a proof of principle we study the response of dendritic cells to their major guidance cues, chemokines. The majority of data on chemokine gradient sensing is based on in vitro studies employing soluble gradients. Despite evidence suggesting that in vivo chemokines are often immobilized to sugar residues, limited information is available how cells respond to immobilized chemokines. We tracked migration of dendritic cells towards immobilized gradients of the chemokine CCL21 and varying superimposed soluble gradients of CCL19. Differential migratory patterns illustrate the potential of our setup to quantitatively study the competitive response to both types of gradients. Beyond chemokines our approach is broadly applicable to alternative systems of chemo- and haptotaxis such as cells migrating along gradients of adhesion receptor ligands vs. any soluble cue. \r\n" acknowledgement: 'This work was supported by the Swiss National Science Foundation (Ambizione fellowship; PZ00P3-154733 to M.M.), the Swiss Multiple Sclerosis Society (research support to M.M.), a fellowship from the Boehringer Ingelheim Fonds (BIF) to J.S., the European Research Council (grant ERC GA 281556) and a START award from the Austrian Science Foundation (FWF) to M.S. #BioimagingFacility' article_number: '36440' author: - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Veronika full_name: Bierbaum, Veronika id: 3FD04378-F248-11E8-B48F-1D18A9856A87 last_name: Bierbaum - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Tino full_name: Frank, Tino last_name: Frank - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Mark Tobias full_name: Bollenbach, Mark Tobias id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87 last_name: Bollenbach orcid: 0000-0003-4398-476X - first_name: Savaş full_name: Tay, Savaş last_name: Tay - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Matthias full_name: Mehling, Matthias id: 3C23B994-F248-11E8-B48F-1D18A9856A87 last_name: Mehling orcid: 0000-0001-8599-1226 citation: ama: Schwarz J, Bierbaum V, Merrin J, et al. A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients. Scientific Reports. 2016;6. doi:10.1038/srep36440 apa: Schwarz, J., Bierbaum, V., Merrin, J., Frank, T., Hauschild, R., Bollenbach, M. T., … Mehling, M. (2016). A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients. Scientific Reports. Nature Publishing Group. https://doi.org/10.1038/srep36440 chicago: Schwarz, Jan, Veronika Bierbaum, Jack Merrin, Tino Frank, Robert Hauschild, Mark Tobias Bollenbach, Savaş Tay, Michael K Sixt, and Matthias Mehling. “A Microfluidic Device for Measuring Cell Migration towards Substrate Bound and Soluble Chemokine Gradients.” Scientific Reports. Nature Publishing Group, 2016. https://doi.org/10.1038/srep36440. ieee: J. Schwarz et al., “A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients,” Scientific Reports, vol. 6. Nature Publishing Group, 2016. ista: Schwarz J, Bierbaum V, Merrin J, Frank T, Hauschild R, Bollenbach MT, Tay S, Sixt MK, Mehling M. 2016. A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients. Scientific Reports. 6, 36440. mla: Schwarz, Jan, et al. “A Microfluidic Device for Measuring Cell Migration towards Substrate Bound and Soluble Chemokine Gradients.” Scientific Reports, vol. 6, 36440, Nature Publishing Group, 2016, doi:10.1038/srep36440. short: J. Schwarz, V. Bierbaum, J. Merrin, T. Frank, R. Hauschild, M.T. Bollenbach, S. Tay, M.K. Sixt, M. Mehling, Scientific Reports 6 (2016). date_created: 2018-12-11T11:50:27Z date_published: 2016-11-07T00:00:00Z date_updated: 2021-01-12T06:48:41Z day: '07' ddc: - '579' department: - _id: MiSi - _id: NanoFab - _id: Bio - _id: ToBo doi: 10.1038/srep36440 ec_funded: 1 file: - access_level: open_access content_type: application/pdf creator: system date_created: 2018-12-12T10:09:32Z date_updated: 2018-12-12T10:09:32Z file_id: '4756' file_name: IST-2017-744-v1+1_srep36440.pdf file_size: 2353456 relation: main_file file_date_updated: 2018-12-12T10:09:32Z has_accepted_license: '1' intvolume: ' 6' language: - iso: eng month: '11' oa: 1 oa_version: Published Version project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Scientific Reports publication_status: published publisher: Nature Publishing Group publist_id: '6204' pubrep_id: '744' quality_controlled: '1' scopus_import: 1 status: public title: A microfluidic device for measuring cell migration towards substrate bound and soluble chemokine gradients tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 6 year: '2016' ... --- _id: '1201' abstract: - lang: eng text: In this issue of Cell, Skau et al. show that the formin FMN2 organizes a perinuclear actin cytoskeleton that protects the nucleus and its genomic content of migrating cells squeezing through small spaces. author: - first_name: Jörg full_name: Renkawitz, Jörg id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Renkawitz J, Sixt MK. Formin’ a nuclear protection. Cell. 2016;167(6):1448-1449. doi:10.1016/j.cell.2016.11.024 apa: Renkawitz, J., & Sixt, M. K. (2016). Formin’ a nuclear protection. Cell. Cell Press. https://doi.org/10.1016/j.cell.2016.11.024 chicago: Renkawitz, Jörg, and Michael K Sixt. “Formin’ a Nuclear Protection.” Cell. Cell Press, 2016. https://doi.org/10.1016/j.cell.2016.11.024. ieee: J. Renkawitz and M. K. Sixt, “Formin’ a nuclear protection,” Cell, vol. 167, no. 6. Cell Press, pp. 1448–1449, 2016. ista: Renkawitz J, Sixt MK. 2016. Formin’ a nuclear protection. Cell. 167(6), 1448–1449. mla: Renkawitz, Jörg, and Michael K. Sixt. “Formin’ a Nuclear Protection.” Cell, vol. 167, no. 6, Cell Press, 2016, pp. 1448–49, doi:10.1016/j.cell.2016.11.024. short: J. Renkawitz, M.K. Sixt, Cell 167 (2016) 1448–1449. date_created: 2018-12-11T11:50:41Z date_published: 2016-12-01T00:00:00Z date_updated: 2021-01-12T06:49:03Z day: '01' department: - _id: MiSi doi: 10.1016/j.cell.2016.11.024 intvolume: ' 167' issue: '6' language: - iso: eng month: '12' oa_version: None page: 1448 - 1449 publication: Cell publication_status: published publisher: Cell Press publist_id: '6149' quality_controlled: '1' scopus_import: 1 status: public title: Formin’ a nuclear protection type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 167 year: '2016' ... --- _id: '1285' abstract: - lang: eng text: Cell migration is central to a multitude of physiological processes, including embryonic development, immune surveillance, and wound healing, and deregulated migration is key to cancer dissemination. Decades of investigations have uncovered many of the molecular and physical mechanisms underlying cell migration. Together with protrusion extension and cell body retraction, adhesion to the substrate via specific focal adhesion points has long been considered an essential step in cell migration. Although this is true for cells moving on two-dimensional substrates, recent studies have demonstrated that focal adhesions are not required for cells moving in three dimensions, in which confinement is sufficient to maintain a cell in contact with its substrate. Here, we review the investigations that have led to challenging the requirement of specific adhesions for migration, discuss the physical mechanisms proposed for cell body translocation during focal adhesion-independent migration, and highlight the remaining open questions for the future. acknowledgement: We would like to thank Dani Bodor for critical comments on the manuscript and Guillaume Salbreux for discussions. The authors are supported by the United Kingdom's Medical Research Council (MRC) (E.K.P. and I.M.A.; core funding to the MRC Laboratory for Molecular Cell Biology), by the European Research Council [ERC GA 311637 (E.K.P.) and ERC GA 281556 (M.S.)], and by a START award from the Austrian Science Foundation (M.S.). author: - first_name: Ewa full_name: Paluch, Ewa last_name: Paluch - first_name: Irene full_name: Aspalter, Irene last_name: Aspalter - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Paluch E, Aspalter I, Sixt MK. Focal adhesion-independent cell migration. Annual Review of Cell and Developmental Biology. 2016;32:469-490. doi:10.1146/annurev-cellbio-111315-125341 apa: Paluch, E., Aspalter, I., & Sixt, M. K. (2016). Focal adhesion-independent cell migration. Annual Review of Cell and Developmental Biology. Annual Reviews. https://doi.org/10.1146/annurev-cellbio-111315-125341 chicago: Paluch, Ewa, Irene Aspalter, and Michael K Sixt. “Focal Adhesion-Independent Cell Migration.” Annual Review of Cell and Developmental Biology. Annual Reviews, 2016. https://doi.org/10.1146/annurev-cellbio-111315-125341. ieee: E. Paluch, I. Aspalter, and M. K. Sixt, “Focal adhesion-independent cell migration,” Annual Review of Cell and Developmental Biology, vol. 32. Annual Reviews, pp. 469–490, 2016. ista: Paluch E, Aspalter I, Sixt MK. 2016. Focal adhesion-independent cell migration. Annual Review of Cell and Developmental Biology. 32, 469–490. mla: Paluch, Ewa, et al. “Focal Adhesion-Independent Cell Migration.” Annual Review of Cell and Developmental Biology, vol. 32, Annual Reviews, 2016, pp. 469–90, doi:10.1146/annurev-cellbio-111315-125341. short: E. Paluch, I. Aspalter, M.K. Sixt, Annual Review of Cell and Developmental Biology 32 (2016) 469–490. date_created: 2018-12-11T11:51:08Z date_published: 2016-10-06T00:00:00Z date_updated: 2021-01-12T06:49:37Z day: '06' department: - _id: MiSi doi: 10.1146/annurev-cellbio-111315-125341 ec_funded: 1 intvolume: ' 32' language: - iso: eng month: '10' oa_version: None page: 469 - 490 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Annual Review of Cell and Developmental Biology publication_status: published publisher: Annual Reviews publist_id: '6031' quality_controlled: '1' scopus_import: 1 status: public title: Focal adhesion-independent cell migration type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 32 year: '2016' ... --- _id: '1490' abstract: - lang: eng text: To induce adaptive immunity, dendritic cells (DCs) migrate through afferent lymphatic vessels (LVs) to draining lymph nodes (dLNs). This process occurs in several consecutive steps. Upon entry into lymphatic capillaries, DCs first actively crawl into downstream collecting vessels. From there, they are next passively and rapidly transported to the dLN by lymph flow. Here, we describe a role for the chemokine CCL21 in intralymphatic DC crawling. Performing time-lapse imaging in murine skin, we found that blockade of CCL21-but not the absence of lymph flow-completely abolished DC migration from capillaries toward collecting vessels and reduced the ability of intralymphatic DCs to emigrate from skin. Moreover, we found that in vitro low laminar flow established a CCL21 gradient along lymphatic endothelial monolayers, thereby inducing downstream-directed DC migration. These findings reveal a role for intralymphatic CCL21 in promoting DC trafficking to dLNs, through the formation of a flow-induced gradient. author: - first_name: Erica full_name: Russo, Erica last_name: Russo - first_name: Alvaro full_name: Teijeira, Alvaro last_name: Teijeira - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 - first_name: Ann full_name: Willrodt, Ann last_name: Willrodt - first_name: Joël full_name: Bloch, Joël last_name: Bloch - first_name: Maximilian full_name: Nitschké, Maximilian last_name: Nitschké - first_name: Laura full_name: Santambrogio, Laura last_name: Santambrogio - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Cornelia full_name: Halin, Cornelia last_name: Halin citation: ama: Russo E, Teijeira A, Vaahtomeri K, et al. Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels. Cell Reports. 2016;14(7):1723-1734. doi:10.1016/j.celrep.2016.01.048 apa: Russo, E., Teijeira, A., Vaahtomeri, K., Willrodt, A., Bloch, J., Nitschké, M., … Halin, C. (2016). Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels. Cell Reports. Cell Press. https://doi.org/10.1016/j.celrep.2016.01.048 chicago: Russo, Erica, Alvaro Teijeira, Kari Vaahtomeri, Ann Willrodt, Joël Bloch, Maximilian Nitschké, Laura Santambrogio, Dontscho Kerjaschki, Michael K Sixt, and Cornelia Halin. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic Cells through Afferent Lymphatic Vessels.” Cell Reports. Cell Press, 2016. https://doi.org/10.1016/j.celrep.2016.01.048. ieee: E. Russo et al., “Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels,” Cell Reports, vol. 14, no. 7. Cell Press, pp. 1723–1734, 2016. ista: Russo E, Teijeira A, Vaahtomeri K, Willrodt A, Bloch J, Nitschké M, Santambrogio L, Kerjaschki D, Sixt MK, Halin C. 2016. Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels. Cell Reports. 14(7), 1723–1734. mla: Russo, Erica, et al. “Intralymphatic CCL21 Promotes Tissue Egress of Dendritic Cells through Afferent Lymphatic Vessels.” Cell Reports, vol. 14, no. 7, Cell Press, 2016, pp. 1723–34, doi:10.1016/j.celrep.2016.01.048. short: E. Russo, A. Teijeira, K. Vaahtomeri, A. Willrodt, J. Bloch, M. Nitschké, L. Santambrogio, D. Kerjaschki, M.K. Sixt, C. Halin, Cell Reports 14 (2016) 1723–1734. date_created: 2018-12-11T11:52:19Z date_published: 2016-02-23T00:00:00Z date_updated: 2021-01-12T06:51:07Z day: '23' ddc: - '570' department: - _id: MiSi doi: 10.1016/j.celrep.2016.01.048 file: - access_level: open_access checksum: c98c1151d5f1e5ce1643a83d8d7f3c29 content_type: application/pdf creator: system date_created: 2018-12-12T10:12:30Z date_updated: 2020-07-14T12:44:58Z file_id: '4948' file_name: IST-2016-515-v1+1_1-s2.0-S2211124716300262-main.pdf file_size: 5489897 relation: main_file file_date_updated: 2020-07-14T12:44:58Z has_accepted_license: '1' intvolume: ' 14' issue: '7' language: - iso: eng month: '02' oa: 1 oa_version: Published Version page: 1723 - 1734 publication: Cell Reports publication_status: published publisher: Cell Press publist_id: '5697' pubrep_id: '515' quality_controlled: '1' scopus_import: 1 status: public title: Intralymphatic CCL21 promotes tissue egress of dendritic cells through afferent lymphatic vessels tmp: image: /images/cc_by_nc_nd.png legal_code_url: https://creativecommons.org/licenses/by-nc-nd/4.0/legalcode name: Creative Commons Attribution-NonCommercial-NoDerivatives 4.0 International (CC BY-NC-ND 4.0) short: CC BY-NC-ND (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 14 year: '2016' ... --- _id: '1599' abstract: - lang: eng text: "The addition of polysialic acid to N- and/or O-linked glycans, referred to as polysialylation, is a rare posttranslational modification that is mainly known to control the developmental plasticity of the nervous system. Here we show that CCR7, the central chemokine receptor controlling immune cell trafficking to secondary lymphatic organs, carries polysialic acid. This modification is essential for the recognition of the CCR7 ligand CCL21. As a consequence, dendritic cell trafficking is abrogated in polysialyltransferase-deficient mice, manifesting as disturbed lymph node homeostasis and unresponsiveness to inflammatory stimuli. Structure-function analysis of chemokine-receptor interactions reveals that CCL21 adopts an autoinhibited conformation, which is released upon interaction with polysialic acid. Thus, we describe a glycosylation-mediated immune cell trafficking disorder and its mechanistic basis.\r\n" acknowledged_ssus: - _id: SSU acknowledgement: 'We thank S. Schüchner and E. Ogris for kindly providing the antibody to GFP, M. Helmbrecht and A. Huber for providing Nrp2−/− mice, the IST Scientific Support Facilities for excellent services, and J. Renkawitz and K. Vaahtomeri for critically reading the manuscript. ' article_processing_charge: No article_type: original author: - first_name: Eva full_name: Kiermaier, Eva id: 3EB04B78-F248-11E8-B48F-1D18A9856A87 last_name: Kiermaier orcid: 0000-0001-6165-5738 - first_name: Christine full_name: Moussion, Christine id: 3356F664-F248-11E8-B48F-1D18A9856A87 last_name: Moussion - first_name: Christopher full_name: Veldkamp, Christopher last_name: Veldkamp - first_name: Rita full_name: Gerardy Schahn, Rita last_name: Gerardy Schahn - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Larry full_name: Williams, Larry last_name: Williams - first_name: Gary full_name: Chaffee, Gary last_name: Chaffee - first_name: Andrew full_name: Phillips, Andrew last_name: Phillips - first_name: Friedrich full_name: Freiberger, Friedrich last_name: Freiberger - first_name: Richard full_name: Imre, Richard last_name: Imre - first_name: Deni full_name: Taleski, Deni last_name: Taleski - first_name: Richard full_name: Payne, Richard last_name: Payne - first_name: Asolina full_name: Braun, Asolina last_name: Braun - first_name: Reinhold full_name: Förster, Reinhold last_name: Förster - first_name: Karl full_name: Mechtler, Karl last_name: Mechtler - first_name: Martina full_name: Mühlenhoff, Martina last_name: Mühlenhoff - first_name: Brian full_name: Volkman, Brian last_name: Volkman - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Kiermaier E, Moussion C, Veldkamp C, et al. Polysialylation controls dendritic cell trafficking by regulating chemokine recognition. Science. 2016;351(6269):186-190. doi:10.1126/science.aad0512 apa: Kiermaier, E., Moussion, C., Veldkamp, C., Gerardy  Schahn, R., de Vries, I., Williams, L., … Sixt, M. K. (2016). Polysialylation controls dendritic cell trafficking by regulating chemokine recognition. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.aad0512 chicago: Kiermaier, Eva, Christine Moussion, Christopher Veldkamp, Rita Gerardy  Schahn, Ingrid de Vries, Larry Williams, Gary Chaffee, et al. “Polysialylation Controls Dendritic Cell Trafficking by Regulating Chemokine Recognition.” Science. American Association for the Advancement of Science, 2016. https://doi.org/10.1126/science.aad0512. ieee: E. Kiermaier et al., “Polysialylation controls dendritic cell trafficking by regulating chemokine recognition,” Science, vol. 351, no. 6269. American Association for the Advancement of Science, pp. 186–190, 2016. ista: Kiermaier E, Moussion C, Veldkamp C, Gerardy  Schahn R, de Vries I, Williams L, Chaffee G, Phillips A, Freiberger F, Imre R, Taleski D, Payne R, Braun A, Förster R, Mechtler K, Mühlenhoff M, Volkman B, Sixt MK. 2016. Polysialylation controls dendritic cell trafficking by regulating chemokine recognition. Science. 351(6269), 186–190. mla: Kiermaier, Eva, et al. “Polysialylation Controls Dendritic Cell Trafficking by Regulating Chemokine Recognition.” Science, vol. 351, no. 6269, American Association for the Advancement of Science, 2016, pp. 186–90, doi:10.1126/science.aad0512. short: E. Kiermaier, C. Moussion, C. Veldkamp, R. Gerardy  Schahn, I. de Vries, L. Williams, G. Chaffee, A. Phillips, F. Freiberger, R. Imre, D. Taleski, R. Payne, A. Braun, R. Förster, K. Mechtler, M. Mühlenhoff, B. Volkman, M.K. Sixt, Science 351 (2016) 186–190. date_created: 2018-12-11T11:52:57Z date_published: 2016-01-08T00:00:00Z date_updated: 2021-01-12T06:51:52Z day: '08' department: - _id: MiSi doi: 10.1126/science.aad0512 ec_funded: 1 external_id: pmid: - '26657283' intvolume: ' 351' issue: '6269' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5583642/ month: '01' oa: 1 oa_version: Submitted Version page: 186 - 190 pmid: 1 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25A76F58-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '289720' name: Stromal Cell-immune Cell Interactions in Health and Disease - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Science publication_status: published publisher: American Association for the Advancement of Science publist_id: '5570' quality_controlled: '1' scopus_import: 1 status: public title: Polysialylation controls dendritic cell trafficking by regulating chemokine recognition type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 351 year: '2016' ... --- _id: '1597' abstract: - lang: eng text: Chemokines are the main guidance cues directing leukocyte migration. Opposed to early assumptions, chemokines do not necessarily act as soluble cues but are often immobilized within tissues, e.g., dendritic cell migration toward lymphatic vessels is guided by a haptotactic gradient of the chemokine CCL21. Controlled assay systems to quantitatively study haptotaxis in vitro are still missing. In this chapter, we describe an in vitro haptotaxis assay optimized for the unique properties of dendritic cells. The chemokine CCL21 is immobilized in a bioactive state, using laser-assisted protein adsorption by photobleaching. The cells follow this immobilized CCL21 gradient in a haptotaxis chamber, which provides three dimensionally confined migration conditions. acknowledged_ssus: - _id: Bio acknowledgement: This work was supported by the Boehringer Ingelheim Fonds, the European Research Council (ERC StG 281556), and a START Award of the Austrian Science Foundation (FWF). We thank Robert Hauschild, Anne Reversat, and Jack Merrin for valuable input and the Imaging Facility of IST Austria for excellent support. article_processing_charge: No article_type: original author: - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Schwarz J, Sixt MK. Quantitative analysis of dendritic cell haptotaxis. Methods in Enzymology. 