--- _id: '10536' abstract: - lang: eng text: TGFβ overexpression is commonly detected in cancer patients and correlates with poor prognosis and metastasis. Cancer progression is often associated with an enhanced recruitment of myeloid-derived cells to the tumor microenvironment. Here we show that functional TGFβ-signaling in myeloid cells is required for metastasis to the lungs and the liver. Myeloid-specific deletion of Tgfbr2 resulted in reduced spontaneous lung metastasis, which was associated with a reduction of proinflammatory cytokines in the metastatic microenvironment. Notably, CD8+ T cell depletion in myeloid-specific Tgfbr2-deficient mice rescued lung metastasis. Myeloid-specific Tgfbr2-deficiency resulted in reduced liver metastasis with an almost complete absence of myeloid cells within metastatic foci. On contrary, an accumulation of Tgfβ-responsive myeloid cells was associated with an increased recruitment of monocytes and granulocytes and higher proinflammatory cytokine levels in control mice. Monocytic cells isolated from metastatic livers of Tgfbr2-deficient mice showed increased polarization towards the M1 phenotype, Tnfα and Il-1β expression, reduced levels of M2 markers and reduced production of chemokines responsible for myeloid-cell recruitment. No significant differences in Tgfβ levels were observed at metastatic sites of any model. These data demonstrate that Tgfβ signaling in monocytic myeloid cells suppresses CD8+ T cell activity during lung metastasis, while these cells actively contribute to tumor growth during liver metastasis. Thus, myeloid cells modulate metastasis through different mechanisms in a tissue-specific manner. acknowledgement: The authors acknowledge the assistance of the Laboratory Animal Services Center (LASC) – UZH, Center for Microscopy and Image Analysis, and the Flow Cytometry Center of the University of Zurich. article_number: '765151' article_processing_charge: No article_type: original author: - first_name: Cristina full_name: Stefanescu, Cristina last_name: Stefanescu - first_name: Merel full_name: Van Gogh, Merel last_name: Van Gogh - first_name: Marko full_name: Roblek, Marko id: 3047D808-F248-11E8-B48F-1D18A9856A87 last_name: Roblek orcid: 0000-0001-9588-1389 - first_name: Mathias full_name: Heikenwalder, Mathias last_name: Heikenwalder - first_name: Lubor full_name: Borsig, Lubor last_name: Borsig citation: ama: Stefanescu C, Van Gogh M, Roblek M, Heikenwalder M, Borsig L. TGFβ signaling in myeloid cells promotes lung and liver metastasis through different mechanisms. Frontiers in Oncology. 2021;11. doi:10.3389/fonc.2021.765151 apa: Stefanescu, C., Van Gogh, M., Roblek, M., Heikenwalder, M., & Borsig, L. (2021). TGFβ signaling in myeloid cells promotes lung and liver metastasis through different mechanisms. Frontiers in Oncology. Frontiers. https://doi.org/10.3389/fonc.2021.765151 chicago: Stefanescu, Cristina, Merel Van Gogh, Marko Roblek, Mathias Heikenwalder, and Lubor Borsig. “TGFβ Signaling in Myeloid Cells Promotes Lung and Liver Metastasis through Different Mechanisms.” Frontiers in Oncology. Frontiers, 2021. https://doi.org/10.3389/fonc.2021.765151. ieee: C. Stefanescu, M. Van Gogh, M. Roblek, M. Heikenwalder, and L. Borsig, “TGFβ signaling in myeloid cells promotes lung and liver metastasis through different mechanisms,” Frontiers in Oncology, vol. 11. Frontiers, 2021. ista: Stefanescu C, Van Gogh M, Roblek M, Heikenwalder M, Borsig L. 2021. TGFβ signaling in myeloid cells promotes lung and liver metastasis through different mechanisms. Frontiers in Oncology. 11, 765151. mla: Stefanescu, Cristina, et al. “TGFβ Signaling in Myeloid Cells Promotes Lung and Liver Metastasis through Different Mechanisms.” Frontiers in Oncology, vol. 11, 765151, Frontiers, 2021, doi:10.3389/fonc.2021.765151. short: C. Stefanescu, M. Van Gogh, M. Roblek, M. Heikenwalder, L. Borsig, Frontiers in Oncology 11 (2021). date_created: 2021-12-12T23:01:27Z date_published: 2021-11-18T00:00:00Z date_updated: 2023-08-17T06:20:32Z day: '18' ddc: - '610' department: - _id: DaSi doi: 10.3389/fonc.2021.765151 external_id: isi: - '000726603400001' pmid: - '34868988' file: - access_level: open_access checksum: 56cbac80e6891ce750511a30161b7792 content_type: application/pdf creator: alisjak date_created: 2021-12-13T13:32:37Z date_updated: 2021-12-13T13:32:37Z file_id: '10539' file_name: 2021_Frontiers_Stefanescu.pdf file_size: 9245199 relation: main_file success: 1 file_date_updated: 2021-12-13T13:32:37Z has_accepted_license: '1' intvolume: ' 11' isi: 1 language: - iso: eng month: '11' oa: 1 oa_version: Published Version pmid: 1 publication: Frontiers in Oncology publication_identifier: eissn: - 2234-943X publication_status: published publisher: Frontiers quality_controlled: '1' scopus_import: '1' status: public title: TGFβ signaling in myeloid cells promotes lung and liver metastasis through different mechanisms 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: '2021' ... --- _id: '7466' abstract: - lang: eng text: Unpaired ligands are secreted signals that act via a GP130-like receptor, domeless, to activate JAK/STAT signalling in Drosophila. Like many mammalian cytokines, unpaireds can be activated by infection and other stresses and can promote insulin resistance in target tissues. However, the importance of this effect in non-inflammatory physiology is unknown. Here, we identify a requirement for unpaired-JAK signalling as a metabolic regulator in healthy adult Drosophila muscle. Adult muscles show basal JAK-STAT signalling activity in the absence of any immune challenge. Plasmatocytes (Drosophila macrophages) are an important source of this tonic signal. Loss of the dome receptor on adult muscles significantly reduces lifespan and causes local and systemic metabolic pathology. These pathologies result from hyperactivation of AKT and consequent deregulation of metabolism. Thus, we identify a cytokine signal that must be received in muscle to control AKT activity and metabolic homeostasis. article_number: e51595 article_processing_charge: No article_type: original author: - first_name: Katrin full_name: Kierdorf, Katrin last_name: Kierdorf - first_name: Fabian full_name: Hersperger, Fabian last_name: Hersperger - first_name: Jessica full_name: Sharrock, Jessica last_name: Sharrock - first_name: Crystal M. full_name: Vincent, Crystal M. last_name: Vincent - first_name: Pinar full_name: Ustaoglu, Pinar last_name: Ustaoglu - first_name: Jiawen full_name: Dou, Jiawen last_name: Dou - first_name: Attila full_name: György, Attila id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87 last_name: György orcid: 0000-0002-1819-198X - first_name: Olaf full_name: Groß, Olaf last_name: Groß - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 - first_name: Marc S. full_name: Dionne, Marc S. last_name: Dionne citation: ama: Kierdorf K, Hersperger F, Sharrock J, et al. Muscle function and homeostasis require cytokine inhibition of AKT activity in Drosophila. eLife. 2020;9. doi:10.7554/eLife.51595 apa: Kierdorf, K., Hersperger, F., Sharrock, J., Vincent, C. M., Ustaoglu, P., Dou, J., … Dionne, M. S. (2020). Muscle function and homeostasis require cytokine inhibition of AKT activity in Drosophila. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.51595 chicago: Kierdorf, Katrin, Fabian Hersperger, Jessica Sharrock, Crystal M. Vincent, Pinar Ustaoglu, Jiawen Dou, Attila György, Olaf Groß, Daria E Siekhaus, and Marc S. Dionne. “Muscle Function and Homeostasis Require Cytokine Inhibition of AKT Activity in Drosophila.” ELife. eLife Sciences Publications, 2020. https://doi.org/10.7554/eLife.51595. ieee: K. Kierdorf et al., “Muscle function and homeostasis require cytokine inhibition of AKT activity in Drosophila,” eLife, vol. 9. eLife Sciences Publications, 2020. ista: Kierdorf K, Hersperger F, Sharrock J, Vincent CM, Ustaoglu P, Dou J, György A, Groß O, Siekhaus DE, Dionne MS. 2020. Muscle function and homeostasis require cytokine inhibition of AKT activity in Drosophila. eLife. 9, e51595. mla: Kierdorf, Katrin, et al. “Muscle Function and Homeostasis Require Cytokine Inhibition of AKT Activity in Drosophila.” ELife, vol. 9, e51595, eLife Sciences Publications, 2020, doi:10.7554/eLife.51595. short: K. Kierdorf, F. Hersperger, J. Sharrock, C.M. Vincent, P. Ustaoglu, J. Dou, A. György, O. Groß, D.E. Siekhaus, M.S. Dionne, ELife 9 (2020). date_created: 2020-02-09T23:00:51Z date_published: 2020-01-20T00:00:00Z date_updated: 2023-08-17T14:36:39Z day: '20' ddc: - '570' department: - _id: DaSi doi: 10.7554/eLife.51595 external_id: isi: - '000512304800001' file: - access_level: open_access checksum: 3a072be843f416c7a7d532a51dc0addb content_type: application/pdf creator: dernst date_created: 2020-02-10T08:53:16Z