2016;570:567-581. doi:10.1016/bs.mie.2015.11.004 apa: Schwarz, J., & Sixt, M. K. (2016). Quantitative analysis of dendritic cell haptotaxis. Methods in Enzymology. Elsevier. https://doi.org/10.1016/bs.mie.2015.11.004 chicago: Schwarz, Jan, and Michael K Sixt. “Quantitative Analysis of Dendritic Cell Haptotaxis.” Methods in Enzymology. Elsevier, 2016. https://doi.org/10.1016/bs.mie.2015.11.004. ieee: J. Schwarz and M. K. Sixt, “Quantitative analysis of dendritic cell haptotaxis,” Methods in Enzymology, vol. 570. Elsevier, pp. 567–581, 2016. ista: Schwarz J, Sixt MK. 2016. Quantitative analysis of dendritic cell haptotaxis. Methods in Enzymology. 570, 567–581. mla: Schwarz, Jan, and Michael K. Sixt. “Quantitative Analysis of Dendritic Cell Haptotaxis.” Methods in Enzymology, vol. 570, Elsevier, 2016, pp. 567–81, doi:10.1016/bs.mie.2015.11.004. short: J. Schwarz, M.K. Sixt, Methods in Enzymology 570 (2016) 567–581. date_created: 2018-12-11T11:52:56Z date_published: 2016-01-01T00:00:00Z date_updated: 2021-01-12T06:51:51Z day: '01' department: - _id: MiSi doi: 10.1016/bs.mie.2015.11.004 ec_funded: 1 external_id: pmid: - '26921962' intvolume: ' 570' language: - iso: eng month: '01' oa_version: None page: 567 - 581 pmid: 1 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25A8E5EA-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: Y 564-B12 name: Cytoskeletal force generation and transduction of leukocytes (FWF) publication: Methods in Enzymology publication_status: published publisher: Elsevier publist_id: '5573' quality_controlled: '1' scopus_import: 1 status: public title: Quantitative analysis of dendritic cell haptotaxis type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 570 year: '2016' ... --- _id: '1321' abstract: - lang: eng text: Most migrating cells extrude their front by the force of actin polymerization. Polymerization requires an initial nucleation step, which is mediated by factors establishing either parallel filaments in the case of filopodia or branched filaments that form the branched lamellipodial network. Branches are considered essential for regular cell motility and are initiated by the Arp2/3 complex, which in turn is activated by nucleation-promoting factors of the WASP and WAVE families. Here we employed rapid amoeboid crawling leukocytes and found that deletion of the WAVE complex eliminated actin branching and thus lamellipodia formation. The cells were left with parallel filaments at the leading edge, which translated, depending on the differentiation status of the cell, into a unipolar pointed cell shape or cells with multiple filopodia. Remarkably, unipolar cells migrated with increased speed and enormous directional persistence, while they were unable to turn towards chemotactic gradients. Cells with multiple filopodia retained chemotactic activity but their migration was progressively impaired with increasing geometrical complexity of the extracellular environment. These findings establish that diversified leading edge protrusions serve as explorative structures while they slow down actual locomotion. acknowledged_ssus: - _id: SSU acknowledgement: "This work was supported by the German Research Foundation (DFG) Priority Program SP 1464 to T.E.B.S. and M.S., and European Research Council (ERC GA 281556) and Human Frontiers Program grants to M.S.\r\nService Units of IST Austria for excellent technical support." article_processing_charge: No article_type: original author: - first_name: Alexander F full_name: Leithner, Alexander F id: 3B1B77E4-F248-11E8-B48F-1D18A9856A87 last_name: Leithner orcid: 0000-0002-1073-744X - first_name: Alexander full_name: Eichner, Alexander id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87 last_name: Eichner - first_name: Jan full_name: Müller, Jan id: AD07FDB4-0F61-11EA-8158-C4CC64CEAA8D last_name: Müller - first_name: Anne full_name: Reversat, Anne id: 35B76592-F248-11E8-B48F-1D18A9856A87 last_name: Reversat orcid: 0000-0003-0666-8928 - first_name: Markus full_name: Brown, Markus id: 3DAB9AFC-F248-11E8-B48F-1D18A9856A87 last_name: Brown - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: David full_name: De Gorter, David last_name: De Gorter - first_name: Florian full_name: Schur, Florian id: 48AD8942-F248-11E8-B48F-1D18A9856A87 last_name: Schur orcid: 0000-0003-4790-8078 - first_name: Jonathan full_name: Bayerl, Jonathan last_name: Bayerl - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Stefan full_name: Wieser, Stefan id: 355AA5A0-F248-11E8-B48F-1D18A9856A87 last_name: Wieser orcid: 0000-0002-2670-2217 - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Frank full_name: Lai, Frank last_name: Lai - first_name: Markus full_name: Moser, Markus last_name: Moser - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki - first_name: Klemens full_name: Rottner, Klemens last_name: Rottner - first_name: Victor full_name: Small, Victor last_name: Small - first_name: Theresia full_name: Stradal, Theresia last_name: Stradal - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Leithner AF, Eichner A, Müller J, et al. Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. 2016;18:1253-1259. doi:10.1038/ncb3426 apa: Leithner, A. F., Eichner, A., Müller, J., Reversat, A., Brown, M., Schwarz, J., … Sixt, M. K. (2016). Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. Nature Publishing Group. https://doi.org/10.1038/ncb3426 chicago: Leithner, Alexander F, Alexander Eichner, Jan Müller, Anne Reversat, Markus Brown, Jan Schwarz, Jack Merrin, et al. “Diversified Actin Protrusions Promote Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature Cell Biology. Nature Publishing Group, 2016. https://doi.org/10.1038/ncb3426. ieee: A. F. Leithner et al., “Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes,” Nature Cell Biology, vol. 18. Nature Publishing Group, pp. 1253–1259, 2016. ista: Leithner AF, Eichner A, Müller J, Reversat A, Brown M, Schwarz J, Merrin J, De Gorter D, Schur FK, Bayerl J, de Vries I, Wieser S, Hauschild R, Lai F, Moser M, Kerjaschki D, Rottner K, Small V, Stradal T, Sixt MK. 2016. Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes. Nature Cell Biology. 18, 1253–1259. mla: Leithner, Alexander F., et al. “Diversified Actin Protrusions Promote Environmental Exploration but Are Dispensable for Locomotion of Leukocytes.” Nature Cell Biology, vol. 18, Nature Publishing Group, 2016, pp. 1253–59, doi:10.1038/ncb3426. short: A.F. Leithner, A. Eichner, J. Müller, A. Reversat, M. Brown, J. Schwarz, J. Merrin, D. De Gorter, F.K. Schur, J. Bayerl, I. de Vries, S. Wieser, R. Hauschild, F. Lai, M. Moser, D. Kerjaschki, K. Rottner, V. Small, T. Stradal, M.K. Sixt, Nature Cell Biology 18 (2016) 1253–1259. date_created: 2018-12-11T11:51:21Z date_published: 2016-10-24T00:00:00Z date_updated: 2024-03-27T23:30:16Z day: '24' ddc: - '570' department: - _id: MiSi - _id: NanoFab - _id: Bio doi: 10.1038/ncb3426 ec_funded: 1 file: - access_level: open_access checksum: e1411cb7c99a2d9089c178a6abef25e7 content_type: application/pdf creator: dernst date_created: 2020-05-14T16:33:46Z date_updated: 2020-07-14T12:44:43Z file_id: '7844' file_name: 2018_NatureCell_Leithner.pdf file_size: 4433280 relation: main_file file_date_updated: 2020-07-14T12:44:43Z has_accepted_license: '1' intvolume: ' 18' language: - iso: eng month: '10' oa: 1 oa_version: Submitted Version page: 1253 - 1259 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Nature Cell Biology publication_status: published publisher: Nature Publishing Group publist_id: '5949' quality_controlled: '1' related_material: record: - id: '323' relation: dissertation_contains status: public scopus_import: 1 status: public title: Diversified actin protrusions promote environmental exploration but are dispensable for locomotion of leukocytes tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 18 year: '2016' ... --- _id: '1553' abstract: - lang: eng text: Cell movement has essential functions in development, immunity, and cancer. Various cell migration patterns have been reported, but no general rule has emerged so far. Here, we show on the basis of experimental data in vitro and in vivo that cell persistence, which quantifies the straightness of trajectories, is robustly coupled to cell migration speed. We suggest that this universal coupling constitutes a generic law of cell migration, which originates in the advection of polarity cues by an actin cytoskeleton undergoing flows at the cellular scale. Our analysis relies on a theoretical model that we validate by measuring the persistence of cells upon modulation of actin flow speeds and upon optogenetic manipulation of the binding of an actin regulator to actin filaments. Beyond the quantitative prediction of the coupling, the model yields a generic phase diagram of cellular trajectories, which recapitulates the full range of observed migration patterns. author: - first_name: Paolo full_name: Maiuri, Paolo last_name: Maiuri - first_name: Jean full_name: Rupprecht, Jean last_name: Rupprecht - first_name: Stefan full_name: Wieser, Stefan id: 355AA5A0-F248-11E8-B48F-1D18A9856A87 last_name: Wieser orcid: 0000-0002-2670-2217 - first_name: Verena full_name: Ruprecht, Verena id: 4D71A03A-F248-11E8-B48F-1D18A9856A87 last_name: Ruprecht orcid: 0000-0003-4088-8633 - first_name: Olivier full_name: Bénichou, Olivier last_name: Bénichou - first_name: Nicolas full_name: Carpi, Nicolas last_name: Carpi - first_name: Mathieu full_name: Coppey, Mathieu last_name: Coppey - first_name: Simon full_name: De Beco, Simon last_name: De Beco - first_name: Nir full_name: Gov, Nir last_name: Gov - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 - first_name: Carolina full_name: Lage Crespo, Carolina last_name: Lage Crespo - first_name: Franziska full_name: Lautenschlaeger, Franziska last_name: Lautenschlaeger - first_name: Maël full_name: Le Berre, Maël last_name: Le Berre - first_name: Ana full_name: Lennon Duménil, Ana last_name: Lennon Duménil - first_name: Matthew full_name: Raab, Matthew last_name: Raab - first_name: Hawa full_name: Thiam, Hawa last_name: Thiam - first_name: Matthieu full_name: Piel, Matthieu last_name: Piel - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Raphaël full_name: Voituriez, Raphaël last_name: Voituriez citation: ama: Maiuri P, Rupprecht J, Wieser S, et al. Actin flows mediate a universal coupling between cell speed and cell persistence. Cell. 2015;161(2):374-386. doi:10.1016/j.cell.2015.01.056 apa: Maiuri, P., Rupprecht, J., Wieser, S., Ruprecht, V., Bénichou, O., Carpi, N., … Voituriez, R. (2015). Actin flows mediate a universal coupling between cell speed and cell persistence. Cell. Cell Press. https://doi.org/10.1016/j.cell.2015.01.056 chicago: Maiuri, Paolo, Jean Rupprecht, Stefan Wieser, Verena Ruprecht, Olivier Bénichou, Nicolas Carpi, Mathieu Coppey, et al. “Actin Flows Mediate a Universal Coupling between Cell Speed and Cell Persistence.” Cell. Cell Press, 2015. https://doi.org/10.1016/j.cell.2015.01.056. ieee: P. Maiuri et al., “Actin flows mediate a universal coupling between cell speed and cell persistence,” Cell, vol. 161, no. 2. Cell Press, pp. 374–386, 2015. ista: Maiuri P, Rupprecht J, Wieser S, Ruprecht V, Bénichou O, Carpi N, Coppey M, De Beco S, Gov N, Heisenberg C-PJ, Lage Crespo C, Lautenschlaeger F, Le Berre M, Lennon Duménil A, Raab M, Thiam H, Piel M, Sixt MK, Voituriez R. 2015. Actin flows mediate a universal coupling between cell speed and cell persistence. Cell. 161(2), 374–386. mla: Maiuri, Paolo, et al. “Actin Flows Mediate a Universal Coupling between Cell Speed and Cell Persistence.” Cell, vol. 161, no. 2, Cell Press, 2015, pp. 374–86, doi:10.1016/j.cell.2015.01.056. short: P. Maiuri, J. Rupprecht, S. Wieser, V. Ruprecht, O. Bénichou, N. Carpi, M. Coppey, S. De Beco, N. Gov, C.-P.J. Heisenberg, C. Lage Crespo, F. Lautenschlaeger, M. Le Berre, A. Lennon Duménil, M. Raab, H. Thiam, M. Piel, M.K. Sixt, R. Voituriez, Cell 161 (2015) 374–386. date_created: 2018-12-11T11:52:41Z date_published: 2015-04-09T00:00:00Z date_updated: 2021-01-12T06:51:33Z day: '09' department: - _id: MiSi - _id: CaHe doi: 10.1016/j.cell.2015.01.056 ec_funded: 1 intvolume: ' 161' issue: '2' language: - iso: eng month: '04' oa_version: None page: 374 - 386 project: - _id: 2529486C-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: T 560-B17 name: Cell- and Tissue Mechanics in Zebrafish Germ Layer Formation - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25ABD200-B435-11E9-9278-68D0E5697425 grant_number: RGP0058/2011 name: 'Cell migration in complex environments: from in vivo experiments to theoretical models' publication: Cell publication_status: published publisher: Cell Press publist_id: '5618' quality_controlled: '1' scopus_import: 1 status: public title: Actin flows mediate a universal coupling between cell speed and cell persistence type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 161 year: '2015' ... --- _id: '1561' abstract: - lang: eng text: Replication-deficient recombinant adenoviruses are potent vectors for the efficient transient expression of exogenous genes in resting immune cells. However, most leukocytes are refractory to efficient adenoviral transduction as they lack expression of the coxsackie/adenovirus receptor (CAR). To circumvent this obstacle, we generated the R26/CAG-CARΔ1StopF (where R26 is ROSA26 and CAG is CMV early enhancer/chicken β actin promoter) knock-in mouse line. This strain allows monitoring of in situ Cre recombinase activity through expression of CARΔ1. Simultaneously, CARΔ1 expression permits selective and highly efficient adenoviral transduction of immune cell populations, such as mast cells or T cells, directly ex vivo in bulk cultures without prior cell purification or activation. Furthermore, we show that CARΔ1 expression dramatically improves adenoviral infection of in vitro differentiated conventional and plasmacytoid dendritic cells (DCs), basophils, mast cells, as well as Hoxb8-immortalized hematopoietic progenitor cells. This novel dual function mouse strain will hence be a valuable tool to rapidly dissect the function of specific genes in leukocyte physiology. author: - first_name: Klaus full_name: Heger, Klaus last_name: Heger - first_name: Maike full_name: Kober, Maike last_name: Kober - first_name: David full_name: Rieß, David last_name: Rieß - first_name: Christoph full_name: Drees, Christoph last_name: Drees - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Arianna full_name: Bertossi, Arianna last_name: Bertossi - first_name: Axel full_name: Roers, Axel last_name: Roers - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Marc full_name: Schmidt Supprian, Marc last_name: Schmidt Supprian citation: ama: Heger K, Kober M, Rieß D, et al. A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors. European Journal of Immunology. 2015;45(6):1614-1620. doi:10.1002/eji.201545457 apa: Heger, K., Kober, M., Rieß, D., Drees, C., de Vries, I., Bertossi, A., … Schmidt Supprian, M. (2015). A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors. European Journal of Immunology. Wiley. https://doi.org/10.1002/eji.201545457 chicago: Heger, Klaus, Maike Kober, David Rieß, Christoph Drees, Ingrid de Vries, Arianna Bertossi, Axel Roers, Michael K Sixt, and Marc Schmidt Supprian. “A Novel Cre Recombinase Reporter Mouse Strain Facilitates Selective and Efficient Infection of Primary Immune Cells with Adenoviral Vectors.” European Journal of Immunology. Wiley, 2015. https://doi.org/10.1002/eji.201545457. ieee: K. Heger et al., “A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors,” European Journal of Immunology, vol. 45, no. 6. Wiley, pp. 1614–1620, 2015. ista: Heger K, Kober M, Rieß D, Drees C, de Vries I, Bertossi A, Roers A, Sixt MK, Schmidt Supprian M. 2015. A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors. European Journal of Immunology. 45(6), 1614–1620. mla: Heger, Klaus, et al. “A Novel Cre Recombinase Reporter Mouse Strain Facilitates Selective and Efficient Infection of Primary Immune Cells with Adenoviral Vectors.” European Journal of Immunology, vol. 45, no. 6, Wiley, 2015, pp. 1614–20, doi:10.1002/eji.201545457. short: K. Heger, M. Kober, D. Rieß, C. Drees, I. de Vries, A. Bertossi, A. Roers, M.K. Sixt, M. Schmidt Supprian, European Journal of Immunology 45 (2015) 1614–1620. date_created: 2018-12-11T11:52:44Z date_published: 2015-06-01T00:00:00Z date_updated: 2021-01-12T06:51:36Z day: '01' department: - _id: MiSi doi: 10.1002/eji.201545457 intvolume: ' 45' issue: '6' language: - iso: eng month: '06' oa_version: None page: 1614 - 1620 publication: European Journal of Immunology publication_status: published publisher: Wiley publist_id: '5610' quality_controlled: '1' scopus_import: 1 status: public title: A novel Cre recombinase reporter mouse strain facilitates selective and efficient infection of primary immune cells with adenoviral vectors type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 45 year: '2015' ... --- _id: '1560' abstract: - lang: eng text: Stromal cells in the subcapsular sinus of the lymph node 'decide' which cells and molecules are allowed access to the deeper parenchyma. The glycoprotein PLVAP is a crucial component of this selector function. author: - first_name: Miroslav full_name: Hons, Miroslav id: 4167FE56-F248-11E8-B48F-1D18A9856A87 last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Hons M, Sixt MK. The lymph node filter revealed. Nature Immunology. 2015;16(4):338-340. doi:10.1038/ni.3126 apa: Hons, M., & Sixt, M. K. (2015). The lymph node filter revealed. Nature Immunology. Nature Publishing Group. https://doi.org/10.1038/ni.3126 chicago: Hons, Miroslav, and Michael K Sixt. “The Lymph Node Filter Revealed.” Nature Immunology. Nature Publishing Group, 2015. https://doi.org/10.1038/ni.3126. ieee: M. Hons and M. K. Sixt, “The lymph node filter revealed,” Nature Immunology, vol. 16, no. 4. Nature Publishing Group, pp. 338–340, 2015. ista: Hons M, Sixt MK. 2015. The lymph node filter revealed. Nature Immunology. 16(4), 338–340. mla: Hons, Miroslav, and Michael K. Sixt. “The Lymph Node Filter Revealed.” Nature Immunology, vol. 16, no. 4, Nature Publishing Group, 2015, pp. 338–40, doi:10.1038/ni.3126. short: M. Hons, M.K. Sixt, Nature Immunology 16 (2015) 338–340. date_created: 2018-12-11T11:52:43Z date_published: 2015-03-19T00:00:00Z date_updated: 2021-01-12T06:51:36Z day: '19' department: - _id: MiSi doi: 10.1038/ni.3126 intvolume: ' 16' issue: '4' language: - iso: eng month: '03' oa_version: None page: 338 - 340 publication: Nature Immunology publication_status: published publisher: Nature Publishing Group publist_id: '5611' quality_controlled: '1' scopus_import: 1 status: public title: The lymph node filter revealed type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 16 year: '2015' ... --- _id: '1575' abstract: - lang: eng text: The immune response relies on the migration of leukocytes and on their ability to stop in precise anatomical locations to fulfil their task. How leukocyte migration and function are coordinated is unknown. Here we show that in immature dendritic cells, which patrol their environment by engulfing extracellular material, cell migration and antigen capture are antagonistic. This antagonism results from transient enrichment of myosin IIA at the cell front, which disrupts the back-to-front gradient of the motor protein, slowing down locomotion but promoting antigen capture. We further highlight that myosin IIA enrichment at the cell front requires the MHC class II-associated invariant chain (Ii). Thus, by controlling myosin IIA localization, Ii imposes on dendritic cells an intermittent antigen capture behaviour that might facilitate environment patrolling. We propose that the requirement for myosin II in both cell migration and specific cell functions may provide a general mechanism for their coordination in time and space. acknowledgement: M.C. and M.L.H. were supported by fellowships from the Fondation pour la Recherche Médicale and the Association pour la Recherche contre le Cancer, respectively. This work was funded by grants from the City of Paris and the European Research Council to A.