date_updated: 2020-07-14T12:47:59Z file_id: '7470' file_name: 2020_eLife_Kierdorf.pdf file_size: 4959933 relation: main_file file_date_updated: 2020-07-14T12:47:59Z has_accepted_license: '1' intvolume: ' 9' isi: 1 language: - iso: eng month: '01' oa: 1 oa_version: Published Version project: - _id: 253B6E48-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29638 name: Drosophila TNFa´s Funktion in Immunzellen publication: eLife publication_identifier: eissn: - 2050084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' scopus_import: '1' status: public title: Muscle function and homeostasis require cytokine inhibition of AKT activity in Drosophila 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: '8983' abstract: - lang: eng text: Metabolic adaptation is a critical feature of migrating cells. It tunes the metabolic programs of migrating cells to allow them to efficiently exert their crucial roles in development, inflammatory responses and tumor metastasis. Cell migration through physically challenging contexts requires energy. However, how the metabolic reprogramming that underlies in vivo cell invasion is controlled is still unanswered. In my PhD project, I identify a novel conserved metabolic shift in Drosophila melanogaster immune cells that by modulating their bioenergetic potential controls developmentally programmed tissue invasion. We show that this regulation requires a novel conserved nuclear protein, named Atossa. Atossa enhances the transcription of a set of proteins, including an RNA helicase Porthos and two metabolic enzymes, each of which increases the tissue invasion of leading Drosophila macrophages and can rescue the atossa mutant phenotype. Porthos selectively regulates the translational efficiency of a subset of mRNAs containing a 5’-UTR cis-regulatory TOP-like sequence. These 5’TOPL mRNA targets encode mitochondrial-related proteins, including subunits of mitochondrial oxidative phosphorylation (OXPHOS) components III and V and other metabolic-related proteins. Porthos powers up mitochondrial OXPHOS to engender a sufficient ATP supply, which is required for tissue invasion of leading macrophages. Atossa’s two vertebrate orthologs rescue the invasion defect. In my PhD project, I elucidate that Atossa displays a conserved developmental metabolic control to modulate metabolic capacities and the cellular energy state, through altered transcription and translation, to aid the tissue infiltration of leading cells into energy demanding barriers. acknowledged_ssus: - _id: Bio - _id: LifeSc - _id: E-Lib - _id: CampIT acknowledgement: Also, I would like to express my appreciation and thanks to the Bioimaging facility, LSF, GSO, library, and IT people at IST Austria. alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Shamsi full_name: Emtenani, Shamsi id: 49D32318-F248-11E8-B48F-1D18A9856A87 last_name: Emtenani orcid: 0000-0001-6981-6938 citation: ama: Emtenani S. Metabolic regulation of Drosophila macrophage tissue invasion. 2020. doi:10.15479/AT:ISTA:8983 apa: Emtenani, S. (2020). Metabolic regulation of Drosophila macrophage tissue invasion. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:8983 chicago: Emtenani, Shamsi. “Metabolic Regulation of Drosophila Macrophage Tissue Invasion.” Institute of Science and Technology Austria, 2020. https://doi.org/10.15479/AT:ISTA:8983. ieee: S. Emtenani, “Metabolic regulation of Drosophila macrophage tissue invasion,” Institute of Science and Technology Austria, 2020. ista: Emtenani S. 2020. Metabolic regulation of Drosophila macrophage tissue invasion. Institute of Science and Technology Austria. mla: Emtenani, Shamsi. Metabolic Regulation of Drosophila Macrophage Tissue Invasion. Institute of Science and Technology Austria, 2020, doi:10.15479/AT:ISTA:8983. short: S. Emtenani, Metabolic Regulation of Drosophila Macrophage Tissue Invasion, Institute of Science and Technology Austria, 2020. date_created: 2020-12-30T15:41:26Z date_published: 2020-12-30T00:00:00Z date_updated: 2023-09-07T13:24:17Z day: '30' ddc: - '570' degree_awarded: PhD department: - _id: DaSi doi: 10.15479/AT:ISTA:8983 file: - access_level: open_access checksum: ec2797ab7a6f253b35df0572b36d1b43 content_type: application/pdf creator: semtenan date_created: 2020-12-30T15:34:01Z date_updated: 2021-12-31T23:30:04Z embargo: 2021-12-30 file_id: '8984' file_name: Thesis_Shamsi_Emtenani_pdfA.pdf file_size: 10848175 relation: main_file - access_level: closed checksum: cc30e6608a9815414024cf548dff3b3a content_type: application/pdf creator: semtenan date_created: 2020-12-30T15:37:36Z date_updated: 2021-12-31T23:30:04Z embargo_to: open_access file_id: '8985' file_name: Thesis_Shamsi_Emtenani_source file.pdf file_size: 10073648 relation: source_file file_date_updated: 2021-12-31T23:30:04Z has_accepted_license: '1' language: - iso: eng month: '12' oa: 1 oa_version: Published Version page: '141' publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria related_material: record: - id: '8557' relation: part_of_dissertation status: public - id: '6187' relation: part_of_dissertation status: public status: public supervisor: - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 title: Metabolic regulation of Drosophila macrophage tissue invasion type: dissertation user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 year: '2020' ... --- _id: '8557' abstract: - lang: eng text: The infiltration of immune cells into tissues underlies the establishment of tissue resident macrophages, and responses to infections and tumors. Yet the mechanisms immune cells utilize to negotiate tissue barriers in living organisms are not well understood, and a role for cortical actin has not been examined. Here we find that the tissue invasion of Drosophila macrophages, also known as plasmatocytes or hemocytes, utilizes enhanced cortical F-actin levels stimulated by the Drosophila member of the fos proto oncogene transcription factor family (Dfos, Kayak). RNA sequencing analysis and live imaging show that Dfos enhances F-actin levels around the entire macrophage surface by increasing mRNA levels of the membrane spanning molecular scaffold tetraspanin TM4SF, and the actin cross-linking filamin Cheerio which are themselves required for invasion. Cortical F-actin levels are critical as expressing a dominant active form of Diaphanous, a actin polymerizing Formin, can rescue the Dfos Dominant Negative macrophage invasion defect. In vivo imaging shows that Dfos is required to enhance the efficiency of the initial phases of macrophage tissue entry. Genetic evidence argues that this Dfos-induced program in macrophages counteracts the constraint produced by the tension of surrounding tissues and buffers the mechanical properties of the macrophage nucleus from affecting tissue entry. We thus identify tuning the cortical actin cytoskeleton through Dfos as a key process allowing efficient forward movement of an immune cell into surrounding tissues. acknowledged_ssus: - _id: LifeSc acknowledgement: 'We thank the following for their contributions: The Drosophila Genomics Resource Center supported by NIH grant 2P40OD010949-10A1 for plasmids, K. Brueckner. B. Stramer, M. Uhlirova, O. Schuldiner, the Bloomington Drosophila Stock Center supported by NIH grant P40OD018537 and the Vienna Drosophila Resource Center for fly stocks, FlyBase (Thurmond et al., 2019) for essential genomic information, and the BDGP in situ database for data (Tomancak et al., 2002, 2007). For antibodies, we thank the Developmental Studies Hybridoma Bank, which was created by the Eunice Kennedy Shriver National Institute of Child Health and Human Development of the NIH, and is maintained at the University of Iowa, as well as J. Zeitlinger for her generous gift of Dfos antibody. We thank the Vienna BioCenter Core Facilities for RNA sequencing and analysis and the Life Scientific Service Units at IST Austria for technical support and assistance with microscopy and FACS analysis. We thank C.P. Heisenberg, P. Martin, M. Sixt and Siekhaus group members for discussions and T.Hurd, A. Ratheesh and P. Rangan for comments on the manuscript. A.G. was supported by the Austrian Science Fund (FWF) grant DASI_FWF01_P29638S, D.E.S. by Marie Curie CIG 334077/IRTIM. M.S. is supported by the FWF, PhD program W1212 915 and the European Research Council (ERC) Advanced grant (ERC-2015-AdG TNT-Tumors 694883). S.W. is supported by an OEAW, DOC fellowship.' article_processing_charge: No author: - first_name: Vera full_name: Belyaeva, Vera id: 47F080FE-F248-11E8-B48F-1D18A9856A87 last_name: Belyaeva - first_name: Stephanie full_name: Wachner, Stephanie id: 2A95E7B0-F248-11E8-B48F-1D18A9856A87 last_name: Wachner - first_name: Igor full_name: Gridchyn, Igor id: 4B60654C-F248-11E8-B48F-1D18A9856A87 last_name: Gridchyn orcid: 0000-0002-1807-1929 - first_name: Markus full_name: Linder, Markus last_name: Linder - first_name: Shamsi full_name: Emtenani, Shamsi id: 49D32318-F248-11E8-B48F-1D18A9856A87 last_name: Emtenani orcid: 0000-0001-6981-6938 - first_name: Attila full_name: György, Attila id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87 last_name: György orcid: 0000-0002-1819-198X - first_name: Maria full_name: Sibilia, Maria last_name: Sibilia - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 citation: ama: Belyaeva V, Wachner S, Gridchyn I, et al. Cortical actin properties controlled by Drosophila Fos aid macrophage infiltration against surrounding tissue resistance. bioRxiv. doi:10.1101/2020.09.18.301481 apa: Belyaeva, V., Wachner, S., Gridchyn, I., Linder, M., Emtenani, S., György, A., … Siekhaus, D. E. (n.d.). Cortical actin properties controlled by Drosophila Fos aid macrophage infiltration against surrounding tissue resistance. bioRxiv. https://doi.org/10.1101/2020.09.18.301481 chicago: Belyaeva, Vera, Stephanie Wachner, Igor Gridchyn, Markus Linder, Shamsi Emtenani, Attila György, Maria Sibilia, and Daria E Siekhaus. “Cortical Actin Properties Controlled by Drosophila Fos Aid Macrophage Infiltration against Surrounding Tissue Resistance.” BioRxiv, n.d. https://doi.org/10.1101/2020.09.18.301481. ieee: V. Belyaeva et al., “Cortical actin properties controlled by Drosophila Fos aid macrophage infiltration against surrounding tissue resistance,” bioRxiv. . ista: Belyaeva V, Wachner S, Gridchyn I, Linder M, Emtenani S, György A, Sibilia M, Siekhaus DE. Cortical actin properties controlled by Drosophila Fos aid macrophage infiltration against surrounding tissue resistance. bioRxiv, 10.1101/2020.09.18.301481. mla: Belyaeva, Vera, et al. “Cortical Actin Properties Controlled by Drosophila Fos Aid Macrophage Infiltration against Surrounding Tissue Resistance.” BioRxiv, doi:10.1101/2020.09.18.301481. short: V. Belyaeva, S. Wachner, I. Gridchyn, M. Linder, S. Emtenani, A. György, M. Sibilia, D.E. Siekhaus, BioRxiv (n.d.). date_created: 2020-09-23T09:36:47Z date_published: 2020-09-18T00:00:00Z date_updated: 2024-03-27T23:30:24Z day: '18' department: - _id: DaSi - _id: JoCs doi: 10.1101/2020.09.18.301481 ec_funded: 1 language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1101/2020.09.18.301481 month: '09' oa: 1 oa_version: Preprint project: - _id: 253B6E48-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29638 name: Drosophila TNFa´s Funktion in Immunzellen - _id: 2536F660-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '334077' name: Investigating the role of transporters in invasive migration through junctions - _id: 26199CA4-B435-11E9-9278-68D0E5697425 grant_number: '24800' name: Tissue barrier penetration is crucial for immunity and metastasis publication: bioRxiv publication_status: submitted related_material: record: - id: '10614' relation: later_version status: public - id: '8983' relation: dissertation_contains status: public status: public title: Cortical actin properties controlled by Drosophila Fos aid macrophage infiltration against surrounding tissue resistance type: preprint user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2020' ... --- _id: '6190' abstract: - lang: eng text: "Increased levels of the chemokine CCL2 in cancer patients are associated with poor prognosis. Experimental evidence suggests that CCL2 correlates with inflammatory monocyte recruitment and induction of vascular activation, but the functionality remains open. Here, we show that endothelial Ccr2 facilitates pulmonary metastasis using an endothelial-specific Ccr2-deficient mouse model (Ccr2ecKO). Similar levels of circulating monocytes and equal leukocyte recruitment to metastatic lesions of Ccr2ecKO and Ccr2fl/fl littermates were observed. The absence of endothelial Ccr2 strongly reduced pulmonary metastasis, while the primary tumor growth was unaffected. Despite a comparable cytokine milieu in Ccr2ecKO and Ccr2fl/fl littermates the absence of vascular permeability induction was observed only in Ccr2ecKO mice. CCL2 stimulation of pulmonary endothelial cells resulted in increased phosphorylation of MLC2, endothelial cell retraction, and vascular leakiness that was blocked by an addition of a CCR2 inhibitor. These data demonstrate that endothelial CCR2 expression is required for tumor cell extravasation and pulmonary metastasis.