-M.L.-D. (Strapacemi 243103), the Association Nationale pour la Recherche (ANR-09-PIRI-0027-PCVI) and the InnaBiosanté foundation (Micemico) to A.-M.L.-D., M.P. and R.V., and the DCBIOL Labex from the French Government (ANR-10-IDEX-0001-02-PSL* and ANR-11-LABX-0043). The super-resolution SIM microscope was funded through an ERC Advanced Investigator Grant (250367) to Edith Heard (CNRS UMR3215/Inserm U934, Institut Curie). article_number: '7526' author: - first_name: Mélanie full_name: Chabaud, Mélanie last_name: Chabaud - first_name: Mélina full_name: Heuzé, Mélina last_name: Heuzé - first_name: Marine full_name: Bretou, Marine last_name: Bretou - first_name: Pablo full_name: Vargas, Pablo last_name: Vargas - first_name: Paolo full_name: Maiuri, Paolo last_name: Maiuri - first_name: Paola full_name: Solanes, Paola last_name: Solanes - first_name: Mathieu full_name: Maurin, Mathieu last_name: Maurin - first_name: Emmanuel full_name: Terriac, Emmanuel last_name: Terriac - first_name: Maël full_name: Le Berre, Maël last_name: Le Berre - first_name: Danielle full_name: Lankar, Danielle last_name: Lankar - first_name: Tristan full_name: Piolot, Tristan last_name: Piolot - first_name: Robert full_name: Adelstein, Robert last_name: Adelstein - first_name: Yingfan full_name: Zhang, Yingfan last_name: Zhang - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Jordan full_name: Jacobelli, Jordan last_name: Jacobelli - first_name: Olivier full_name: Bénichou, Olivier last_name: Bénichou - first_name: Raphaël full_name: Voituriez, Raphaël last_name: Voituriez - first_name: Matthieu full_name: Piel, Matthieu last_name: Piel - first_name: Ana full_name: Lennon Duménil, Ana last_name: Lennon Duménil citation: ama: Chabaud M, Heuzé M, Bretou M, et al. Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells. Nature Communications. 2015;6. doi:10.1038/ncomms8526 apa: Chabaud, M., Heuzé, M., Bretou, M., Vargas, P., Maiuri, P., Solanes, P., … Lennon Duménil, A. (2015). Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms8526 chicago: Chabaud, Mélanie, Mélina Heuzé, Marine Bretou, Pablo Vargas, Paolo Maiuri, Paola Solanes, Mathieu Maurin, et al. “Cell Migration and Antigen Capture Are Antagonistic Processes Coupled by Myosin II in Dendritic Cells.” Nature Communications. Nature Publishing Group, 2015. https://doi.org/10.1038/ncomms8526. ieee: M. Chabaud et al., “Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells,” Nature Communications, vol. 6. Nature Publishing Group, 2015. ista: Chabaud M, Heuzé M, Bretou M, Vargas P, Maiuri P, Solanes P, Maurin M, Terriac E, Le Berre M, Lankar D, Piolot T, Adelstein R, Zhang Y, Sixt MK, Jacobelli J, Bénichou O, Voituriez R, Piel M, Lennon Duménil A. 2015. Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells. Nature Communications. 6, 7526. mla: Chabaud, Mélanie, et al. “Cell Migration and Antigen Capture Are Antagonistic Processes Coupled by Myosin II in Dendritic Cells.” Nature Communications, vol. 6, 7526, Nature Publishing Group, 2015, doi:10.1038/ncomms8526. short: M. Chabaud, M. Heuzé, M. Bretou, P. Vargas, P. Maiuri, P. Solanes, M. Maurin, E. Terriac, M. Le Berre, D. Lankar, T. Piolot, R. Adelstein, Y. Zhang, M.K. Sixt, J. Jacobelli, O. Bénichou, R. Voituriez, M. Piel, A. Lennon Duménil, Nature Communications 6 (2015). date_created: 2018-12-11T11:52:48Z date_published: 2015-06-25T00:00:00Z date_updated: 2021-01-12T06:51:42Z day: '25' ddc: - '570' department: - _id: MiSi doi: 10.1038/ncomms8526 file: - access_level: open_access checksum: bae12e86be2adb28253f890b8bba8315 content_type: application/pdf creator: system date_created: 2018-12-12T10:11:58Z date_updated: 2020-07-14T12:45:02Z file_id: '4915' file_name: IST-2016-476-v1+1_ncomms8526.pdf file_size: 4530215 relation: main_file file_date_updated: 2020-07-14T12:45:02Z has_accepted_license: '1' intvolume: ' 6' language: - iso: eng month: '06' oa: 1 oa_version: Published Version publication: Nature Communications publication_status: published publisher: Nature Publishing Group publist_id: '5596' pubrep_id: '476' quality_controlled: '1' scopus_import: 1 status: public title: Cell migration and antigen capture are antagonistic processes coupled by myosin II in dendritic cells tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 6 year: '2015' ... --- _id: '1676' author: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Erez full_name: Raz, Erez last_name: Raz citation: ama: 'Sixt MK, Raz E. Editorial overview: Cell adhesion and migration. Current Opinion in Cell Biology. 2015;36(10):4-6. doi:10.1016/j.ceb.2015.09.004' apa: 'Sixt, M. K., & Raz, E. (2015). Editorial overview: Cell adhesion and migration. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2015.09.004' chicago: 'Sixt, Michael K, and Erez Raz. “Editorial Overview: Cell Adhesion and Migration.” Current Opinion in Cell Biology. Elsevier, 2015. https://doi.org/10.1016/j.ceb.2015.09.004.' ieee: 'M. K. Sixt and E. Raz, “Editorial overview: Cell adhesion and migration,” Current Opinion in Cell Biology, vol. 36, no. 10. Elsevier, pp. 4–6, 2015.' ista: 'Sixt MK, Raz E. 2015. Editorial overview: Cell adhesion and migration. Current Opinion in Cell Biology. 36(10), 4–6.' mla: 'Sixt, Michael K., and Erez Raz. “Editorial Overview: Cell Adhesion and Migration.” Current Opinion in Cell Biology, vol. 36, no. 10, Elsevier, 2015, pp. 4–6, doi:10.1016/j.ceb.2015.09.004.' short: M.K. Sixt, E. Raz, Current Opinion in Cell Biology 36 (2015) 4–6. date_created: 2018-12-11T11:53:25Z date_published: 2015-10-01T00:00:00Z date_updated: 2021-01-12T06:52:27Z day: '01' department: - _id: MiSi doi: 10.1016/j.ceb.2015.09.004 intvolume: ' 36' issue: '10' language: - iso: eng month: '10' oa_version: None page: 4 - 6 publication: Current Opinion in Cell Biology publication_status: published publisher: Elsevier publist_id: '5473' scopus_import: 1 status: public title: 'Editorial overview: Cell adhesion and migration' type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 36 year: '2015' ... --- _id: '1687' abstract: - lang: eng text: Guided cell movement is essential for development and integrity of animals and crucially involved in cellular immune responses. Leukocytes are professional migratory cells that can navigate through most types of tissues and sense a wide range of directional cues. The responses of these cells to attractants have been mainly explored in tissue culture settings. How leukocytes make directional decisions in situ, within the challenging environment of a tissue maze, is less understood. Here we review recent advances in how leukocytes sense chemical cues in complex tissue settings and make links with paradigms of directed migration in development and Dictyostelium discoideum amoebae. author: - first_name: Milka full_name: Sarris, Milka last_name: Sarris - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Sarris M, Sixt MK. Navigating in tissue mazes: Chemoattractant interpretation in complex environments. Current Opinion in Cell Biology. 2015;36(10):93-102. doi:10.1016/j.ceb.2015.08.001' apa: 'Sarris, M., & Sixt, M. K. (2015). Navigating in tissue mazes: Chemoattractant interpretation in complex environments. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2015.08.001' chicago: 'Sarris, Milka, and Michael K Sixt. “Navigating in Tissue Mazes: Chemoattractant Interpretation in Complex Environments.” Current Opinion in Cell Biology. Elsevier, 2015. https://doi.org/10.1016/j.ceb.2015.08.001.' ieee: 'M. Sarris and M. K. Sixt, “Navigating in tissue mazes: Chemoattractant interpretation in complex environments,” Current Opinion in Cell Biology, vol. 36, no. 10. Elsevier, pp. 93–102, 2015.' ista: 'Sarris M, Sixt MK. 2015. Navigating in tissue mazes: Chemoattractant interpretation in complex environments. Current Opinion in Cell Biology. 36(10), 93–102.' mla: 'Sarris, Milka, and Michael K. Sixt. “Navigating in Tissue Mazes: Chemoattractant Interpretation in Complex Environments.” Current Opinion in Cell Biology, vol. 36, no. 10, Elsevier, 2015, pp. 93–102, doi:10.1016/j.ceb.2015.08.001.' short: M. Sarris, M.K. Sixt, Current Opinion in Cell Biology 36 (2015) 93–102. date_created: 2018-12-11T11:53:28Z date_published: 2015-10-01T00:00:00Z date_updated: 2021-01-12T06:52:31Z day: '01' ddc: - '570' department: - _id: MiSi doi: 10.1016/j.ceb.2015.08.001 ec_funded: 1 file: - access_level: open_access checksum: c29973924b790aab02fdd91857759cfb content_type: application/pdf creator: system date_created: 2018-12-12T10:11:21Z date_updated: 2020-07-14T12:45:12Z file_id: '4875' file_name: IST-2016-445-v1+1_1-s2.0-S0955067415001064-main.pdf file_size: 797964 relation: main_file file_date_updated: 2020-07-14T12:45:12Z has_accepted_license: '1' intvolume: ' 36' issue: '10' language: - iso: eng month: '10' oa: 1 oa_version: Published Version page: 93 - 102 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Current Opinion in Cell Biology publication_status: published publisher: Elsevier publist_id: '5458' pubrep_id: '445' quality_controlled: '1' scopus_import: 1 status: public title: 'Navigating in tissue mazes: Chemoattractant interpretation in complex environments' tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 36 year: '2015' ... --- _id: '1686' author: - first_name: Eva full_name: Kiermaier, Eva id: 3EB04B78-F248-11E8-B48F-1D18A9856A87 last_name: Kiermaier orcid: 0000-0001-6165-5738 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Kiermaier E, Sixt MK. Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection. Science. 2015;349(6252):1055-1056. doi:10.1126/science.aad0867' apa: 'Kiermaier, E., & Sixt, M. K. (2015). Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.aad0867' chicago: 'Kiermaier, Eva, and Michael K Sixt. “Fragmented Communication between Immune Cells: Neutrophils Blaze a Trail with Migratory Cues for T Cells to Follow to Sites of Infection.” Science. American Association for the Advancement of Science, 2015. https://doi.org/10.1126/science.aad0867.' ieee: 'E. Kiermaier and M. K. Sixt, “Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection,” Science, vol. 349, no. 6252. American Association for the Advancement of Science, pp. 1055–1056, 2015.' ista: 'Kiermaier E, Sixt MK. 2015. Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection. Science. 349(6252), 1055–1056.' mla: 'Kiermaier, Eva, and Michael K. Sixt. “Fragmented Communication between Immune Cells: Neutrophils Blaze a Trail with Migratory Cues for T Cells to Follow to Sites of Infection.” Science, vol. 349, no. 6252, American Association for the Advancement of Science, 2015, pp. 1055–56, doi:10.1126/science.aad0867.' short: E. Kiermaier, M.K. Sixt, Science 349 (2015) 1055–1056. date_created: 2018-12-11T11:53:28Z date_published: 2015-09-04T00:00:00Z date_updated: 2021-01-12T06:52:31Z day: '04' department: - _id: MiSi doi: 10.1126/science.aad0867 intvolume: ' 349' issue: '6252' language: - iso: eng month: '09' oa_version: None page: 1055 - 1056 publication: Science publication_status: published publisher: American Association for the Advancement of Science publist_id: '5459' quality_controlled: '1' scopus_import: 1 status: public title: 'Fragmented communication between immune cells: Neutrophils blaze a trail with migratory cues for T cells to follow to sites of infection' type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 349 year: '2015' ... --- _id: '477' abstract: - lang: eng text: Dendritic cells are potent antigen-presenting cells endowed with the unique ability to initiate adaptive immune responses upon inflammation. Inflammatory processes are often associated with an increased production of serotonin, which operates by activating specific receptors. However, the functional role of serotonin receptors in regulation of dendritic cell functions is poorly understood. Here, we demonstrate that expression of serotonin receptor 5-HT7 (5-HT7TR) as well as its downstream effector Cdc42 is upregulated in dendritic cells upon maturation. Although dendritic cell maturation was independent of 5-HT7TR, receptor stimulation affected dendritic cell morphology through Cdc42-mediated signaling. In addition, basal activity of 5-HT7TR was required for the proper expression of the chemokine receptor CCR7, which is a key factor that controls dendritic cell migration. Consistent with this, we observed that 5-HT7TR enhances chemotactic motility of dendritic cells in vitro by modulating their directionality and migration velocity. Accordingly, migration of dendritic cells in murine colon explants was abolished after pharmacological receptor inhibition. Our results indicate that there is a crucial role for 5-HT7TR-Cdc42-mediated signaling in the regulation of dendritic cell morphology and motility, suggesting that 5-HT7TR could be a new target for treatment of a variety of inflammatory and immune disorders. author: - first_name: Katrin full_name: Holst, Katrin last_name: Holst - first_name: Daria full_name: Guseva, Daria last_name: Guseva - first_name: Susann full_name: Schindler, Susann last_name: Schindler - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Armin full_name: Braun, Armin last_name: Braun - first_name: Himpriya full_name: Chopra, Himpriya last_name: Chopra - first_name: Oliver full_name: Pabst, Oliver last_name: Pabst - first_name: Evgeni full_name: Ponimaskin, Evgeni last_name: Ponimaskin citation: ama: Holst K, Guseva D, Schindler S, et al. The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells. Journal of Cell Science. 2015;128(15):2866-2880. doi:10.1242/jcs.167999 apa: Holst, K., Guseva, D., Schindler, S., Sixt, M. K., Braun, A., Chopra, H., … Ponimaskin, E. (2015). The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells. Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.167999 chicago: Holst, Katrin, Daria Guseva, Susann Schindler, Michael K Sixt, Armin Braun, Himpriya Chopra, Oliver Pabst, and Evgeni Ponimaskin. “The Serotonin Receptor 5-HT7R Regulates the Morphology and Migratory Properties of Dendritic Cells.” Journal of Cell Science. Company of Biologists, 2015. https://doi.org/10.1242/jcs.167999. ieee: K. Holst et al., “The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells,” Journal of Cell Science, vol. 128, no. 15. Company of Biologists, pp. 2866–2880, 2015. ista: Holst K, Guseva D, Schindler S, Sixt MK, Braun A, Chopra H, Pabst O, Ponimaskin E. 2015. The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells. Journal of Cell Science. 128(15), 2866–2880. mla: Holst, Katrin, et al. “The Serotonin Receptor 5-HT7R Regulates the Morphology and Migratory Properties of Dendritic Cells.” Journal of Cell Science, vol. 128, no. 15, Company of Biologists, 2015, pp. 2866–80, doi:10.1242/jcs.167999. short: K. Holst, D. Guseva, S. Schindler, M.K. Sixt, A. Braun, H. Chopra, O. Pabst, E. Ponimaskin, Journal of Cell Science 128 (2015) 2866–2880. date_created: 2018-12-11T11:46:41Z date_published: 2015-06-15T00:00:00Z date_updated: 2021-01-12T08:00:54Z day: '15' department: - _id: MiSi doi: 10.1242/jcs.167999 intvolume: ' 128' issue: '15' language: - iso: eng month: '06' oa_version: None page: 2866 - 2880 publication: Journal of Cell Science publication_status: published publisher: Company of Biologists publist_id: '7343' quality_controlled: '1' scopus_import: 1 status: public title: The serotonin receptor 5-HT7R regulates the morphology and migratory properties of dendritic cells type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 128 year: '2015' ... --- _id: '1618' abstract: - lang: eng text: CCL19 and CCL21 are chemokines involved in the trafficking of immune cells, particularly within the lymphatic system, through activation of CCR7. Concurrent expression of PSGL-1 and CCR7 in naive T-cells enhances recruitment of these cells to secondary lymphoid organs by CCL19 and CCL21. Here the solution structure of CCL19 is reported. It contains a canonical chemokine domain. Chemical shift mapping shows the N-termini of PSGL-1 and CCR7 have overlapping binding sites for CCL19 and binding is competitive. Implications for the mechanism of PSGL-1's enhancement of resting T-cell recruitment are discussed. article_processing_charge: No author: - first_name: Christopher full_name: Veldkamp, Christopher last_name: Veldkamp - first_name: Eva full_name: Kiermaier, Eva id: 3EB04B78-F248-11E8-B48F-1D18A9856A87 last_name: Kiermaier orcid: 0000-0001-6165-5738 - first_name: Skylar full_name: Gabel Eissens, Skylar last_name: Gabel Eissens - first_name: Miranda full_name: Gillitzer, Miranda last_name: Gillitzer - first_name: David full_name: Lippner, David last_name: Lippner - first_name: Frank full_name: Disilvio, Frank last_name: Disilvio - first_name: Casey full_name: Mueller, Casey last_name: Mueller - first_name: Paeton full_name: Wantuch, Paeton last_name: Wantuch - first_name: Gary full_name: Chaffee, Gary last_name: Chaffee - first_name: Michael full_name: Famiglietti, Michael last_name: Famiglietti - first_name: Danielle full_name: Zgoba, Danielle last_name: Zgoba - first_name: Asha full_name: Bailey, Asha last_name: Bailey - first_name: Yaya full_name: Bah, Yaya last_name: Bah - first_name: Samantha full_name: Engebretson, Samantha last_name: Engebretson - first_name: David full_name: Graupner, David last_name: Graupner - first_name: Emily full_name: Lackner, Emily last_name: Lackner - first_name: Vincent full_name: Larosa, Vincent last_name: Larosa - first_name: Tysha full_name: Medeiros, Tysha last_name: Medeiros - first_name: Michael full_name: Olson, Michael last_name: Olson - first_name: Andrew full_name: Phillips, Andrew last_name: Phillips - first_name: Harley full_name: Pyles, Harley last_name: Pyles - first_name: Amanda full_name: Richard, Amanda last_name: Richard - first_name: Scott full_name: Schoeller, Scott last_name: Schoeller - first_name: Boris full_name: Touzeau, Boris last_name: Touzeau - first_name: Larry full_name: Williams, Larry last_name: Williams - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Francis full_name: Peterson, Francis last_name: Peterson citation: ama: Veldkamp C, Kiermaier E, Gabel Eissens S, et al. Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites. Biochemistry. 2015;54(27):4163-4166. doi:10.1021/acs.biochem.5b00560 apa: Veldkamp, C., Kiermaier, E., Gabel Eissens, S., Gillitzer, M., Lippner, D., Disilvio, F., … Peterson, F. (2015). Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites. Biochemistry. American Chemical Society. https://doi.org/10.1021/acs.biochem.5b00560 chicago: Veldkamp, Christopher, Eva Kiermaier, Skylar Gabel Eissens, Miranda Gillitzer, David Lippner, Frank Disilvio, Casey Mueller, et al. “Solution Structure of CCL19 and Identification of Overlapping CCR7 and PSGL-1 Binding Sites.” Biochemistry. American Chemical Society, 2015. https://doi.org/10.1021/acs.biochem.5b00560. ieee: C. Veldkamp et al., “Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites,” Biochemistry, vol. 54, no. 27. American Chemical Society, pp. 4163–4166, 2015. ista: Veldkamp C, Kiermaier E, Gabel Eissens S, Gillitzer M, Lippner D, Disilvio F, Mueller C, Wantuch P, Chaffee G, Famiglietti M, Zgoba D, Bailey A, Bah Y, Engebretson S, Graupner D, Lackner E, Larosa V, Medeiros T, Olson M, Phillips A, Pyles H, Richard A, Schoeller S, Touzeau B, Williams L, Sixt MK, Peterson F. 2015. Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites. Biochemistry. 