\r\n\r\nImplications: The findings provide mechanistic insight into how CCL2–CCR2 signaling in endothelial cells promotes their activation through myosin light chain phosphorylation, resulting in endothelial retraction and enhanced tumor cell migration and metastasis." article_processing_charge: No article_type: original author: - first_name: Marko full_name: Roblek, Marko id: 3047D808-F248-11E8-B48F-1D18A9856A87 last_name: Roblek orcid: 0000-0001-9588-1389 - first_name: Darya full_name: Protsyuk, Darya last_name: Protsyuk - first_name: Paul F. full_name: Becker, Paul F. last_name: Becker - first_name: Cristina full_name: Stefanescu, Cristina last_name: Stefanescu - first_name: Christian full_name: Gorzelanny, Christian last_name: Gorzelanny - first_name: Jesus F. full_name: Glaus Garzon, Jesus F. last_name: Glaus Garzon - first_name: Lucia full_name: Knopfova, Lucia last_name: Knopfova - first_name: Mathias full_name: Heikenwalder, Mathias last_name: Heikenwalder - first_name: Bruno full_name: Luckow, Bruno last_name: Luckow - first_name: Stefan W. full_name: Schneider, Stefan W. last_name: Schneider - first_name: Lubor full_name: Borsig, Lubor last_name: Borsig citation: ama: Roblek M, Protsyuk D, Becker PF, et al. CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis. Molecular Cancer Research. 2019;17(3):783-793. doi:10.1158/1541-7786.MCR-18-0530 apa: Roblek, M., Protsyuk, D., Becker, P. F., Stefanescu, C., Gorzelanny, C., Glaus Garzon, J. F., … Borsig, L. (2019). CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis. Molecular Cancer Research. AACR. https://doi.org/10.1158/1541-7786.MCR-18-0530 chicago: Roblek, Marko, Darya Protsyuk, Paul F. Becker, Cristina Stefanescu, Christian Gorzelanny, Jesus F. Glaus Garzon, Lucia Knopfova, et al. “CCL2 Is a Vascular Permeability Factor Inducing CCR2-Dependent Endothelial Retraction during Lung Metastasis.” Molecular Cancer Research. AACR, 2019. https://doi.org/10.1158/1541-7786.MCR-18-0530. ieee: M. Roblek et al., “CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis,” Molecular Cancer Research, vol. 17, no. 3. AACR, pp. 783–793, 2019. ista: Roblek M, Protsyuk D, Becker PF, Stefanescu C, Gorzelanny C, Glaus Garzon JF, Knopfova L, Heikenwalder M, Luckow B, Schneider SW, Borsig L. 2019. CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis. Molecular Cancer Research. 17(3), 783–793. mla: Roblek, Marko, et al. “CCL2 Is a Vascular Permeability Factor Inducing CCR2-Dependent Endothelial Retraction during Lung Metastasis.” Molecular Cancer Research, vol. 17, no. 3, AACR, 2019, pp. 783–93, doi:10.1158/1541-7786.MCR-18-0530. short: M. Roblek, D. Protsyuk, P.F. Becker, C. Stefanescu, C. Gorzelanny, J.F. Glaus Garzon, L. Knopfova, M. Heikenwalder, B. Luckow, S.W. Schneider, L. Borsig, Molecular Cancer Research 17 (2019) 783–793. date_created: 2019-03-31T21:59:12Z date_published: 2019-03-01T00:00:00Z date_updated: 2023-08-25T08:57:01Z day: '01' department: - _id: DaSi doi: 10.1158/1541-7786.MCR-18-0530 external_id: isi: - '000460099800012' pmid: - '30552233' intvolume: ' 17' isi: 1 issue: '3' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1158/1541-7786.MCR-18-0530 month: '03' oa: 1 oa_version: Published Version page: 783-793 pmid: 1 publication: Molecular Cancer Research publication_identifier: eissn: - '15573125' issn: - '15417786' publication_status: published publisher: AACR quality_controlled: '1' scopus_import: '1' status: public title: CCL2 is a vascular permeability factor inducing CCR2-dependent endothelial retraction during lung metastasis type: journal_article user_id: 4359f0d1-fa6c-11eb-b949-802e58b17ae8 volume: 17 year: '2019' ... --- _id: '7097' abstract: - lang: eng text: Early endosomes, also called sorting endosomes, are known to mature into late endosomesvia the Rab5-mediated endolysosomal trafficking pathway. Thus, early endosome existence isthought to be maintained by the continual fusion of transport vesicles from the plasmamembrane and thetrans-Golgi network (TGN). Here we show instead that endocytosis isdispensable and post-Golgi vesicle transport is crucial for the formation of endosomes andthe subsequent endolysosomal traffic regulated by yeast Rab5 Vps21p. Fittingly, all threeproteins required for endosomal nucleotide exchange on Vps21p arefirst recruited to theTGN before transport to the endosome, namely the GEF Vps9p and the epsin-relatedadaptors Ent3/5p. The TGN recruitment of these components is distinctly controlled, withVps9p appearing to require the Arf1p GTPase, and the Rab11s, Ypt31p/32p. These resultsprovide a different view of endosome formation and identify the TGN as a critical location forregulating progress through the endolysosomal trafficking pathway. article_number: '419' article_processing_charge: No article_type: original author: - first_name: Makoto full_name: Nagano, Makoto last_name: Nagano - first_name: Junko Y. full_name: Toshima, Junko Y. last_name: Toshima - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 - first_name: Jiro full_name: Toshima, Jiro last_name: Toshima citation: ama: Nagano M, Toshima JY, Siekhaus DE, Toshima J. Rab5-mediated endosome formation is regulated at the trans-Golgi network. Communications Biology. 2019;2(1). doi:10.1038/s42003-019-0670-5 apa: Nagano, M., Toshima, J. Y., Siekhaus, D. E., & Toshima, J. (2019). Rab5-mediated endosome formation is regulated at the trans-Golgi network. Communications Biology. Springer Nature. https://doi.org/10.1038/s42003-019-0670-5 chicago: Nagano, Makoto, Junko Y. Toshima, Daria E Siekhaus, and Jiro Toshima. “Rab5-Mediated Endosome Formation Is Regulated at the Trans-Golgi Network.” Communications Biology. Springer Nature, 2019. https://doi.org/10.1038/s42003-019-0670-5. ieee: M. Nagano, J. Y. Toshima, D. E. Siekhaus, and J. Toshima, “Rab5-mediated endosome formation is regulated at the trans-Golgi network,” Communications Biology, vol. 2, no. 1. Springer Nature, 2019. ista: Nagano M, Toshima JY, Siekhaus DE, Toshima J. 2019. Rab5-mediated endosome formation is regulated at the trans-Golgi network. Communications Biology. 2(1), 419. mla: Nagano, Makoto, et al. “Rab5-Mediated Endosome Formation Is Regulated at the Trans-Golgi Network.” Communications Biology, vol. 2, no. 1, 419, Springer Nature, 2019, doi:10.1038/s42003-019-0670-5. short: M. Nagano, J.Y. Toshima, D.E. Siekhaus, J. Toshima, Communications Biology 2 (2019). date_created: 2019-11-25T07:55:01Z date_published: 2019-11-15T00:00:00Z date_updated: 2023-08-30T07:27:55Z day: '15' ddc: - '570' department: - _id: DaSi doi: 10.1038/s42003-019-0670-5 external_id: isi: - '000496767800005' file: - access_level: open_access checksum: c63c69a264fc8a0e52f2b0d482f3bdae content_type: application/pdf creator: dernst date_created: 2019-11-25T07:58:05Z date_updated: 2020-07-14T12:47:49Z file_id: '7098' file_name: 2019_CommunicBiology_Nagano.pdf file_size: 2626069 relation: main_file file_date_updated: 2020-07-14T12:47:49Z has_accepted_license: '1' intvolume: ' 2' isi: 1 issue: '1' language: - iso: eng month: '11' oa: 1 oa_version: Published Version publication: Communications Biology publication_identifier: issn: - 2399-3642 publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Rab5-mediated endosome formation is regulated at the trans-Golgi network 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: 2 year: '2019' ... --- _id: '7180' abstract: - lang: eng text: Arabidopsis PIN2 protein directs transport of the phytohormone auxin from the root tip into the root elongation zone. Variation in hormone transport, which depends on a delicate interplay between PIN2 sorting to and from polar plasma membrane domains, determines root growth. By employing a constitutively degraded version of PIN2, we identify brassinolides as antagonists of PIN2 endocytosis. This response does not require de novo protein synthesis, but involves early events in canonical brassinolide signaling. Brassinolide-controlled adjustments in PIN2 sorting and intracellular distribution governs formation of a lateral PIN2 gradient in gravistimulated roots, coinciding with adjustments in auxin signaling and directional root growth. Strikingly, simulations indicate that PIN2 gradient formation is no prerequisite for root bending but rather dampens asymmetric auxin flow and signaling. Crosstalk between brassinolide signaling and endocytic PIN2 sorting, thus, appears essential for determining the rate of gravity-induced root curvature via attenuation of differential cell elongation. article_number: '5516' article_processing_charge: No article_type: original author: - first_name: Katarzyna full_name: Retzer, Katarzyna last_name: Retzer - first_name: Maria full_name: Akhmanova, Maria id: 3425EC26-F248-11E8-B48F-1D18A9856A87 last_name: Akhmanova orcid: 0000-0003-1522-3162 - first_name: Nataliia full_name: Konstantinova, Nataliia last_name: Konstantinova - first_name: Kateřina full_name: Malínská, Kateřina last_name: Malínská - first_name: Johannes full_name: Leitner, Johannes last_name: Leitner - first_name: Jan full_name: Petrášek, Jan last_name: Petrášek - first_name: Christian full_name: Luschnig, Christian last_name: Luschnig citation: ama: Retzer K, Akhmanova M, Konstantinova N, et al. Brassinosteroid signaling delimits root gravitropism via sorting of the Arabidopsis PIN2 auxin transporter. Nature Communications. 