54(27), 4163–4166. mla: Veldkamp, Christopher, et al. “Solution Structure of CCL19 and Identification of Overlapping CCR7 and PSGL-1 Binding Sites.” Biochemistry, vol. 54, no. 27, American Chemical Society, 2015, pp. 4163–66, doi:10.1021/acs.biochem.5b00560. short: C. Veldkamp, E. Kiermaier, S. Gabel Eissens, M. Gillitzer, D. Lippner, F. Disilvio, C. Mueller, P. Wantuch, G. Chaffee, M. Famiglietti, D. Zgoba, A. Bailey, Y. Bah, S. Engebretson, D. Graupner, E. Lackner, V. Larosa, T. Medeiros, M. Olson, A. Phillips, H. Pyles, A. Richard, S. Schoeller, B. Touzeau, L. Williams, M.K. Sixt, F. Peterson, Biochemistry 54 (2015) 4163–4166. date_created: 2018-12-11T11:53:03Z date_published: 2015-06-26T00:00:00Z date_updated: 2023-03-30T11:32:57Z day: '26' department: - _id: MiSi doi: 10.1021/acs.biochem.5b00560 ec_funded: 1 external_id: pmid: - '26115234' intvolume: ' 54' issue: '27' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4809050/ month: '06' oa: 1 oa_version: Submitted Version page: 4163 - 4166 pmid: 1 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) publication: Biochemistry publication_status: published publisher: American Chemical Society publist_id: '5548' quality_controlled: '1' scopus_import: '1' status: public title: Solution structure of CCL19 and identification of overlapping CCR7 and PSGL-1 binding sites type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 54 year: '2015' ... --- _id: '1537' abstract: - lang: eng text: 3D amoeboid cell migration is central to many developmental and disease-related processes such as cancer metastasis. Here, we identify a unique prototypic amoeboid cell migration mode in early zebrafish embryos, termed stable-bleb migration. Stable-bleb cells display an invariant polarized balloon-like shape with exceptional migration speed and persistence. Progenitor cells can be reversibly transformed into stable-bleb cells irrespective of their primary fate and motile characteristics by increasing myosin II activity through biochemical or mechanical stimuli. Using a combination of theory and experiments, we show that, in stable-bleb cells, cortical contractility fluctuations trigger a stochastic switch into amoeboid motility, and a positive feedback between cortical flows and gradients in contractility maintains stable-bleb cell polarization. We further show that rearward cortical flows drive stable-bleb cell migration in various adhesive and non-adhesive environments, unraveling a highly versatile amoeboid migration phenotype. acknowledged_ssus: - _id: SSU acknowledgement: 'We would like to thank R. Hausschild and E. Papusheva for technical assistance and the service facilities at the IST Austria for continuous support. The caRhoA plasmid was a kind gift of T. Kudoh and A. Takesono. We thank M. Piel and E. Paluch for exchanging unpublished data. ' author: - first_name: Verena full_name: Ruprecht, Verena id: 4D71A03A-F248-11E8-B48F-1D18A9856A87 last_name: Ruprecht orcid: 0000-0003-4088-8633 - first_name: Stefan full_name: Wieser, Stefan id: 355AA5A0-F248-11E8-B48F-1D18A9856A87 last_name: Wieser orcid: 0000-0002-2670-2217 - first_name: Andrew full_name: Callan Jones, Andrew last_name: Callan Jones - first_name: Michael full_name: Smutny, Michael id: 3FE6E4E8-F248-11E8-B48F-1D18A9856A87 last_name: Smutny orcid: 0000-0002-5920-9090 - first_name: Hitoshi full_name: Morita, Hitoshi id: 4C6E54C6-F248-11E8-B48F-1D18A9856A87 last_name: Morita - first_name: Keisuke full_name: Sako, Keisuke id: 3BED66BE-F248-11E8-B48F-1D18A9856A87 last_name: Sako orcid: 0000-0002-6453-8075 - first_name: Vanessa full_name: Barone, Vanessa id: 419EECCC-F248-11E8-B48F-1D18A9856A87 last_name: Barone orcid: 0000-0003-2676-3367 - first_name: Monika full_name: Ritsch Marte, Monika last_name: Ritsch Marte - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Raphaël full_name: Voituriez, Raphaël last_name: Voituriez - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 citation: ama: Ruprecht V, Wieser S, Callan Jones A, et al. Cortical contractility triggers a stochastic switch to fast amoeboid cell motility. Cell. 2015;160(4):673-685. doi:10.1016/j.cell.2015.01.008 apa: Ruprecht, V., Wieser, S., Callan Jones, A., Smutny, M., Morita, H., Sako, K., … Heisenberg, C.-P. J. (2015). Cortical contractility triggers a stochastic switch to fast amoeboid cell motility. Cell. Cell Press. https://doi.org/10.1016/j.cell.2015.01.008 chicago: Ruprecht, Verena, Stefan Wieser, Andrew Callan Jones, Michael Smutny, Hitoshi Morita, Keisuke Sako, Vanessa Barone, et al. “Cortical Contractility Triggers a Stochastic Switch to Fast Amoeboid Cell Motility.” Cell. Cell Press, 2015. https://doi.org/10.1016/j.cell.2015.01.008. ieee: V. Ruprecht et al., “Cortical contractility triggers a stochastic switch to fast amoeboid cell motility,” Cell, vol. 160, no. 4. Cell Press, pp. 673–685, 2015. ista: Ruprecht V, Wieser S, Callan Jones A, Smutny M, Morita H, Sako K, Barone V, Ritsch Marte M, Sixt MK, Voituriez R, Heisenberg C-PJ. 2015. Cortical contractility triggers a stochastic switch to fast amoeboid cell motility. Cell. 160(4), 673–685. mla: Ruprecht, Verena, et al. “Cortical Contractility Triggers a Stochastic Switch to Fast Amoeboid Cell Motility.” Cell, vol. 160, no. 4, Cell Press, 2015, pp. 673–85, doi:10.1016/j.cell.2015.01.008. short: V. Ruprecht, S. Wieser, A. Callan Jones, M. Smutny, H. Morita, K. Sako, V. Barone, M. Ritsch Marte, M.K. Sixt, R. Voituriez, C.-P.J. Heisenberg, Cell 160 (2015) 673–685. date_created: 2018-12-11T11:52:35Z date_published: 2015-02-12T00:00:00Z date_updated: 2023-09-07T12:05:08Z day: '12' ddc: - '570' department: - _id: CaHe - _id: MiSi doi: 10.1016/j.cell.2015.01.008 file: - access_level: open_access checksum: 228d3edf40627d897b3875088a0ac51f content_type: application/pdf creator: system date_created: 2018-12-12T10:13:21Z date_updated: 2020-07-14T12:45:01Z file_id: '5003' file_name: IST-2016-484-v1+1_1-s2.0-S0092867415000094-main.pdf file_size: 4362653 relation: main_file file_date_updated: 2020-07-14T12:45:01Z has_accepted_license: '1' intvolume: ' 160' issue: '4' language: - iso: eng month: '02' oa: 1 oa_version: Published Version page: 673 - 685 project: - _id: 2529486C-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: T 560-B17 name: Cell- and Tissue Mechanics in Zebrafish Germ Layer Formation - _id: 2527D5CC-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: I 812-B12 name: Cell Cortex and Germ Layer Formation in Zebrafish Gastrulation publication: Cell publication_status: published publisher: Cell Press publist_id: '5634' pubrep_id: '484' quality_controlled: '1' related_material: record: - id: '961' relation: dissertation_contains status: public scopus_import: 1 status: public title: Cortical contractility triggers a stochastic switch to fast amoeboid cell motility tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 160 year: '2015' ... --- _id: '1877' abstract: - lang: eng text: During inflammation, lymph nodes swell with an influx of immune cells. New findings identify a signalling pathway that induces relaxation in the contractile cells that give structure to these organs. article_type: letter_note author: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Kari full_name: Vaahtomeri, Kari id: 368EE576-F248-11E8-B48F-1D18A9856A87 last_name: Vaahtomeri orcid: 0000-0001-7829-3518 citation: ama: 'Sixt MK, Vaahtomeri K. Physiology: Relax and come in. Nature. 2014;514(7523):441-442. doi:10.1038/514441a' apa: 'Sixt, M. K., & Vaahtomeri, K. (2014). Physiology: Relax and come in. Nature. Springer Nature. https://doi.org/10.1038/514441a' chicago: 'Sixt, Michael K, and Kari Vaahtomeri. “Physiology: Relax and Come In.” Nature. Springer Nature, 2014. https://doi.org/10.1038/514441a.' ieee: 'M. K. Sixt and K. Vaahtomeri, “Physiology: Relax and come in,” Nature, vol. 514, no. 7523. Springer Nature, pp. 441–442, 2014.' ista: 'Sixt MK, Vaahtomeri K. 2014. Physiology: Relax and come in. Nature. 514(7523), 441–442.' mla: 'Sixt, Michael K., and Kari Vaahtomeri. “Physiology: Relax and Come In.” Nature, vol. 514, no. 7523, Springer Nature, 2014, pp. 441–42, doi:10.1038/514441a.' short: M.K. Sixt, K. Vaahtomeri, Nature 514 (2014) 441–442. date_created: 2018-12-11T11:54:30Z date_published: 2014-10-23T00:00:00Z date_updated: 2021-01-12T06:53:47Z day: '23' department: - _id: MiSi doi: 10.1038/514441a intvolume: ' 514' issue: '7523' language: - iso: eng month: '10' oa_version: None page: 441 - 442 publication: Nature publication_status: published publisher: Springer Nature publist_id: '5219' quality_controlled: '1' scopus_import: 1 status: public title: 'Physiology: Relax and come in' type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 514 year: '2014' ... --- _id: '1910' abstract: - lang: eng text: angerhans cells (LCs) are a unique subset of dendritic cells (DCs) that express epithelial adhesion molecules, allowing them to form contacts with epithelial cells and reside in epidermal/epithelial tissues. The dynamic regulation of epithelial adhesion plays a decisive role in the life cycle of LCs. It controls whether LCs remain immature and sessile within the epidermis or mature and egress to initiate immune responses. So far, the molecular machinery regulating epithelial adhesion molecules during LC maturation remains elusive. Here, we generated pure populations of immature human LCs in vitro to systematically probe for gene-expression changes during LC maturation. LCs down-regulate a set of epithelial genes including E-cadherin, while they upregulate the mesenchymal marker N-cadherin known to facilitate cell migration. In addition, N-cadherin is constitutively expressed by monocyte-derived DCs known to exhibit characteristics of both inflammatory-type and interstitial/dermal DCs. Moreover, the transcription factors ZEB1 and ZEB2 (ZEB is zinc-finger E-box-binding homeobox) are upregulated in migratory LCs. ZEB1 and ZEB2 have been shown to induce epithelial-to-mesenchymal transition (EMT) and invasive behavior in cancer cells undergoing metastasis. Our results provide the first hint that the molecular EMT machinery might facilitate LC mobilization. Moreover, our study suggests that N-cadherin plays a role during DC migration. acknowledgement: 'FWF. Grant Number: P22058-B20' author: - first_name: Sabine full_name: Konradi, Sabine last_name: Konradi - first_name: Nighat full_name: Yasmin, Nighat last_name: Yasmin - first_name: Denise full_name: Haslwanter, Denise last_name: Haslwanter - first_name: Michele full_name: Weber, Michele id: 3A3FC708-F248-11E8-B48F-1D18A9856A87 last_name: Weber - first_name: Bernd full_name: Gesslbauer, Bernd last_name: Gesslbauer - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Herbert full_name: Strobl, Herbert last_name: Strobl citation: ama: Konradi S, Yasmin N, Haslwanter D, et al. Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2. European Journal of Immunology. 2014;44(2):553-560. doi:10.1002/eji.201343681 apa: Konradi, S., Yasmin, N., Haslwanter, D., Weber, M., Gesslbauer, B., Sixt, M. K., & Strobl, H. (2014). Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2. European Journal of Immunology. Wiley-Blackwell. https://doi.org/10.1002/eji.201343681 chicago: Konradi, Sabine, Nighat Yasmin, Denise Haslwanter, Michele Weber, Bernd Gesslbauer, Michael K Sixt, and Herbert Strobl. “Langerhans Cell Maturation Is Accompanied by Induction of N-Cadherin and the Transcriptional Regulators of Epithelial-Mesenchymal Transition ZEB1/2.” European Journal of Immunology. Wiley-Blackwell, 2014. https://doi.org/10.1002/eji.201343681. ieee: S. Konradi et al., “Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2,” European Journal of Immunology, vol. 44, no. 2. Wiley-Blackwell, pp. 553–560, 2014. ista: Konradi S, Yasmin N, Haslwanter D, Weber M, Gesslbauer B, Sixt MK, Strobl H. 2014. Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2. European Journal of Immunology. 44(2), 553–560. mla: Konradi, Sabine, et al. “Langerhans Cell Maturation Is Accompanied by Induction of N-Cadherin and the Transcriptional Regulators of Epithelial-Mesenchymal Transition ZEB1/2.” European Journal of Immunology, vol. 44, no. 2, Wiley-Blackwell, 2014, pp. 553–60, doi:10.1002/eji.201343681. short: S. Konradi, N. Yasmin, D. Haslwanter, M. Weber, B. Gesslbauer, M.K. Sixt, H. Strobl, European Journal of Immunology 44 (2014) 553–560. date_created: 2018-12-11T11:54:40Z date_published: 2014-02-01T00:00:00Z date_updated: 2021-01-12T06:54:01Z day: '01' department: - _id: MiSi doi: 10.1002/eji.201343681 intvolume: ' 44' issue: '2' language: - iso: eng month: '02' oa_version: None page: 553 - 560 publication: European Journal of Immunology publication_status: published publisher: Wiley-Blackwell publist_id: '5185' scopus_import: 1 status: public title: Langerhans cell maturation is accompanied by induction of N-cadherin and the transcriptional regulators of epithelial-mesenchymal transition ZEB1/2 type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 44 year: '2014' ... --- _id: '2158' abstract: - lang: eng text: Directional guidance of migrating cells is relatively well explored in the reductionist setting of cell culture experiments. Here spatial gradients of chemical cues as well as gradients of mechanical substrate characteristics prove sufficient to attract single cells as well as their collectives. How such gradients present and act in the context of an organism is far less clear. Here we review recent advances in understanding how guidance cues emerge and operate in the physiological context. acknowledgement: This effort was supported by the Intramural Research Program of the Center for Cancer Research, NCI, National Institutes of Health and the European Research Council (ERC). author: - first_name: Ritankar full_name: Majumdar, Ritankar last_name: Majumdar - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Carole full_name: Parent, Carole last_name: Parent citation: ama: Majumdar R, Sixt MK, Parent C. New paradigms in the establishment and maintenance of gradients during directed cell migration. Current Opinion in Cell Biology. 2014;30(1):33-40. doi:10.1016/j.ceb.2014.05.010 apa: Majumdar, R., Sixt, M. K., & Parent, C. (2014). New paradigms in the establishment and maintenance of gradients during directed cell migration. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2014.05.010 chicago: Majumdar, Ritankar, Michael K Sixt, and Carole Parent. “New Paradigms in the Establishment and Maintenance of Gradients during Directed Cell Migration.” Current Opinion in Cell Biology. Elsevier, 2014. https://doi.org/10.1016/j.ceb.2014.05.010. ieee: R. Majumdar, M. K. Sixt, and C. Parent, “New paradigms in the establishment and maintenance of gradients during directed cell migration,” Current Opinion in Cell Biology, vol. 30, no. 1. Elsevier, pp. 33–40, 2014. ista: Majumdar R, Sixt MK, Parent C. 2014. New paradigms in the establishment and maintenance of gradients during directed cell migration. Current Opinion in Cell Biology. 30(1), 33–40. mla: Majumdar, Ritankar, et al. “New Paradigms in the Establishment and Maintenance of Gradients during Directed Cell Migration.” Current Opinion in Cell Biology, vol. 30, no. 1, Elsevier, 2014, pp. 33–40, doi:10.1016/j.ceb.2014.05.010. short: R. Majumdar, M.K. Sixt, C. Parent, Current Opinion in Cell Biology 30 (2014) 33–40. date_created: 2018-12-11T11:56:03Z date_published: 2014-10-01T00:00:00Z date_updated: 2021-01-12T06:55:40Z day: '01' department: - _id: MiSi doi: 10.1016/j.ceb.2014.05.010 external_id: pmid: - '24959970' intvolume: ' 30' issue: '1' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4177954/ month: '10' oa: 1 oa_version: Submitted Version page: 33 - 40 pmid: 1 publication: Current Opinion in Cell Biology publication_status: published publisher: Elsevier publist_id: '4848' quality_controlled: '1' scopus_import: 1 status: public title: New paradigms in the establishment and maintenance of gradients during directed cell migration type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 30 year: '2014' ... --- _id: '2214' abstract: - lang: eng text: A hallmark of immune cell trafficking is directional guidance via gradients of soluble or surface bound chemokines. Vascular endothelial cells produce, transport and deposit either their own chemokines or chemokines produced by the underlying stroma. Endothelial heparan sulfate (HS) was suggested to be a critical scaffold for these chemokine pools, but it is unclear how steep chemokine gradients are sustained between the lumenal and ablumenal aspects of blood vessels. Addressing this question by semi-quantitative immunostaining of HS moieties around blood vessels with a pan anti-HS IgM mAb, we found a striking HS enrichment in the basal lamina of resting and inflamed post capillary skin venules, as well as in high endothelial venules (HEVs) of lymph nodes. Staining of skin vessels with a glycocalyx probe further suggested that their lumenal glycocalyx contains much lower HS density than their basolateral extracellular matrix (ECM). This polarized HS pattern was observed also in isolated resting and inflamed microvascular dermal cells. Notably, progressive skin inflammation resulted in massive ECM deposition and in further HS enrichment around skin post capillary venules and their associated pericytes. Inflammation-dependent HS enrichment was not compromised in mice deficient in the main HS degrading enzyme, heparanase. Our results suggest that the blood vasculature patterns steep gradients of HS scaffolds between their lumenal and basolateral endothelial aspects, and that inflammatory processes can further enrich the HS content nearby inflamed vessels. We propose that chemokine gradients between the lumenal and ablumenal sides of vessels could be favored by these sharp HS scaffold gradients. acknowledgement: Michael Sixt's research is supported by the European Research Council (ERC Starting grant). article_number: e85699 author: - first_name: Liat full_name: Stoler Barak, Liat last_name: Stoler Barak - first_name: Christine full_name: Moussion, Christine id: 3356F664-F248-11E8-B48F-1D18A9856A87 last_name: Moussion - first_name: Elias full_name: Shezen, Elias last_name: Shezen - first_name: Miki full_name: Hatzav, Miki last_name: Hatzav - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Ronen full_name: Alon, Ronen last_name: Alon citation: ama: Stoler Barak L, Moussion C, Shezen E, Hatzav M, Sixt MK, Alon R. Blood vessels pattern heparan sulfate gradients between their apical and basolateral aspects. PLoS One. 2014;9(1). doi:10.1371/journal.pone.0085699 apa: Stoler Barak, L., Moussion, C., Shezen, E., Hatzav, M., Sixt, M. K., & Alon, R. (2014). Blood vessels pattern heparan sulfate gradients between their apical and basolateral aspects. PLoS One. Public Library of Science. https://doi.org/10.1371/journal.pone.0085699 chicago: Stoler Barak, Liat, Christine Moussion, Elias Shezen, Miki Hatzav, Michael K Sixt, and Ronen Alon. “Blood Vessels Pattern Heparan Sulfate Gradients between Their Apical and Basolateral Aspects.” PLoS One. Public Library of Science, 2014. https://doi.org/10.1371/journal.pone.0085699. ieee: L. Stoler Barak, C. Moussion, E. Shezen, M. Hatzav, M. K. Sixt, and R. Alon, “Blood vessels pattern heparan sulfate gradients between their apical and basolateral aspects,” PLoS One, vol. 9, no. 1. Public Library of Science, 2014. ista: Stoler Barak L, Moussion C, Shezen E, Hatzav M, Sixt MK, Alon R. 2014. Blood vessels pattern heparan sulfate gradients between their apical and basolateral aspects. PLoS One. 9(1), e85699. mla: Stoler Barak, Liat, et al. “Blood Vessels Pattern Heparan Sulfate Gradients between Their Apical and Basolateral Aspects.” PLoS One, vol. 9, no. 1, e85699, Public Library of Science, 2014, doi:10.1371/journal.pone.0085699. short: L. Stoler Barak, C. Moussion, E. Shezen, M. Hatzav, M.K. Sixt, R. Alon, PLoS One 9 (2014). date_created: 2018-12-11T11:56:22Z date_published: 2014-01-22T00:00:00Z date_updated: 2021-01-12T06:56:03Z day: '22' ddc: - '570' department: - _id: MiSi doi: 10.1371/journal.pone.0085699 ec_funded: 1 file: - access_level: open_access checksum: 84a8033bda2e07e39405f5acc85f4eca content_type: application/pdf creator: system date_created: 2018-12-12T10:07:48Z date_updated: 2020-07-14T12:45:33Z file_id: '4646' file_name: IST-2016-433-v1+1_journal.pone.0085699.pdf file_size: 12634775 relation: main_file file_date_updated: 2020-07-14T12:45:33Z has_accepted_license: '1' intvolume: ' 9' issue: '1' language: - iso: eng month: '01' oa: 1 oa_version: Published Version project: - _id: 25A76F58-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '289720' name: Stromal Cell-immune Cell Interactions in Health and Disease publication: PLoS One publication_status: published publisher: Public Library of Science publist_id: '4756' pubrep_id: '433' quality_controlled: '1' scopus_import: 1 status: public title: Blood vessels pattern heparan sulfate gradients between their apical and basolateral aspects tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 9 year: '2014' ... --- _id: '2242' abstract: - lang: eng text: MicroRNAs (miRNAs) are small RNAs that play important regulatory roles in many cellular pathways. MiRNAs associate with members of the Argonaute protein family and bind to partially complementary sequences on mRNAs and induce translational repression or mRNA decay. Using deep sequencing and Northern blotting, we characterized miRNA expression in wild type and miR-155-deficient dendritic cells (DCs) and macrophages. Analysis of different stimuli (LPS, LDL, eLDL, oxLDL) reveals a direct influence of miR-155 on the expression levels of other miRNAs. For example, miR-455 is negatively regulated in miR-155-deficient cells possibly due to inhibition of the transcription factor C/EBPbeta by miR-155. Based on our comprehensive data sets, we propose a model of hierarchical miRNA expression dominated by miR-155 in DCs and macrophages. author: - first_name: Anne full_name: Dueck, Anne last_name: Dueck - first_name: Alexander full_name: Eichner, Alexander id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87 last_name: Eichner - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Gunter full_name: Meister, Gunter last_name: Meister citation: ama: Dueck A, Eichner A, Sixt MK, Meister G. A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation. FEBS Letters. 2014;588(4):632-640. doi:10.1016/j.febslet.2014.01.009 apa: Dueck, A., Eichner, A., Sixt, M. K., & Meister, G. (2014). A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation. FEBS Letters. Elsevier. https://doi.org/10.1016/j.febslet.2014.01.009 chicago: Dueck, Anne, Alexander Eichner, Michael K Sixt, and Gunter Meister. “A MiR-155-Dependent MicroRNA Hierarchy in Dendritic Cell Maturation and Macrophage Activation.” FEBS Letters. Elsevier, 2014. https://doi.org/10.1016/j.febslet.2014.01.009. ieee: A. Dueck, A. Eichner, M. K. Sixt, and G. Meister, “A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation,” FEBS Letters, vol. 588, no. 4. Elsevier, pp. 632–640, 2014. ista: Dueck A, Eichner A, Sixt MK, Meister G. 2014. A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation. FEBS Letters. 588(4), 632–640. mla: Dueck, Anne, et al. “A MiR-155-Dependent MicroRNA Hierarchy in Dendritic Cell Maturation and Macrophage Activation.” FEBS Letters, vol. 588, no. 4, Elsevier, 2014, pp. 632–40, doi:10.1016/j.febslet.2014.01.009. short: A. Dueck, A. Eichner, M.K. Sixt, G. Meister, FEBS Letters 588 (2014) 632–640. date_created: 2018-12-11T11:56:31Z date_published: 2014-02-14T00:00:00Z date_updated: 2021-01-12T06:56:14Z day: '14' department: - _id: MiSi doi: 10.1016/j.febslet.2014.01.009 intvolume: ' 588' issue: '4' language: - iso: eng month: '02' oa_version: None page: 632 - 640 publication: FEBS Letters publication_identifier: issn: - '00145793' publication_status: published publisher: Elsevier publist_id: '4714' quality_controlled: '1' scopus_import: 1 status: public title: A miR-155-dependent microRNA hierarchy in dendritic cell maturation and macrophage activation type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 588 year: '2014' ... --- _id: '2830' author: - first_name: Christine full_name: Moussion, Christine id: 3356F664-F248-11E8-B48F-1D18A9856A87 last_name: Moussion - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Moussion C, Sixt MK. A conduit to amplify innate immunity. Immunity. 2013;38(5):853-854. doi:10.1016/j.immuni.2013.05.005 apa: Moussion, C., & Sixt, M. K. (2013). A conduit to amplify innate immunity. Immunity. Cell Press. https://doi.org/10.1016/j.immuni.2013.05.005 chicago: Moussion, Christine, and Michael K Sixt. “A Conduit to Amplify Innate Immunity.” Immunity. Cell Press, 2013. https://doi.org/10.1016/j.immuni.2013.05.005. ieee: C. Moussion and M. K. Sixt, “A conduit to amplify innate immunity,” Immunity, vol. 38, no. 5. Cell Press, pp. 853–854, 2013. ista: Moussion C, Sixt MK. 2013. A conduit to amplify innate immunity. Immunity. 38(5), 853–854. mla: Moussion, Christine, and Michael K. Sixt. “A Conduit to Amplify Innate Immunity.” Immunity, vol. 38, no. 5, Cell Press, 2013, pp. 853–54, doi:10.1016/j.immuni.2013.05.005. short: C. Moussion, M.K. Sixt, Immunity 38 (2013) 853–854. date_created: 2018-12-11T11:59:49Z date_published: 2013-05-23T00:00:00Z date_updated: 2021-01-12T07:00:01Z day: '23' department: - _id: MiSi doi: 10.1016/j.immuni.2013.05.005 intvolume: ' 38' issue: '5' language: - iso: eng month: '05' oa_version: None page: 853 - 854 publication: Immunity publication_status: published publisher: Cell Press publist_id: '3969' quality_controlled: '1' scopus_import: 1 status: public title: A conduit to amplify innate immunity type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 38 year: '2013' ... --- _id: '2839' abstract: - lang: eng text: Directional guidance of cells via gradients of chemokines is considered crucial for embryonic development, cancer dissemination, and immune responses. Nevertheless, the concept still lacks direct experimental confirmation in vivo. Here, we identify endogenous gradients of the chemokine CCL21 within mouse skin and show that they guide dendritic cells toward lymphatic vessels. Quantitative imaging reveals depots of CCL21 within lymphatic endothelial cells and steeply decaying gradients within the perilymphatic interstitium. These gradients match the migratory patterns of the dendritic cells, which directionally approach vessels from a distance of up to 90-micrometers. Interstitial CCL21 is immobilized to heparan sulfates, and its experimental delocalization or swamping the endogenous gradients abolishes directed migration. These findings functionally establish the concept of haptotaxis, directed migration along immobilized gradients, in tissues. acknowledgement: We thank M. Frank for technical assistance and S. Cremer, P. Schmalhorst, and E. Kiermaier for critical reading of the manuscript. This work was supported by a Humboldt Foundation postdoctoral fellowship (to M.W.), the German Research Foundation (Si1323 1,2 to M.S.), the Human Frontier Science Program (HFSP RGP0058/2011 to M.S.), the European Research Council (ERC StG 281556 to M.S.), and the Swiss National Science Foundation (31003A 127474 to D.F.L., 130488 to S.A.L.). article_processing_charge: No article_type: original author: - first_name: Michele full_name: Weber, Michele id: 3A3FC708-F248-11E8-B48F-1D18A9856A87 last_name: Weber - first_name: Robert full_name: Hauschild, Robert id: 4E01D6B4-F248-11E8-B48F-1D18A9856A87 last_name: Hauschild orcid: 0000-0001-9843-3522 - first_name: Jan full_name: Schwarz, Jan id: 346C1EC6-F248-11E8-B48F-1D18A9856A87 last_name: Schwarz - first_name: Christine full_name: Moussion, Christine id: 3356F664-F248-11E8-B48F-1D18A9856A87 last_name: Moussion - first_name: Ingrid full_name: De Vries, Ingrid id: 4C7D837E-F248-11E8-B48F-1D18A9856A87 last_name: De Vries - first_name: Daniel full_name: Legler, Daniel last_name: Legler - first_name: Sanjiv full_name: Luther, Sanjiv last_name: Luther - first_name: Mark Tobias full_name: Bollenbach, Mark Tobias id: 3E6DB97A-F248-11E8-B48F-1D18A9856A87 last_name: Bollenbach orcid: 0000-0003-4398-476X - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Weber M, Hauschild R, Schwarz J, et al. Interstitial dendritic cell guidance by haptotactic chemokine gradients. Science. 2013;339(6117):328-332. doi:10.1126/science.1228456 apa: Weber, M., Hauschild, R., Schwarz, J., Moussion, C., de Vries, I., Legler, D., … Sixt, M. K. (2013). Interstitial dendritic cell guidance by haptotactic chemokine gradients. Science. American Association for the Advancement of Science. https://doi.org/10.1126/science.1228456 chicago: Weber, Michele, Robert Hauschild, Jan Schwarz, Christine Moussion, Ingrid de Vries, Daniel Legler, Sanjiv Luther, Mark Tobias Bollenbach, and Michael K Sixt. “Interstitial Dendritic Cell Guidance by Haptotactic Chemokine Gradients.” Science. American Association for the Advancement of Science, 2013. https://doi.org/10.1126/science.1228456. ieee: M. Weber et al., “Interstitial dendritic cell guidance by haptotactic chemokine gradients,” Science, vol. 339, no. 6117. American Association for the Advancement of Science, pp. 328–332, 2013. ista: Weber M, Hauschild R, Schwarz J, Moussion C, de Vries I, Legler D, Luther S, Bollenbach MT, Sixt MK. 2013. Interstitial dendritic cell guidance by haptotactic chemokine gradients. Science. 339(6117), 328–332. mla: Weber, Michele, et al. “Interstitial Dendritic Cell Guidance by Haptotactic Chemokine Gradients.” Science, vol. 339, no. 6117, American Association for the Advancement of Science, 2013, pp. 328–32, doi:10.1126/science.1228456. short: M. Weber, R. Hauschild, J. Schwarz, C. Moussion, I. de Vries, D. Legler, S. Luther, M.T. Bollenbach, M.K. Sixt, Science 339 (2013) 328–332. date_created: 2018-12-11T11:59:52Z date_published: 2013-01-18T00:00:00Z date_updated: 2022-06-10T10:21:40Z day: '18' department: - _id: MiSi - _id: Bio doi: 10.1126/science.1228456 ec_funded: 1 intvolume: ' 339' issue: '6117' language: - iso: eng main_file_link: - open_access: '1' url: https://kops.uni-konstanz.de/bitstream/123456789/26341/2/Weber_263418.pdf month: '01' oa: 1 oa_version: Published Version page: 328 - 332 project: - _id: 25A603A2-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '281556' name: Cytoskeletal force generation and force transduction of migrating leukocytes (EU) - _id: 25ABD200-B435-11E9-9278-68D0E5697425 grant_number: RGP0058/2011 name: 'Cell migration in complex environments: from in vivo experiments to theoretical models' publication: Science publication_status: published publisher: American Association for the Advancement of Science publist_id: '3959' quality_controlled: '1' scopus_import: '1' status: public title: Interstitial dendritic cell guidance by haptotactic chemokine gradients type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 339 year: '2013' ... --- _id: '522' abstract: - lang: eng text: Podoplanin, a mucin-like plasma membrane protein, is expressed by lymphatic endothelial cells and responsible for separation of blood and lymphatic circulation through activation of platelets. Here we show that podoplanin is also expressed by thymic fibroblastic reticular cells (tFRC), a novel thymic medulla stroma cell type associated with thymic conduits, and involved in development of natural regulatory T cells (nTreg). Young mice deficient in podoplanin lack nTreg owing to retardation of CD4+CD25+ thymocytes in the cortex and missing differentiation of Foxp3+ thymocytes in the medulla. This might be due to CCL21 that delocalizes upon deletion of the CCL21-binding podoplanin from medullar tFRC to cortex areas. The animals do not remain devoid of nTreg but generate them delayed within the first month resulting in Th2-biased hypergammaglobulinemia but not in the death-causing autoimmune phenotype of Foxp3-deficient Scurfy mice. author: - first_name: Elke full_name: Fuertbauer, Elke last_name: Fuertbauer - first_name: Jan full_name: Zaujec, Jan last_name: Zaujec - first_name: Pavel full_name: Uhrin, Pavel last_name: Uhrin - first_name: Ingrid full_name: Raab, Ingrid last_name: Raab - first_name: Michele full_name: Weber, Michele id: 3A3FC708-F248-11E8-B48F-1D18A9856A87 last_name: Weber - first_name: Helga full_name: Schachner, Helga last_name: Schachner - first_name: Miroslav full_name: Bauer, Miroslav last_name: Bauer - first_name: Gerhard full_name: Schütz, Gerhard last_name: Schütz - first_name: Bernd full_name: Binder, Bernd last_name: Binder - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Dontscho full_name: Kerjaschki, Dontscho last_name: Kerjaschki - first_name: Hannes full_name: Stockinger, Hannes last_name: Stockinger citation: ama: Fuertbauer E, Zaujec J, Uhrin P, et al. Thymic medullar conduits-associated podoplanin promotes natural regulatory T cells. Immunology Letters. 2013;154(1-2):31-41. doi:10.1016/j.imlet.2013.07.007 apa: Fuertbauer, E., Zaujec, J., Uhrin, P., Raab, I., Weber, M., Schachner, H., … Stockinger, H. (2013). Thymic medullar conduits-associated podoplanin promotes natural regulatory T cells. Immunology Letters. Elsevier. https://doi.org/10.1016/j.imlet.2013.07.007 chicago: Fuertbauer, Elke, Jan Zaujec, Pavel Uhrin, Ingrid Raab, Michele Weber, Helga Schachner, Miroslav Bauer, et al. “Thymic Medullar Conduits-Associated Podoplanin Promotes Natural Regulatory T Cells.” Immunology Letters. Elsevier, 2013. https://doi.org/10.1016/j.imlet.2013.07.007. ieee: E. Fuertbauer et al., “Thymic medullar conduits-associated podoplanin promotes natural regulatory T cells,” Immunology Letters, vol. 154, no. 1–2. Elsevier, pp. 31–41, 2013. ista: Fuertbauer E, Zaujec J, Uhrin P, Raab I, Weber M, Schachner H, Bauer M, Schütz G, Binder B, Sixt MK, Kerjaschki D, Stockinger H. 2013. Thymic medullar conduits-associated podoplanin promotes natural regulatory T cells. Immunology Letters. 154(1–2), 31–41. mla: Fuertbauer, Elke, et al. “Thymic Medullar Conduits-Associated Podoplanin Promotes Natural Regulatory T Cells.” Immunology Letters, vol. 154, no. 1–2, Elsevier, 2013, pp. 31–41, doi:10.1016/j.imlet.2013.07.007. short: E. Fuertbauer, J. Zaujec, P. Uhrin, I. Raab, M. Weber, H. Schachner, M. Bauer, G. Schütz, B. Binder, M.K. Sixt, D. Kerjaschki, H. Stockinger, Immunology Letters 154 (2013) 31–41. date_created: 2018-12-11T11:46:57Z date_published: 2013-07-01T00:00:00Z date_updated: 2021-01-12T08:01:22Z day: '01' department: - _id: MiSi doi: 10.1016/j.imlet.2013.07.007 intvolume: ' 154' issue: 1-2 language: - iso: eng month: '07' oa_version: None page: 31 - 41 publication: Immunology Letters publication_status: published publisher: Elsevier publist_id: '7300' quality_controlled: '1' scopus_import: 1 status: public title: Thymic medullar conduits-associated podoplanin promotes natural regulatory T cells type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 154 year: '2013' ... --- _id: '10900' abstract: - lang: eng text: Leukocyte migration through the interstitial space is crucial for the maintenance of tolerance and immunity. The main cues for leukocyte trafficking are chemokines thought to directionally guide these cells towards their targets. However, model systems that facilitate quantification of chemokine-guided leukocyte migration in vivo are uncommon. Here we describe an ex vivo crawl-in assay using explanted mouse ears that allows the visualization of chemokine-dependent dendritic cell (DC) motility in the dermal interstitium in real time. We present methods for the preparation of mouse ear sheets and their use in multidimensional confocal imaging experiments to monitor and analyze the directional migration of fluorescently labelled DCs through the dermis and into afferent lymphatic vessels. The assay provides a more physiological approach to study leukocyte migration than in vitro three-dimensional (3D) or 2-dimensional (2D) migration assays such as collagen gels and transwell assays. acknowledgement: We would like to thank Alexander Eichner and Ingrid de Vries for discussion and critical reading of the manuscript, and Mary Frank for assistance with the recording of videos and images in Fig. 1. M.S. is supported through funding from the German Research Foundation (DFG). M.W. acknowledges the Alexander von Humboldt Foundation for funding. alternative_title: - Methods in Molecular Biology article_processing_charge: No author: - first_name: Michele full_name: Weber, Michele id: 3A3FC708-F248-11E8-B48F-1D18A9856A87 last_name: Weber - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Weber M, Sixt MK. Live Cell Imaging of Chemotactic Dendritic Cell Migration in Explanted Mouse Ear Preparations. In: Cardona A, Ubogu E, eds. Chemokines. Vol 1013. MIMB. Totowa, NJ: Humana Press; 2013:215-226. doi:10.1007/978-1-62703-426-5_14' apa: 'Weber, M., & Sixt, M. K. (2013). Live Cell Imaging of Chemotactic Dendritic Cell Migration in Explanted Mouse Ear Preparations. In A. Cardona & E. Ubogu (Eds.), Chemokines (Vol. 1013, pp. 215–226). Totowa, NJ: Humana Press. https://doi.org/10.1007/978-1-62703-426-5_14' chicago: 'Weber, Michele, and Michael K Sixt. “Live Cell Imaging of Chemotactic Dendritic Cell Migration in Explanted Mouse Ear Preparations.” In Chemokines, edited by Astrid Cardona and Eroboghene Ubogu, 1013:215–26. MIMB. Totowa, NJ: Humana Press, 2013. https://doi.org/10.1007/978-1-62703-426-5_14.' ieee: 'M. Weber and M. K. Sixt, “Live Cell Imaging of Chemotactic Dendritic Cell Migration in Explanted Mouse Ear Preparations,” in Chemokines, vol. 1013, A. Cardona and E. Ubogu, Eds. Totowa, NJ: Humana Press, 2013, pp. 215–226.' ista: 'Weber M, Sixt MK. 2013.Live Cell Imaging of Chemotactic Dendritic Cell Migration in Explanted Mouse Ear Preparations. In: Chemokines. Methods in Molecular Biology, vol. 1013, 215–226.' mla: Weber, Michele, and Michael K. Sixt. “Live Cell Imaging of Chemotactic Dendritic Cell Migration in Explanted Mouse Ear Preparations.” Chemokines, edited by Astrid Cardona and Eroboghene Ubogu, vol. 1013, Humana Press, 2013, pp. 215–26, doi:10.1007/978-1-62703-426-5_14. short: M. Weber, M.K. Sixt, in:, A. Cardona, E. Ubogu (Eds.), Chemokines, Humana Press, Totowa, NJ, 2013, pp. 215–226. date_created: 2022-03-21T07:47:41Z date_published: 2013-04-03T00:00:00Z date_updated: 2023-09-05T13:15:33Z day: '03' department: - _id: MiSi doi: 10.1007/978-1-62703-426-5_14 editor: - first_name: Astrid full_name: Cardona, Astrid last_name: Cardona - first_name: Eroboghene full_name: Ubogu, Eroboghene last_name: Ubogu external_id: pmid: - '23625502' intvolume: ' 1013' language: - iso: eng month: '04' oa_version: None page: 215-226 place: Totowa, NJ pmid: 1 publication: Chemokines publication_identifier: eisbn: - '9781627034265' eissn: - 1940-6029 isbn: - '9781627034258' issn: - 1064-3745 publication_status: published publisher: Humana Press quality_controlled: '1' scopus_import: '1' series_title: MIMB status: public title: Live Cell Imaging of Chemotactic Dendritic Cell Migration in Explanted Mouse Ear Preparations type: book_chapter user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 1013 year: '2013' ... --- _id: '3158' abstract: - lang: eng text: We describe here the development and characterization of a conditionally inducible mouse model expressing Lifeact-GFP, a peptide that reports the dynamics of filamentous actin. We have used this model to study platelets, megakaryocytes and melanoblasts and we provide evidence that Lifeact-GFP is a useful reporter in these cell types ex vivo. In the case of platelets and megakaryocytes, these cells are not transfectable by traditional methods, so conditional activation of Lifeact allows the study of actin dynamics in these cells live. We studied melanoblasts in native skin explants from embryos, allowing the visualization of live actin dynamics during cytokinesis and migration. Our study revealed that melanoblasts lacking the small GTPase Rac1 show a delay in the formation of new pseudopodia following cytokinesis that accounts for the previously reported cytokinesis delay in these cells. Thus, through use of this mouse model, we were able to gain insights into the actin dynamics of cells that could only previously be studied using fixed specimens or following isolation from their native tissue environment. author: - first_name: Hannah full_name: Schachtner, Hannah last_name: Schachtner - first_name: Ang full_name: Li, Ang last_name: Li - first_name: David full_name: Stevenson, David last_name: Stevenson - first_name: Simon full_name: Calaminus, Simon last_name: Calaminus - first_name: Steven full_name: Thomas, Steven last_name: Thomas - first_name: Steve full_name: Watson, Steve last_name: Watson - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Roland full_name: Wedlich Söldner, Roland last_name: Wedlich Söldner - first_name: Douglas full_name: Strathdee, Douglas last_name: Strathdee - first_name: Laura full_name: Machesky, Laura last_name: Machesky citation: ama: Schachtner H, Li A, Stevenson D, et al. Tissue inducible Lifeact expression allows visualization of actin dynamics in vivo and ex vivo. European Journal of Cell Biology. 2012;91(11-12):923-929. doi:10.1016/j.ejcb.2012.04.002 apa: Schachtner, H., Li, A., Stevenson, D., Calaminus, S., Thomas, S., Watson, S., … Machesky, L. (2012). Tissue inducible Lifeact expression allows visualization of actin dynamics in vivo and ex vivo. European Journal of Cell Biology. Elsevier. https://doi.org/10.1016/j.ejcb.2012.04.002 chicago: Schachtner, Hannah, Ang Li, David Stevenson, Simon Calaminus, Steven Thomas, Steve Watson, Michael K Sixt, Roland Wedlich Söldner, Douglas Strathdee, and Laura Machesky. “Tissue Inducible Lifeact Expression Allows Visualization of Actin Dynamics in Vivo and Ex Vivo.” European Journal of Cell Biology. Elsevier, 2012. https://doi.org/10.1016/j.ejcb.2012.04.002. ieee: H. Schachtner et al., “Tissue inducible Lifeact expression allows visualization of actin dynamics in vivo and ex vivo,” European Journal of Cell Biology, vol. 91, no. 11–12. Elsevier, pp. 923–929, 2012. ista: Schachtner H, Li A, Stevenson D, Calaminus S, Thomas S, Watson S, Sixt MK, Wedlich Söldner R, Strathdee D, Machesky L. 2012. Tissue inducible Lifeact expression allows visualization of actin dynamics in vivo and ex vivo. European Journal of Cell Biology. 91(11–12), 923–929. mla: Schachtner, Hannah, et al. “Tissue Inducible Lifeact Expression Allows Visualization of Actin Dynamics in Vivo and Ex Vivo.” European Journal of Cell Biology, vol. 91, no. 11–12, Elsevier, 2012, pp. 923–29, doi:10.1016/j.ejcb.2012.04.002. short: H. Schachtner, A. Li, D. Stevenson, S. Calaminus, S. Thomas, S. Watson, M.K. Sixt, R. Wedlich Söldner, D. Strathdee, L. Machesky, European Journal of Cell Biology 91 (2012) 923–929. date_created: 2018-12-11T12:01:44Z date_published: 2012-11-01T00:00:00Z date_updated: 2021-01-12T07:41:27Z day: '01' department: - _id: MiSi doi: 10.1016/j.ejcb.2012.04.002 external_id: pmid: - '22658956' intvolume: ' 91' issue: 11-12 language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3930012/ month: '11' oa: 1 oa_version: Submitted Version page: 923 - 929 pmid: 1 publication: European Journal of Cell Biology publication_status: published publisher: Elsevier publist_id: '3534' quality_controlled: '1' scopus_import: 1 status: public title: Tissue inducible Lifeact expression allows visualization of actin dynamics in vivo and ex vivo type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 91 year: '2012' ... --- _id: '506' article_processing_charge: No article_type: original author: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Sixt MK. Cell migration: Fibroblasts find a new way to get ahead. Journal of Cell Biology. 2012;197(3):347-349. doi:10.1083/jcb.201204039' apa: 'Sixt, M. K. (2012). Cell migration: Fibroblasts find a new way to get ahead. Journal of Cell Biology. Rockefeller University Press. https://doi.org/10.1083/jcb.201204039' chicago: 'Sixt, Michael K. “Cell Migration: Fibroblasts Find a New Way to Get Ahead.” Journal of Cell Biology. Rockefeller University Press, 2012. https://doi.org/10.1083/jcb.201204039.' ieee: 'M. K. Sixt, “Cell migration: Fibroblasts find a new way to get ahead,” Journal of Cell Biology, vol. 197, no. 3. Rockefeller University Press, pp. 347–349, 2012.' ista: 'Sixt MK. 2012. Cell migration: Fibroblasts find a new way to get ahead. Journal of Cell Biology. 197(3), 347–349.' mla: 'Sixt, Michael K. “Cell Migration: Fibroblasts Find a New Way to Get Ahead.” Journal of Cell Biology, vol. 197, no. 3, Rockefeller University Press, 2012, pp. 347–49, doi:10.1083/jcb.201204039.' short: M.K. Sixt, Journal of Cell Biology 197 (2012) 347–349. date_created: 2018-12-11T11:46:51Z date_published: 2012-04-30T00:00:00Z date_updated: 2021-01-12T08:01:11Z day: '30' ddc: - '570' department: - _id: MiSi doi: 10.1083/jcb.201204039 file: - access_level: open_access checksum: 45c02be33ebd99fc3077d60b9c90bdfa content_type: application/pdf creator: kschuh date_created: 2019-02-12T09:03:09Z date_updated: 2020-07-14T12:46:36Z file_id: '5957' file_name: 2012_CellBiology_Sixt.pdf file_size: 986566 relation: main_file file_date_updated: 2020-07-14T12:46:36Z has_accepted_license: '1' intvolume: ' 197' issue: '3' language: - iso: eng month: '04' oa: 1 oa_version: Published Version page: 347 - 349 publication: Journal of Cell Biology publication_status: published publisher: Rockefeller University Press publist_id: '7314' quality_controlled: '1' scopus_import: 1 status: public title: 'Cell migration: Fibroblasts find a new way to get ahead' tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 197 year: '2012' ... --- _id: '3371' abstract: - lang: eng text: The Minisymposium “Cell Migration and Motility” was attended by approximately 500 visitors and covered a broad range of questions in the field using diverse model systems. Topics comprised actin dynamics, cell polarity, force transduction, signal transduction, bar- rier transmigration, and chemotactic guidance. article_type: original author: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Carole full_name: Parent, Carole last_name: Parent citation: ama: Sixt MK, Parent C. Cells on the move in Philadelphia. Molecular Biology and Evolution. 2011;22(6):724. doi:10.1091/mbc.E10-12-0958 apa: Sixt, M. K., & Parent, C. (2011). Cells on the move in Philadelphia. Molecular Biology and Evolution. Oxford University Press. https://doi.org/10.1091/mbc.E10-12-0958 chicago: Sixt, Michael K, and Carole Parent. “Cells on the Move in Philadelphia.” Molecular Biology and Evolution. Oxford University Press, 2011. https://doi.org/10.1091/mbc.E10-12-0958. ieee: M. K. Sixt and C. Parent, “Cells on the move in Philadelphia,” Molecular Biology and Evolution, vol. 22, no. 6. Oxford University Press, p. 724, 2011. ista: Sixt MK, Parent C. 2011. Cells on the move in Philadelphia. Molecular Biology and Evolution. 22(6), 724. mla: Sixt, Michael K., and Carole Parent. “Cells on the Move in Philadelphia.” Molecular Biology and Evolution, vol. 22, no. 6, Oxford University Press, 2011, p. 724, doi:10.1091/mbc.E10-12-0958. short: M.K. Sixt, C. Parent, Molecular Biology and Evolution 22 (2011) 724. date_created: 2018-12-11T12:02:57Z date_published: 2011-03-15T00:00:00Z date_updated: 2021-01-12T07:43:01Z day: '15' ddc: - '570' department: - _id: MiSi doi: 10.1091/mbc.E10-12-0958 file: - access_level: open_access checksum: 3467986ab7a64e7694ffd1013b5d9da9 content_type: application/pdf creator: system date_created: 2018-12-12T10:17:29Z date_updated: 2020-07-14T12:46:11Z file_id: '5283' file_name: IST-2015-373-v1+1_Mol._Biol._Cell-2011-Sixt-724.pdf file_size: 105421 relation: main_file file_date_updated: 2020-07-14T12:46:11Z has_accepted_license: '1' intvolume: ' 22' issue: '6' language: - iso: eng month: '03' oa: 1 oa_version: Published Version page: '724' publication: Molecular Biology and Evolution publication_status: published publisher: Oxford University Press publist_id: '3238' pubrep_id: '373' quality_controlled: '1' scopus_import: 1 status: public title: Cells on the move in Philadelphia tmp: image: /images/cc_by_nc_sa.png legal_code_url: https://creativecommons.org/licenses/by-nc-sa/4.0/legalcode name: Creative Commons Attribution-NonCommercial-ShareAlike 4.0 International (CC BY-NC-SA 4.0) short: CC BY-NC-SA (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 22 year: '2011' ... --- _id: '3505' abstract: - lang: eng text: Cell migration on two-dimensional (2D) substrates follows entirely different rules than cell migration in three-dimensional (3D) environments. This is especially relevant for leukocytes that are able to migrate in the absence of adhesion receptors within the confined geometry of artificial 3D extracellular matrix scaffolds and within the interstitial space in vivo. Here, we describe in detail a simple and economical protocol to visualize dendritic cell migration in 3D collagen scaffolds along chemotactic gradients. This method can be adapted to other cell types and may serve as a physiologically relevant paradigm for the directed locomotion of most amoeboid cells. alternative_title: - Methods in Molecular Biology article_processing_charge: No article_type: original author: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Tim full_name: Lämmermann, Tim last_name: Lämmermann citation: ama: Sixt MK, Lämmermann T. In vitro analysis of chemotactic leukocyte migration in 3D environments. Cell Migration. 2011;769:149-165. doi:10.1007/978-1-61779-207-6_11 apa: Sixt, M. K., & Lämmermann, T. (2011). In vitro analysis of chemotactic leukocyte migration in 3D environments. Cell Migration. Springer. https://doi.org/10.1007/978-1-61779-207-6_11 chicago: Sixt, Michael K, and Tim Lämmermann. “In Vitro Analysis of Chemotactic Leukocyte Migration in 3D Environments.” Cell Migration. Springer, 2011. https://doi.org/10.1007/978-1-61779-207-6_11. ieee: M. K. Sixt and T. Lämmermann, “In vitro analysis of chemotactic leukocyte migration in 3D environments,” Cell Migration, vol. 769. Springer, pp. 149–165, 2011. ista: Sixt MK, Lämmermann T. 2011. In vitro analysis of chemotactic leukocyte migration in 3D environments. Cell Migration. 769, 149–165. mla: Sixt, Michael K., and Tim Lämmermann. “In Vitro Analysis of Chemotactic Leukocyte Migration in 3D Environments.” Cell Migration, vol. 769, Springer, 2011, pp. 149–65, doi:10.1007/978-1-61779-207-6_11. short: M.K. Sixt, T. Lämmermann, Cell Migration 769 (2011) 149–165. date_created: 2018-12-11T12:03:41Z date_published: 2011-05-17T00:00:00Z date_updated: 2021-01-12T07:43:55Z day: '17' department: - _id: MiSi doi: 10.1007/978-1-61779-207-6_11 intvolume: ' 769' language: - iso: eng main_file_link: - open_access: '1' url: https://pure.mpg.de/pubman/item/item_3219628_1/component/file_3219630/Sixt%20et%20al..pdf month: '05' oa: 1 oa_version: Published Version page: 149 - 165 publication: Cell Migration publication_status: published publisher: Springer publist_id: '2882' quality_controlled: '1' status: public title: In vitro analysis of chemotactic leukocyte migration in 3D environments type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 769 year: '2011' ... --- _id: '3385' article_type: review author: - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Sixt MK. Interstitial locomotion of leukocytes. Immunology Letters. 2011;138(1):32-34. doi:10.1016/j.imlet.2011.02.013 apa: Sixt, M. K. (2011). Interstitial locomotion of leukocytes. Immunology Letters. Elsevier. https://doi.org/10.1016/j.imlet.2011.02.013 chicago: Sixt, Michael K. “Interstitial Locomotion of Leukocytes.” Immunology Letters. Elsevier, 2011. https://doi.org/10.1016/j.imlet.2011.02.013. ieee: M. K. Sixt, “Interstitial locomotion of leukocytes,” Immunology Letters, vol. 138, no. 1. Elsevier, pp. 32–34, 2011. ista: Sixt MK. 2011. Interstitial locomotion of leukocytes. Immunology Letters. 138(1), 32–34. mla: Sixt, Michael K. “Interstitial Locomotion of Leukocytes.” Immunology Letters, vol. 138, no. 1, Elsevier, 2011, pp. 32–34, doi:10.1016/j.imlet.2011.02.013. short: M.K. Sixt, Immunology Letters 138 (2011) 32–34. date_created: 2018-12-11T12:03:02Z date_published: 2011-07-01T00:00:00Z date_updated: 2021-01-12T07:43:07Z day: '01' department: - _id: MiSi doi: 10.1016/j.imlet.2011.02.013 intvolume: ' 138' issue: '1' language: - iso: eng month: '07' oa_version: None page: 32 - 34 publication: Immunology Letters publication_status: published publisher: Elsevier publist_id: '3222' quality_controlled: '1' scopus_import: 1 status: public title: Interstitial locomotion of leukocytes type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 138 year: '2011' ... --- _id: '491' abstract: - lang: eng text: In their search for antigens, lymphocytes continuously shuttle among blood vessels, lymph vessels, and lymphatic tissues. Chemokines mediate entry of lymphocytes into lymphatic tissues, and sphingosine 1-phosphate (S1P) promotes localization of lymphocytes to the vasculature. Both signals are sensed through G protein-coupled receptors (GPCRs). Most GPCRs undergo ligand-dependent homologous receptor desensitization, a process that decreases their signaling output after previous exposure to high ligand concentration. Such desensitization can explain why lymphocytes do not take an intermediate position between two signals but rather oscillate between them. The desensitization of S1P receptor 1 (S1PR1) is mediated by GPCR kinase 2 (GRK2). Deletion of GRK2 in lymphocytes compromises desensitization by high vascular S1P concentrations, thereby reducing responsiveness to the chemokine signal and trapping the cells in the vascular compartment. The desensitization kinetics of S1PR1 allows lymphocytes to dynamically shuttle between vasculature and lymphatic tissue, although the positional information in both compartments is static. article_number: pe43 author: - first_name: Alexander full_name: Eichner, Alexander id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87 last_name: Eichner - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Eichner A, Sixt MK. Setting the clock for recirculating lymphocytes. Science Signaling. 2011;4(198). doi:10.1126/scisignal.2002617 apa: Eichner, A., & Sixt, M. K. (2011). Setting the clock for recirculating lymphocytes. Science Signaling. American Association for the Advancement of Science. https://doi.org/10.1126/scisignal.2002617 chicago: Eichner, Alexander, and Michael K Sixt. “Setting the Clock for Recirculating Lymphocytes.” Science Signaling. American Association for the Advancement of Science, 2011. https://doi.org/10.1126/scisignal.2002617. ieee: A. Eichner and M. K. Sixt, “Setting the clock for recirculating lymphocytes,” Science Signaling, vol. 4, no. 198. American Association for the Advancement of Science, 2011. ista: Eichner A, Sixt MK. 2011. Setting the clock for recirculating lymphocytes. Science Signaling. 4(198), pe43. mla: Eichner, Alexander, and Michael K. Sixt. “Setting the Clock for Recirculating Lymphocytes.” Science Signaling, vol. 4, no. 198, pe43, American Association for the Advancement of Science, 2011, doi:10.1126/scisignal.2002617. short: A. Eichner, M.K. Sixt, Science Signaling 4 (2011). date_created: 2018-12-11T11:46:46Z date_published: 2011-11-08T00:00:00Z date_updated: 2021-01-12T08:01:02Z day: '08' department: - _id: MiSi doi: 10.1126/scisignal.2002617 intvolume: ' 4' issue: '198' language: - iso: eng month: '11' oa_version: None publication: Science Signaling publication_status: published publisher: American Association for the Advancement of Science publist_id: '7329' quality_controlled: '1' scopus_import: 1 status: public title: Setting the clock for recirculating lymphocytes type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 4 year: '2011' ... --- _id: '518' abstract: - lang: eng text: Cancer stem cells or cancer initiating cells are believed to contribute to cancer recurrence after therapy. MicroRNAs (miRNAs) are short RNA molecules with fundamental roles in gene regulation. The role of miRNAs in cancer stem cells is only poorly understood. Here, we report miRNA expression profiles of glioblastoma stem cell-containing CD133 + cell populations. We find that miR-9, miR-9 * (referred to as miR-9/9 *), miR-17 and miR-106b are highly abundant in CD133 + cells. Furthermore, inhibition of miR-9/9 * or miR-17 leads to reduced neurosphere formation and stimulates cell differentiation. Calmodulin-binding transcription activator 1 (CAMTA1) is a putative transcription factor, which induces the expression of the anti-proliferative cardiac hormone natriuretic peptide A (NPPA). We identify CAMTA1 as an miR-9/9 * and miR-17 target. CAMTA1 expression leads to reduced neurosphere formation and tumour growth in nude mice, suggesting that CAMTA1 can function as tumour suppressor. Consistently, CAMTA1 and NPPA expression correlate with patient survival. Our findings could provide a basis for novel strategies of glioblastoma therapy. article_processing_charge: No article_type: original author: - first_name: Daniel full_name: Schraivogel, Daniel last_name: Schraivogel - first_name: Lasse full_name: Weinmann, Lasse last_name: Weinmann - first_name: Dagmar full_name: Beier, Dagmar last_name: Beier - first_name: Ghazaleh full_name: Tabatabai, Ghazaleh last_name: Tabatabai - first_name: Alexander full_name: Eichner, Alexander id: 4DFA52AE-F248-11E8-B48F-1D18A9856A87 last_name: Eichner - first_name: Jia full_name: Zhu, Jia last_name: Zhu - first_name: Martina full_name: Anton, Martina last_name: Anton - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Michael full_name: Weller, Michael last_name: Weller - first_name: Christoph full_name: Beier, Christoph last_name: Beier - first_name: Gunter full_name: Meister, Gunter last_name: Meister citation: ama: Schraivogel D, Weinmann L, Beier D, et al. CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma stem cells. EMBO Journal. 2011;30(20):4309-4322. doi:10.1038/emboj.2011.301 apa: Schraivogel, D., Weinmann, L., Beier, D., Tabatabai, G., Eichner, A., Zhu, J., … Meister, G. (2011). CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma stem cells. EMBO Journal. Wiley-Blackwell. https://doi.org/10.1038/emboj.2011.301 chicago: Schraivogel, Daniel, Lasse Weinmann, Dagmar Beier, Ghazaleh Tabatabai, Alexander Eichner, Jia Zhu, Martina Anton, et al. “CAMTA1 Is a Novel Tumour Suppressor Regulated by MiR-9/9 * in Glioblastoma Stem Cells.” EMBO Journal. Wiley-Blackwell, 2011. https://doi.org/10.1038/emboj.2011.301. ieee: D. Schraivogel et al., “CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma stem cells,” EMBO Journal, vol. 30, no. 20. Wiley-Blackwell, pp. 4309–4322, 2011. ista: Schraivogel D, Weinmann L, Beier D, Tabatabai G, Eichner A, Zhu J, Anton M, Sixt MK, Weller M, Beier C, Meister G. 2011. CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma stem cells. EMBO Journal. 30(20), 4309–4322. mla: Schraivogel, Daniel, et al. “CAMTA1 Is a Novel Tumour Suppressor Regulated by MiR-9/9 * in Glioblastoma Stem Cells.” EMBO Journal, vol. 30, no. 20, Wiley-Blackwell, 2011, pp. 4309–22, doi:10.1038/emboj.2011.301. short: D. Schraivogel, L. Weinmann, D. Beier, G. Tabatabai, A. Eichner, J. Zhu, M. Anton, M.K. Sixt, M. Weller, C. Beier, G. Meister, EMBO Journal 30 (2011) 4309–4322. date_created: 2018-12-11T11:46:55Z date_published: 2011-10-19T00:00:00Z date_updated: 2021-01-12T08:01:19Z day: '19' department: - _id: MiSi doi: 10.1038/emboj.2011.301 external_id: pmid: - '21857646' intvolume: ' 30' issue: '20' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC3199389/ month: '10' oa: 1 oa_version: Submitted Version page: 4309 - 4322 pmid: 1 publication: EMBO Journal publication_status: published publisher: Wiley-Blackwell publist_id: '7301' quality_controlled: '1' scopus_import: 1 status: public title: CAMTA1 is a novel tumour suppressor regulated by miR-9/9 * in glioblastoma stem cells type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 30 year: '2011' ... --- _id: '3392' abstract: - lang: eng text: Migrating lymphocytes acquire a polarized phenotype with a leading and a trailing edge, or uropod. Although in vitro experiments in cell lines or activated primary cell cultures have established that Rho-p160 coiled-coil kinase (ROCK)-myosin II-mediated uropod contractility is required for integrin de-adhesion on two-dimensional surfaces and nuclear propulsion through narrow pores in three-dimensional matrices, less is known about the role of these two events during the recirculation of primary, nonactivated lymphocytes. Using pharmacological antagonists of ROCK and myosin II, we report that inhibition of uropod contractility blocked integrin-independent mouse T cell migration through narrow, but not large, pores in vitro. T cell crawling on chemokine-coated endothelial cells under shear was severely impaired by ROCK inhibition, whereas transendothelial migration was only reduced through endothelial cells with high, but not low, barrier properties. Using three-dimensional thick-tissue imaging and dynamic two-photon microscopy of T cell motility in lymphoid tissue, we demonstrated a significant role for uropod contractility in intraluminal crawling and transendothelial migration through lymph node, but not bone marrow, endothelial cells. Finally, we demonstrated that ICAM-1, but not anatomical constraints or integrin-independent interactions, reduced parenchymal motility of inhibitor-treated T cells within the dense lymphoid microenvironment, thus assigning context-dependent roles for uropod contraction during lymphocyte recirculation. article_processing_charge: No article_type: original author: - first_name: Silvia full_name: Soriano, Silvia last_name: Soriano - first_name: Miroslav full_name: Hons, Miroslav last_name: Hons orcid: 0000-0002-6625-3348 - first_name: Kathrin full_name: Schumann, Kathrin last_name: Schumann - first_name: Varsha full_name: Kumar, Varsha last_name: Kumar - first_name: Timo full_name: Dennier, Timo last_name: Dennier - first_name: Ruth full_name: Lyck, Ruth last_name: Lyck - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Jens full_name: Stein, Jens last_name: Stein citation: ama: Soriano S, Hons M, Schumann K, et al. In vivo analysis of uropod function during physiological T cell trafficking. Journal of Immunology. 2011;187(5):2356-2364. doi:10.4049/jimmunol.1100935 apa: Soriano, S., Hons, M., Schumann, K., Kumar, V., Dennier, T., Lyck, R., … Stein, J. (2011). In vivo analysis of uropod function during physiological T cell trafficking. Journal of Immunology. American Association of Immunologists. https://doi.org/10.4049/jimmunol.1100935 chicago: Soriano, Silvia, Miroslav Hons, Kathrin Schumann, Varsha Kumar, Timo Dennier, Ruth Lyck, Michael K Sixt, and Jens Stein. “In Vivo Analysis of Uropod Function during Physiological T Cell Trafficking.” Journal of Immunology. American Association of Immunologists, 2011. https://doi.org/10.4049/jimmunol.1100935. ieee: S. Soriano et al., “In vivo analysis of uropod function during physiological T cell trafficking,” Journal of Immunology, vol. 187, no. 5. American Association of Immunologists, pp. 2356–2364, 2011. ista: Soriano S, Hons M, Schumann K, Kumar V, Dennier T, Lyck R, Sixt MK, Stein J. 2011. In vivo analysis of uropod function during physiological T cell trafficking. Journal of Immunology. 187(5), 2356–2364. mla: Soriano, Silvia, et al. “In Vivo Analysis of Uropod Function during Physiological T Cell Trafficking.” Journal of Immunology, vol. 187, no. 5, American Association of Immunologists, 2011, pp. 2356–64, doi:10.4049/jimmunol.1100935. short: S. Soriano, M. Hons, K. Schumann, V. Kumar, T. Dennier, R. Lyck, M.K. Sixt, J. Stein, Journal of Immunology 187 (2011) 2356–2364. date_created: 2018-12-11T12:03:04Z date_published: 2011-09-01T00:00:00Z date_updated: 2023-10-10T13:14:59Z day: '01' department: - _id: MiSi doi: 10.4049/jimmunol.1100935 intvolume: ' 187' issue: '5' language: - iso: eng month: '09' oa_version: None page: 2356 - 2364 publication: Journal of Immunology publication_identifier: eissn: - 1550-6606 issn: - 0022-1767 publication_status: published publisher: American Association of Immunologists publist_id: '3215' quality_controlled: '1' scopus_import: '1' status: public title: In vivo analysis of uropod function during physiological T cell trafficking type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 187 year: '2011' ... --- _id: '3959' abstract: - lang: eng text: Chemokines orchestrate immune cell trafficking by eliciting either directed or random migration and by activating integrins in order to induce cell adhesion. Analyzing dendritic cell (DC) migration, we showed that these distinct cellular responses depended on the mode of chemokine presentation within tissues. The surface-immobilized form of the chemokine CCL21, the heparan sulfate-anchoring ligand of the CC-chemokine receptor 7 (CCR7), caused random movement of DCs that was confined to the chemokine-presenting surface because it triggered integrin-mediated adhesion. Upon direct contact with CCL21, DCs truncated the anchoring residues of CCL21, thereby releasing it from the solid phase. Soluble CCL21 functionally resembles the second CCR7 ligand, CCL19, which lacks anchoring residues and forms soluble gradients. Both soluble CCR7 ligands triggered chemotactic movement, but not surface adhesion. Adhesive random migration and directional steering cooperate to produce dynamic but spatially restricted locomotion patterns closely resembling the cellular dynamics observed in secondary lymphoid organs. author: - first_name: Kathrin full_name: Schumann, Kathrin id: F44D762E-4F9D-11E9-B64C-9EB26CEFFB5F last_name: Schumann - first_name: Tim full_name: Lämmermann, Tim last_name: Lämmermann - first_name: Markus full_name: Bruckner, Markus last_name: Bruckner - first_name: Daniel full_name: Legler, Daniel last_name: Legler - first_name: Julien full_name: Polleux, Julien last_name: Polleux - first_name: Joachim full_name: Spatz, Joachim last_name: Spatz - first_name: Gerold full_name: Schuler, Gerold last_name: Schuler - first_name: Reinhold full_name: Förster, Reinhold last_name: Förster - first_name: Manfred full_name: Lutz, Manfred last_name: Lutz - first_name: Lydia full_name: Sorokin, Lydia last_name: Sorokin - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Schumann K, Lämmermann T, Bruckner M, et al. Immobilized chemokine fields and soluble chemokine gradients cooperatively shape migration patterns of dendritic cells. Immunity. 2010;32(5):703-713. doi:10.1016/j.immuni.2010.04.017 apa: Schumann, K., Lämmermann, T., Bruckner, M., Legler, D., Polleux, J., Spatz, J., … Sixt, M. K. (2010). Immobilized chemokine fields and soluble chemokine gradients cooperatively shape migration patterns of dendritic cells. Immunity. Cell Press. https://doi.org/10.1016/j.immuni.2010.04.017 chicago: Schumann, Kathrin, Tim Lämmermann, Markus Bruckner, Daniel Legler, Julien Polleux, Joachim Spatz, Gerold Schuler, et al. “Immobilized Chemokine Fields and Soluble Chemokine Gradients Cooperatively Shape Migration Patterns of Dendritic Cells.” Immunity. Cell Press, 2010. https://doi.org/10.1016/j.immuni.2010.04.017. ieee: K. Schumann et al., “Immobilized chemokine fields and soluble chemokine gradients cooperatively shape migration patterns of dendritic cells,” Immunity, vol. 32, no. 5. Cell Press, pp. 703–713, 2010. ista: Schumann K, Lämmermann T, Bruckner M, Legler D, Polleux J, Spatz J, Schuler G, Förster R, Lutz M, Sorokin L, Sixt MK. 2010. Immobilized chemokine fields and soluble chemokine gradients cooperatively shape migration patterns of dendritic cells. Immunity. 32(5), 703–713. mla: Schumann, Kathrin, et al. “Immobilized Chemokine Fields and Soluble Chemokine Gradients Cooperatively Shape Migration Patterns of Dendritic Cells.” Immunity, vol. 32, no. 5, Cell Press, 2010, pp. 703–13, doi:10.1016/j.immuni.2010.04.017. short: K. Schumann, T. Lämmermann, M. Bruckner, D. Legler, J. Polleux, J. Spatz, G. Schuler, R. Förster, M. Lutz, L. Sorokin, M.K. Sixt, Immunity 32 (2010) 703–713. date_created: 2018-12-11T12:06:07Z date_published: 2010-05-28T00:00:00Z date_updated: 2021-01-12T07:53:29Z day: '28' doi: 10.1016/j.immuni.2010.04.017 extern: '1' intvolume: ' 32' issue: '5' language: - iso: eng month: '05' oa_version: None page: 703 - 713 publication: Immunity publication_status: published publisher: Cell Press publist_id: '2168' status: public title: Immobilized chemokine fields and soluble chemokine gradients cooperatively shape migration patterns of dendritic cells type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 32 year: '2010' ... --- _id: '3958' abstract: - lang: eng text: Extracellular matrix (ECM) proteins can modify immune reactions, e.g. by sequestering or displaying growth factors and by interacting with immune and glial cells. Here we quantified by quantitative polymerase chain reaction (qPCR) expression of 50 ECM components and 34 ECM degrading enzymes in multiple sclerosis (MS) active and inactive white matter lesions. COL1A1, COL3A1, COL5A1 and COL5A2 chains were induced strongly in active lesions and even more in inactive lesions. These chains interact to form collagen types I, III and V, which are fibrillar collagens. Biglycan and decorin, which can decorate fibrillar collagens, were also induced strongly. The fibrillar collagens, biglycan and decorin were largely found between the endothelium and astrocytic glia limitans in the perivascular space where they formed a meshwork which was closely associated with infiltrating immune cells. In active lesions collagen V was also seen in the heavily infiltrated parenchyma. Fibrillar collagens I and III inhibited in vitro human monocyte production of CCL2 (MCP-1), an inflammatory chemokine involved in recruitment of immune cells. Together, ECM changes in lesions with different activities were quantified and proteins forming a perivascular fibrosis were identified. Induced fibrillar collagens may contribute to limiting enlargement of MS lesions by inhibiting the production of CCL2 by monocytes. author: - first_name: Hema full_name: Mohan, Hema last_name: Mohan - first_name: Markus full_name: Krumbholz, Markus last_name: Krumbholz - first_name: Rakhi full_name: Sharma, Rakhi last_name: Sharma - first_name: Sylvia full_name: Eisele, Sylvia last_name: Eisele - first_name: Andreas full_name: Junker, Andreas last_name: Junker - first_name: Michael K full_name: Michael Sixt id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Jia full_name: Newcombe, Jia last_name: Newcombe - first_name: Hartmut full_name: Wekerle, Hartmut last_name: Wekerle - first_name: Reinhard full_name: Hohlfeld, Reinhard last_name: Hohlfeld - first_name: Hans full_name: Lassmann, Hans last_name: Lassmann - first_name: Edgar full_name: Meinl, Edgar last_name: Meinl citation: ama: 'Mohan H, Krumbholz M, Sharma R, et al. Extracellular matrix in multiple sclerosis lesions: fibrillar collagens, biglycan and decorin are upregulated and associated with infiltrating immune cells. Brain Pathology. 2010;20(5):966-975. doi:10.1111/j.1750-3639.2010.00399.x' apa: 'Mohan, H., Krumbholz, M., Sharma, R., Eisele, S., Junker, A., Sixt, M. K., … Meinl, E. (2010). Extracellular matrix in multiple sclerosis lesions: fibrillar collagens, biglycan and decorin are upregulated and associated with infiltrating immune cells. Brain Pathology. Wiley-Blackwell. https://doi.org/10.1111/j.1750-3639.2010.00399.x' chicago: 'Mohan, Hema, Markus Krumbholz, Rakhi Sharma, Sylvia Eisele, Andreas Junker, Michael K Sixt, Jia Newcombe, et al. “Extracellular Matrix in Multiple Sclerosis Lesions: Fibrillar Collagens, Biglycan and Decorin Are Upregulated and Associated with Infiltrating Immune Cells.” Brain Pathology. Wiley-Blackwell, 2010. https://doi.org/10.1111/j.1750-3639.2010.00399.x.' ieee: 'H. Mohan et al., “Extracellular matrix in multiple sclerosis lesions: fibrillar collagens, biglycan and decorin are upregulated and associated with infiltrating immune cells,” Brain Pathology, vol. 20, no. 5. Wiley-Blackwell, pp. 966–975, 2010.' ista: 'Mohan H, Krumbholz M, Sharma R, Eisele S, Junker A, Sixt MK, Newcombe J, Wekerle H, Hohlfeld R, Lassmann H, Meinl E. 2010. Extracellular matrix in multiple sclerosis lesions: fibrillar collagens, biglycan and decorin are upregulated and associated with infiltrating immune cells. Brain Pathology. 20(5), 966–975.' mla: 'Mohan, Hema, et al. “Extracellular Matrix in Multiple Sclerosis Lesions: Fibrillar Collagens, Biglycan and Decorin Are Upregulated and Associated with Infiltrating Immune Cells.” Brain Pathology, vol. 20, no. 5, Wiley-Blackwell, 2010, pp. 966–75, doi:10.1111/j.1750-3639.2010.00399.x.' short: H. Mohan, M. Krumbholz, R. Sharma, S. Eisele, A. Junker, M.K. Sixt, J. Newcombe, H. Wekerle, R. Hohlfeld, H. Lassmann, E. Meinl, Brain Pathology 20 (2010) 966–975. date_created: 2018-12-11T12:06:07Z date_published: 2010-09-01T00:00:00Z date_updated: 2021-01-12T07:53:28Z day: '01' doi: 10.1111/j.1750-3639.2010.00399.x extern: 1 intvolume: ' 20' issue: '5' month: '09' page: 966 - 975 publication: Brain Pathology publication_status: published publisher: Wiley-Blackwell publist_id: '2169' quality_controlled: 0 status: public title: 'Extracellular matrix in multiple sclerosis lesions: fibrillar collagens, biglycan and decorin are upregulated and associated with infiltrating immune cells' type: journal_article volume: 20 year: '2010' ... --- _id: '3961' abstract: - lang: eng text: For innate and adaptive immune responses it is essential that inflammatory cells use quick and flexible locomotion strategies. Accordingly, most leukocytes can efficiently infiltrate and traverse almost every physiological or artificial environment. Here, we review how leukocytes might achieve this task mechanistically, and summarize recent findings on the principles of cytoskeletal force generation and transduction at the leading edge of leukocytes. We propose a model in which the cells switch between adhesion-receptor-mediated force transmission and locomotion modes that are based on cellular deformations, but independent of adhesion receptors. This plasticity in migration strategies allows leukocytes to adapt to the geometry and molecular composition of their environment. acknowledgement: We are grateful to Michele Weber for critical comments on the manuscript. Work in the laboratory of M.S. is supported by the German Research Foundation, the Peter Hans Hofschneider Foundation for Experimental Biomedicine and the Max Planck Society. J.R. is supported by a PhD fellowship of the Böhringer Ingelheim Fond. We thank Reinhard Fässler and Stefan Jentsch for their continuous support. author: - first_name: Jörg full_name: Jörg Renkawitz id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Michael K full_name: Michael Sixt id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Renkawitz J, Sixt MK. Mechanisms of force generation and force transmission during interstitial leukocyte migration. EMBO Reports. 2010;11(10):744-750. doi:10.1038/embor.2010.147 apa: Renkawitz, J., & Sixt, M. K. (2010). Mechanisms of force generation and force transmission during interstitial leukocyte migration. EMBO Reports. Wiley-Blackwell. https://doi.org/10.1038/embor.2010.147 chicago: Renkawitz, Jörg, and Michael K Sixt. “Mechanisms of Force Generation and Force Transmission during Interstitial Leukocyte Migration.” EMBO Reports. Wiley-Blackwell, 2010. https://doi.org/10.1038/embor.2010.147. ieee: J. Renkawitz and M. K. Sixt, “Mechanisms of force generation and force transmission during interstitial leukocyte migration,” EMBO Reports, vol. 11, no. 10. Wiley-Blackwell, pp. 744–750, 2010. ista: Renkawitz J, Sixt MK. 2010. Mechanisms of force generation and force transmission during interstitial leukocyte migration. EMBO Reports. 11(10), 744–750. mla: Renkawitz, Jörg, and Michael K. Sixt. “Mechanisms of Force Generation and Force Transmission during Interstitial Leukocyte Migration.” EMBO Reports, vol. 11, no. 10, Wiley-Blackwell, 2010, pp. 744–50, doi:10.1038/embor.2010.147. short: J. Renkawitz, M.K. Sixt, EMBO Reports 11 (2010) 744–750. date_created: 2018-12-11T12:06:08Z date_published: 2010-09-24T00:00:00Z date_updated: 2021-01-12T07:53:30Z day: '24' doi: 10.1038/embor.2010.147 extern: 1 intvolume: ' 11' issue: '10' month: '09' page: 744 - 750 publication: EMBO Reports publication_status: published publisher: Wiley-Blackwell publist_id: '2166' quality_controlled: 0 status: public title: Mechanisms of force generation and force transmission during interstitial leukocyte migration type: journal_article volume: 11 year: '2010' ... --- _id: '3960' abstract: - lang: eng text: When lymphocytes follow chemotactic cues, they can adopt different migratory modes depending on the geometry and molecular composition of their extracellular environment. In this issue of The EMBO Journal, Klemke et al (2010) describe a novel Ras-dependent chemokine receptor signalling pathway that leads to activation of cofilin, which in turn amplifies actin turnover. This signalling module is exclusively required for lymphocyte migration in three-dimensional (3D) environments, but not for locomotion on two-dimensional (2D) surfaces. author: - first_name: Michele full_name: Michele Weber id: 3A3FC708-F248-11E8-B48F-1D18A9856A87 last_name: Weber - first_name: Michael K full_name: Michael Sixt id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Weber M, Sixt MK. MEK signalling tunes actin treadmilling for interstitial lymphocyte migration. EMBO Journal. 2010;29(17):2861-2863. doi:10.1038/emboj.2010.183 apa: Weber, M., & Sixt, M. K. (2010). MEK signalling tunes actin treadmilling for interstitial lymphocyte migration. EMBO Journal. Wiley-Blackwell. https://doi.org/10.1038/emboj.2010.183 chicago: Weber, Michele, and Michael K Sixt. “MEK Signalling Tunes Actin Treadmilling for Interstitial Lymphocyte Migration.” EMBO Journal. Wiley-Blackwell, 2010. https://doi.org/10.1038/emboj.2010.183. ieee: M. Weber and M. K. Sixt, “MEK signalling tunes actin treadmilling for interstitial lymphocyte migration,” EMBO Journal, vol. 29, no. 17. Wiley-Blackwell, pp. 2861–2863, 2010. ista: Weber M, Sixt MK. 2010. MEK signalling tunes actin treadmilling for interstitial lymphocyte migration. EMBO Journal. 29(17), 2861–2863. mla: Weber, Michele, and Michael K. Sixt. “MEK Signalling Tunes Actin Treadmilling for Interstitial Lymphocyte Migration.” EMBO Journal, vol. 29, no. 17, Wiley-Blackwell, 2010, pp. 2861–63, doi:10.1038/emboj.2010.183. short: M. Weber, M.K. Sixt, EMBO Journal 29 (2010) 2861–2863. date_created: 2018-12-11T12:06:07Z date_published: 2010-09-01T00:00:00Z date_updated: 2021-01-12T07:53:29Z day: '01' doi: 10.1038/emboj.2010.183 extern: 1 intvolume: ' 29' issue: '17' main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/issues/190105/ month: '09' oa: 1 page: 2861 - 2863 publication: EMBO Journal publication_status: published publisher: Wiley-Blackwell publist_id: '2167' quality_controlled: 0 status: public title: MEK signalling tunes actin treadmilling for interstitial lymphocyte migration type: journal_article volume: 29 year: '2010' ... --- _id: '3957' author: - first_name: Julia full_name: Riedl, Julia last_name: Riedl - first_name: Kevin full_name: Flynn, Kevin C last_name: Flynn - first_name: Aurelia full_name: Raducanu, Aurelia last_name: Raducanu - first_name: Florian R full_name: Florian Gärtner id: 397A88EE-F248-11E8-B48F-1D18A9856A87 last_name: Gärtner orcid: 0000-0001-6120-3723 - first_name: Gisela full_name: Beck, Gisela last_name: Beck - first_name: Michael full_name: Bosl, Michael last_name: Bosl - first_name: Frank full_name: Bradke, Frank last_name: Bradke - first_name: Steffen full_name: Massberg, Steffen last_name: Massberg - first_name: Attila full_name: Aszodi, Attila last_name: Aszodi - first_name: Michael K full_name: Michael Sixt id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Roland full_name: Wedlich-Söldner, Roland last_name: Wedlich Söldner citation: ama: Riedl J, Flynn K, Raducanu A, et al. Lifeact mice for studying F-actin dynamics. Nature Methods. 2010;7(3):168-169. doi:10.1038/nmeth0310-168 apa: Riedl, J., Flynn, K., Raducanu, A., Gärtner, F. R., Beck, G., Bosl, M., … Wedlich Söldner, R. (2010). Lifeact mice for studying F-actin dynamics. Nature Methods. Nature Publishing Group. https://doi.org/10.1038/nmeth0310-168 chicago: Riedl, Julia, Kevin Flynn, Aurelia Raducanu, Florian R Gärtner, Gisela Beck, Michael Bosl, Frank Bradke, et al. “Lifeact Mice for Studying F-Actin Dynamics.” Nature Methods. Nature Publishing Group, 2010. https://doi.org/10.1038/nmeth0310-168. ieee: J. Riedl et al., “Lifeact mice for studying F-actin dynamics,” Nature Methods, vol. 7, no. 3. Nature Publishing Group, pp. 168–169, 2010. ista: Riedl J, Flynn K, Raducanu A, Gärtner FR, Beck G, Bosl M, Bradke F, Massberg S, Aszodi A, Sixt MK, Wedlich Söldner R. 2010. Lifeact mice for studying F-actin dynamics. Nature Methods. 7(3), 168–169. mla: Riedl, Julia, et al. “Lifeact Mice for Studying F-Actin Dynamics.” Nature Methods, vol. 7, no. 3, Nature Publishing Group, 2010, pp. 168–69, doi:10.1038/nmeth0310-168. short: J. Riedl, K. Flynn, A. Raducanu, F.R. Gärtner, G. Beck, M. Bosl, F. Bradke, S. Massberg, A. Aszodi, M.K. Sixt, R. Wedlich Söldner, Nature Methods 7 (2010) 168–169. date_created: 2018-12-11T12:06:06Z date_published: 2010-03-01T00:00:00Z date_updated: 2021-01-12T07:53:28Z day: '01' doi: 10.1038/nmeth0310-168 extern: 1 intvolume: ' 7' issue: '3' month: '03' page: 168 - 169 publication: Nature Methods publication_status: published publisher: Nature Publishing Group publist_id: '2171' quality_controlled: 0 status: public title: Lifeact mice for studying F-actin dynamics type: journal_article volume: 7 year: '2010' ... --- _id: '3956' abstract: - lang: eng text: The shuttling of leukocytes between the bloodstream and interstitial tissues involves different locomotion strategies that are governed by locally presented soluble and cell-bound signals. Recent studies have furthered our understanding of the rapidly advancing field of leukocyte migration, particularly regarding cellular and subcellular events at the level of the venular wall. Furthermore, emerging cellular models are now addressing the transition from an adherent mode to a non-adherent state, incorporating mechanisms that support an efficient migratory profile of leukocytes in the interstitial tissue beyond the venular wall. author: - first_name: Sussan full_name: Nourshargh, Sussan last_name: Nourshargh - first_name: Peter full_name: Hordijk, Peter L last_name: Hordijk - first_name: Michael K full_name: Michael Sixt id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: 'Nourshargh S, Hordijk P, Sixt MK. Breaching multiple barriers: leukocyte motility through venular walls and the interstitium. Nature Reviews Molecular Cell Biology. 2010;11(5):366-378. doi:10.1038/nrm2889' apa: 'Nourshargh, S., Hordijk, P., & Sixt, M. K. (2010). Breaching multiple barriers: leukocyte motility through venular walls and the interstitium. Nature Reviews Molecular Cell Biology. Nature Publishing Group. https://doi.org/10.1038/nrm2889' chicago: 'Nourshargh, Sussan, Peter Hordijk, and Michael K Sixt. “Breaching Multiple Barriers: Leukocyte Motility through Venular Walls and the Interstitium.” Nature Reviews Molecular Cell Biology. Nature Publishing Group, 2010. https://doi.org/10.1038/nrm2889.' ieee: 'S. Nourshargh, P. Hordijk, and M. K. Sixt, “Breaching multiple barriers: leukocyte motility through venular walls and the interstitium,” Nature Reviews Molecular Cell Biology, vol. 11, no. 5. Nature Publishing Group, pp. 366–378, 2010.' ista: 'Nourshargh S, Hordijk P, Sixt MK. 2010. Breaching multiple barriers: leukocyte motility through venular walls and the interstitium. Nature Reviews Molecular Cell Biology. 11(5), 366–378.' mla: 'Nourshargh, Sussan, et al. “Breaching Multiple Barriers: Leukocyte Motility through Venular Walls and the Interstitium.” Nature Reviews Molecular Cell Biology, vol. 11, no. 5, Nature Publishing Group, 2010, pp. 366–78, doi:10.1038/nrm2889.' short: S. Nourshargh, P. Hordijk, M.K. Sixt, Nature Reviews Molecular Cell Biology 11 (2010) 366–378. date_created: 2018-12-11T12:06:06Z date_published: 2010-05-01T00:00:00Z date_updated: 2021-01-12T07:53:27Z day: '01' doi: 10.1038/nrm2889 extern: 1 intvolume: ' 11' issue: '5' month: '05' page: 366 - 378 publication: Nature Reviews Molecular Cell Biology publication_status: published publisher: Nature Publishing Group publist_id: '2170' quality_controlled: 0 status: public title: 'Breaching multiple barriers: leukocyte motility through venular walls and the interstitium' type: journal_article volume: 11 year: '2010' ... --- _id: '3946' abstract: - lang: eng text: We compare anti-parasite defences at the level of multicellular organisms and insect societies, and find that selection by parasites at these two organisational levels is often very similar and has created a number of parallel evolutionary solutions in the host's immune response. The defence mechanisms of both individuals and insect colonies start with border defences to prevent parasite intake and are followed by soma defences that prevent the establishment and spread of the parasite between the body's cells or the social insect workers. Lastly, germ line defences are employed to inhibit infection of the reproductive tissue of organisms or the reproductive individuals in colonies. We further find sophisticated self/non-self-recognition systems operating at both levels, which appear to be vital in maintaining the integrity of the body or colony as a reproductive entity. We then expand on the regulation of immune responses and end with a contemplation of how evolution may shape the different immune components, both within and between levels. The aim of this review is to highlight common evolutionary principles acting in disease defence at the level of both individual organisms and societies, thereby linking the fields of physiological and ecological immunology. author: - first_name: Sylvia full_name: Cremer, Sylvia id: 2F64EC8C-F248-11E8-B48F-1D18A9856A87 last_name: Cremer orcid: 0000-0002-2193-3868 - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Cremer S, Sixt MK. Analogies in the evolution of individual and social immunity. Philosophical Transactions of the Royal Society of London Series B, Biological Sciences. 2009;364(1513):129-142. doi:10.1098/rstb.2008.0166 apa: Cremer, S., & Sixt, M. K. (2009). Analogies in the evolution of individual and social immunity. Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. Royal Society, The. https://doi.org/10.1098/rstb.2008.0166 chicago: Cremer, Sylvia, and Michael K Sixt. “Analogies in the Evolution of Individual and Social Immunity.” Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. Royal Society, The, 2009. https://doi.org/10.1098/rstb.2008.0166. ieee: S. Cremer and M. K. Sixt, “Analogies in the evolution of individual and social immunity,” Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences, vol. 364, no. 1513. Royal Society, The, pp. 129–142, 2009. ista: Cremer S, Sixt MK. 2009. Analogies in the evolution of individual and social immunity. Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences. 364(1513), 129–142. mla: Cremer, Sylvia, and Michael K. Sixt. “Analogies in the Evolution of Individual and Social Immunity.” Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences, vol. 364, no. 1513, Royal Society, The, 2009, pp. 129–42, doi:10.1098/rstb.2008.0166. short: S. Cremer, M.K. Sixt, Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences 364 (2009) 129–142. date_created: 2018-12-11T12:06:02Z date_published: 2009-01-12T00:00:00Z date_updated: 2021-01-12T07:53:23Z day: '12' doi: 10.1098/rstb.2008.0166 extern: '1' intvolume: ' 364' issue: '1513' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2666697/ month: '01' oa: 1 oa_version: None page: 129 - 142 publication: Philosophical Transactions of the Royal Society of London. Series B, Biological Sciences publication_status: published publisher: Royal Society, The publist_id: '2181' status: public title: Analogies in the evolution of individual and social immunity type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 364 year: '2009' ... --- _id: '3947' abstract: - lang: eng text: Mature dendritic cells (DCs) moving from the skin to the lymph node are a prototypic example of rapidly migrating amoeboid leukocytes. Interstitial DC migration is directionally guided by chemokines, but independent of specific adhesive interactions with the tissue as well as pericellular proteolysis. Instead, the protrusive flow of the actin cytoskeleton directly drives a basal mode of locomotion that is occasionally supported by actomyosin contractions at the trailing edge to propel the cell's rigid nucleus. We here delete the small GTPase Cdc42 in DCs and find that actin flow and actomyosin contraction are still initiated in response to chemotactic cues. Accordingly, the cells are able to polarize and form protrusions. However, in the absence of Cdc42 the protrusions are temporally and spatially dysregulated, which leads to impaired leading edge coordination. Although this defect still allows the cells to move on 2-dimensional surfaces, their in vivo motility is completely abrogated. We show that this difference is entirely caused by the geometric complexity of the environment, as multiple competing protrusions lead to instantaneous entanglement within 3-dimensional extracellular matrix scaffolds. This demonstrates that the decisive factor for migrating DCs is not specific interaction with the extracellular environment, but adequate coordination of cytoskeletal flow. acknowledgement: |- We thank Sylvia Cremer for help with statistics and critical reading of the paper and Reinhard Fässler for continuous support. This work was supported by the German Research Foundation (Bonn, Germany), the Peter Hans Hofschneider Foundation for Experimental Biomedicine (Zürich, Switzerland), and the Max Planck Society (Munich, Germany). author: - first_name: Tim full_name: Lämmermann, Tim last_name: Lämmermann - first_name: Jörg full_name: Jörg Renkawitz id: 3F0587C8-F248-11E8-B48F-1D18A9856A87 last_name: Renkawitz orcid: 0000-0003-2856-3369 - first_name: Xunwei full_name: Wu, Xunwei last_name: Wu - first_name: Karin full_name: Hirsch, Karin last_name: Hirsch - first_name: Cord full_name: Brakebusch, Cord last_name: Brakebusch - first_name: Michael K full_name: Michael Sixt id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 citation: ama: Lämmermann T, Renkawitz J, Wu X, Hirsch K, Brakebusch C, Sixt MK. Cdc42-dependent leading edge coordination is essential for interstitial dendritic cell migration (Plenary Paper). Blood. 2009;113(23):5703-5710. doi:10.1182/blood-2008-11-191882 apa: Lämmermann, T., Renkawitz, J., Wu, X., Hirsch, K., Brakebusch, C., & Sixt, M. K. (2009). Cdc42-dependent leading edge coordination is essential for interstitial dendritic cell migration (Plenary Paper). Blood. American Society of Hematology. https://doi.org/10.1182/blood-2008-11-191882 chicago: Lämmermann, Tim, Jörg Renkawitz, Xunwei Wu, Karin Hirsch, Cord Brakebusch, and Michael K Sixt. “Cdc42-Dependent Leading Edge Coordination Is Essential for Interstitial Dendritic Cell Migration (Plenary Paper).” Blood. American Society of Hematology, 2009. https://doi.org/10.1182/blood-2008-11-191882. ieee: T. Lämmermann, J. Renkawitz, X. Wu, K. Hirsch, C. Brakebusch, and M. K. Sixt, “Cdc42-dependent leading edge coordination is essential for interstitial dendritic cell migration (Plenary Paper),” Blood, vol. 113, no. 23. American Society of Hematology, pp. 5703–5710, 2009. ista: Lämmermann T, Renkawitz J, Wu X, Hirsch K, Brakebusch C, Sixt MK. 2009. Cdc42-dependent leading edge coordination is essential for interstitial dendritic cell migration (Plenary Paper). Blood. 113(23), 5703–5710. mla: Lämmermann, Tim, et al. “Cdc42-Dependent Leading Edge Coordination Is Essential for Interstitial Dendritic Cell Migration (Plenary Paper).” Blood, vol. 113, no. 23, American Society of Hematology, 2009, pp. 5703–10, doi:10.1182/blood-2008-11-191882. short: T. Lämmermann, J. Renkawitz, X. Wu, K. Hirsch, C. Brakebusch, M.K. Sixt, Blood 113 (2009) 5703–5710. date_created: 2018-12-11T12:06:03Z date_published: 2009-06-04T00:00:00Z date_updated: 2021-01-12T07:53:23Z day: '04' doi: 10.1182/blood-2008-11-191882 extern: 1 intvolume: ' 113' issue: '23' month: '06' page: 5703 - 5710 publication: Blood publication_status: published publisher: American Society of Hematology publist_id: '2179' quality_controlled: 0 status: public title: Cdc42-dependent leading edge coordination is essential for interstitial dendritic cell migration (Plenary Paper) type: journal_article volume: 113 year: '2009' ... --- _id: '3948' abstract: - lang: eng text: Inhibiting the alpha(4) subunit of the integrin heterodimers alpha(4)beta(1) and alpha(4)beta(7) with the monoclonal antibody natalizumab is an effective treatment for multiple sclerosis (MS). However, the pharmacological action of natalizumab is not understood conclusively. Previous studies suggested that natalizumab inhibits activation, proliferation, or extravasation of inflammatory cells. To specify which mechanisms, cell types, and alpha(4) heterodimers are affected by the antibody treatment, we studied MS-like experimental autoimmune encephalomyelitis (EAE) in mice lacking the beta(1)-integrin gene either in all hematopoietic cells or selectively in T lymphocytes. Our results show that T cells critically rely on beta(1) integrins to accumulate in the central nervous system (CNS) during EAE, whereas CNS infiltration of beta(1)-deficient myeloid cells remains unaffected, suggesting that T cells are the main target of anti-alpha(4)-antibody blockade. We demonstrate that beta(1)-integrin expression on encephalitogenic T cells is critical for EAE development, and we therefore exclude alpha(4)beta(7) as a target integrin of the antibody treatment. T cells lacking beta(1) integrin are unable to firmly adhere to CNS endothelium in vivo, whereas their priming and expansion remain unaffected. Collectively, these results suggest that the primary action of natalizumab is interference with T cell extravasation via inhibition of alpha(4)beta(1) integrins. author: - first_name: Martina full_name: Bauer, Martina last_name: Bauer - first_name: Cord full_name: Brakebusch, Cord last_name: Brakebusch - first_name: Caroline full_name: Coisne, Caroline last_name: Coisne - first_name: Michael K full_name: Michael Sixt id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Hartmut full_name: Wekerle, Hartmut last_name: Wekerle - first_name: Britta full_name: Engelhardt, Britta last_name: Engelhardt - first_name: Reinhard full_name: Fässler, Reinhard last_name: Fässler citation: ama: Bauer M, Brakebusch C, Coisne C, et al. β1 integrins differentially control extravasation of inflammatory cell subsets into the CNS during autoimmunity. PNAS. 2009;106(6):1920-1925. doi:10.1073/pnas.0808909106 apa: Bauer, M., Brakebusch, C., Coisne, C., Sixt, M. K., Wekerle, H., Engelhardt, B., & Fässler, R. (2009). β1 integrins differentially control extravasation of inflammatory cell subsets into the CNS during autoimmunity. PNAS. National Academy of Sciences. https://doi.org/10.1073/pnas.0808909106 chicago: Bauer, Martina, Cord Brakebusch, Caroline Coisne, Michael K Sixt, Hartmut Wekerle, Britta Engelhardt, and Reinhard Fässler. “Β1 Integrins Differentially Control Extravasation of Inflammatory Cell Subsets into the CNS during Autoimmunity.” PNAS. National Academy of Sciences, 2009. https://doi.org/10.1073/pnas.0808909106. ieee: M. Bauer et al., “β1 integrins differentially control extravasation of inflammatory cell subsets into the CNS during autoimmunity,” PNAS, vol. 106, no. 6. National Academy of Sciences, pp. 1920–1925, 2009. ista: Bauer M, Brakebusch C, Coisne C, Sixt MK, Wekerle H, Engelhardt B, Fässler R. 2009. β1 integrins differentially control extravasation of inflammatory cell subsets into the CNS during autoimmunity. PNAS. 106(6), 1920–1925. mla: Bauer, Martina, et al. “Β1 Integrins Differentially Control Extravasation of Inflammatory Cell Subsets into the CNS during Autoimmunity.” PNAS, vol. 106, no. 6, National Academy of Sciences, 2009, pp. 1920–25, doi:10.1073/pnas.0808909106. short: M. Bauer, C. Brakebusch, C. Coisne, M.K. Sixt, H. Wekerle, B. Engelhardt, R. Fässler, PNAS 106 (2009) 1920–1925. date_created: 2018-12-11T12:06:03Z date_published: 2009-02-10T00:00:00Z date_updated: 2021-01-12T07:53:24Z day: '10' doi: 10.1073/pnas.0808909106 extern: 1 intvolume: ' 106' issue: '6' month: '02' page: 1920 - 1925 publication: PNAS publication_status: published publisher: National Academy of Sciences publist_id: '2180' quality_controlled: 0 status: public title: β1 integrins differentially control extravasation of inflammatory cell subsets into the CNS during autoimmunity type: journal_article volume: 106 year: '2009' ... --- _id: '3949' abstract: - lang: eng text: Adhesion and motility of mammalian leukocytes are essential requirements for innate and adaptive immune defense mechanisms. We show here that the guanine nucleotide exchange factor cytohesin-1, which had previously been demonstrated to be an important component of beta-2 integrin activation in lymphocytes, regulates the activation of the small GTPase RhoA in primary dendritic cells (DCs). Cytohesin-1 and RhoA are both required for the induction of chemokine-dependent conformational changes of the integrin beta-2 subunit of DCs during adhesion under physiological flow conditions. Furthermore, use of RNAi in murine bone marrow DCs (BM-DCs) revealed that interference with cytohesin-1 signaling impairs migration of wild-type dendritic cells in complex 3D environments and in vivo. This phenotype was not observed in the complete absence of integrins. We thus demonstrate an essential role of cytohesin-1/RhoA during ameboid migration in the presence of integrins and further suggest that DCs without integrins switch to a different migration mode. author: - first_name: Thomas full_name: Quast, Thomas last_name: Quast - first_name: Barbara full_name: Tappertzhofen, Barbara last_name: Tappertzhofen - first_name: Cora full_name: Schild, Cora last_name: Schild - first_name: Jessica full_name: Grell, Jessica last_name: Grell - first_name: Niklas full_name: Czeloth, Niklas last_name: Czeloth - first_name: Reinhold full_name: Förster, Reinhold last_name: Förster - first_name: Ronen full_name: Alon, Ronen last_name: Alon - first_name: Line full_name: Fraemohs, Line last_name: Fraemohs - first_name: Katrin full_name: Dreck, Katrin last_name: Dreck - first_name: Christian full_name: Weber, Christian last_name: Weber - first_name: Tim full_name: Lämmermann, Tim last_name: Lämmermann - first_name: Michael K full_name: Michael Sixt id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Waldemar full_name: Kolanus, Waldemar last_name: Kolanus citation: ama: Quast T, Tappertzhofen B, Schild C, et al. Cytohesin-1 controls the activation of RhoA and modulates integrin-dependent adhesion and migration of dendritic cells. Blood. 2009;113(23):5801-5810. doi:10.1182/blood-2008-08-176123 apa: Quast, T., Tappertzhofen, B., Schild, C., Grell, J., Czeloth, N., Förster, R., … Kolanus, W. (2009). Cytohesin-1 controls the activation of RhoA and modulates integrin-dependent adhesion and migration of dendritic cells. Blood. American Society of Hematology. https://doi.org/10.1182/blood-2008-08-176123 chicago: Quast, Thomas, Barbara Tappertzhofen, Cora Schild, Jessica Grell, Niklas Czeloth, Reinhold Förster, Ronen Alon, et al. “Cytohesin-1 Controls the Activation of RhoA and Modulates Integrin-Dependent Adhesion and Migration of Dendritic Cells.” Blood. American Society of Hematology, 2009. https://doi.org/10.1182/blood-2008-08-176123. ieee: T. Quast et al., “Cytohesin-1 controls the activation of RhoA and modulates integrin-dependent adhesion and migration of dendritic cells,” Blood, vol. 113, no. 23. American Society of Hematology, pp. 5801–5810, 2009. ista: Quast T, Tappertzhofen B, Schild C, Grell J, Czeloth N, Förster R, Alon R, Fraemohs L, Dreck K, Weber C, Lämmermann T, Sixt MK, Kolanus W. 2009. Cytohesin-1 controls the activation of RhoA and modulates integrin-dependent adhesion and migration of dendritic cells. Blood. 113(23), 5801–5810. mla: Quast, Thomas, et al. “Cytohesin-1 Controls the Activation of RhoA and Modulates Integrin-Dependent Adhesion and Migration of Dendritic Cells.” Blood, vol. 113, no. 23, American Society of Hematology, 2009, pp. 5801–10, doi:10.1182/blood-2008-08-176123. short: T. Quast, B. Tappertzhofen, C. Schild, J. Grell, N. Czeloth, R. Förster, R. Alon, L. Fraemohs, K. Dreck, C. Weber, T. Lämmermann, M.K. Sixt, W. Kolanus, Blood 113 (2009) 5801–5810. date_created: 2018-12-11T12:06:03Z date_published: 2009-06-04T00:00:00Z date_updated: 2021-01-12T07:53:24Z day: '04' doi: 10.1182/blood-2008-08-176123 extern: 1 intvolume: ' 113' issue: '23' month: '06' page: 5801 - 5810 publication: Blood publication_status: published publisher: American Society of Hematology publist_id: '2177' quality_controlled: 0 status: public title: Cytohesin-1 controls the activation of RhoA and modulates integrin-dependent adhesion and migration of dendritic cells type: journal_article volume: 113 year: '2009' ...