2019;10. doi:10.1038/s41467-019-13543-1 apa: Retzer, K., Akhmanova, M., Konstantinova, N., Malínská, K., Leitner, J., Petrášek, J., & Luschnig, C. (2019). Brassinosteroid signaling delimits root gravitropism via sorting of the Arabidopsis PIN2 auxin transporter. Nature Communications. Springer Nature. https://doi.org/10.1038/s41467-019-13543-1 chicago: Retzer, Katarzyna, Maria Akhmanova, Nataliia Konstantinova, Kateřina Malínská, Johannes Leitner, Jan Petrášek, and Christian Luschnig. “Brassinosteroid Signaling Delimits Root Gravitropism via Sorting of the Arabidopsis PIN2 Auxin Transporter.” Nature Communications. Springer Nature, 2019. https://doi.org/10.1038/s41467-019-13543-1. ieee: K. Retzer et al., “Brassinosteroid signaling delimits root gravitropism via sorting of the Arabidopsis PIN2 auxin transporter,” Nature Communications, vol. 10. Springer Nature, 2019. ista: Retzer K, Akhmanova M, Konstantinova N, Malínská K, Leitner J, Petrášek J, Luschnig C. 2019. Brassinosteroid signaling delimits root gravitropism via sorting of the Arabidopsis PIN2 auxin transporter. Nature Communications. 10, 5516. mla: Retzer, Katarzyna, et al. “Brassinosteroid Signaling Delimits Root Gravitropism via Sorting of the Arabidopsis PIN2 Auxin Transporter.” Nature Communications, vol. 10, 5516, Springer Nature, 2019, doi:10.1038/s41467-019-13543-1. short: K. Retzer, M. Akhmanova, N. Konstantinova, K. Malínská, J. Leitner, J. Petrášek, C. Luschnig, Nature Communications 10 (2019). date_created: 2019-12-15T23:00:43Z date_published: 2019-12-01T00:00:00Z date_updated: 2023-09-06T14:08:21Z day: '01' ddc: - '570' department: - _id: DaSi doi: 10.1038/s41467-019-13543-1 external_id: isi: - '000500508100001' pmid: - '31797871' file: - access_level: open_access checksum: 77e8720a8e0f3091b98159f85be40893 content_type: application/pdf creator: dernst date_created: 2019-12-16T07:37:50Z date_updated: 2020-07-14T12:47:52Z file_id: '7184' file_name: 2019_NatureComm_Retzer.pdf file_size: 5156533 relation: main_file file_date_updated: 2020-07-14T12:47:52Z has_accepted_license: '1' intvolume: ' 10' isi: 1 language: - iso: eng month: '12' oa: 1 oa_version: Published Version pmid: 1 project: - _id: 264CBBAC-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: M02379 name: Modeling epithelial tissue mechanics during cell invasion publication: Nature Communications publication_identifier: eissn: - '20411723' publication_status: published publisher: Springer Nature quality_controlled: '1' scopus_import: '1' status: public title: Brassinosteroid signaling delimits root gravitropism via sorting of the Arabidopsis PIN2 auxin transporter 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: 10 year: '2019' ... --- _id: '8' abstract: - lang: eng text: Despite their different origins, Drosophila glia and hemocytes are related cell populations that provide an immune function. Drosophila hemocytes patrol the body cavity and act as macrophages outside the nervous system whereas glia originate from the neuroepithelium and provide the scavenger population of the nervous system. Drosophila glia are hence the functional orthologs of vertebrate microglia, even though the latter are cells of immune origin that subsequently move into the brain during development. Interestingly, the Drosophila immune cells within (glia) and outside the nervous system (hemocytes) require the same transcription factor Glide/Gcm for their development. This raises the issue of how do glia specifically differentiate in the nervous system and hemocytes in the procephalic mesoderm. The Repo homeodomain transcription factor and pan-glial direct target of Glide/Gcm is known to ensure glial terminal differentiation. Here we show that Repo also takes center stage in the process that discriminates between glia and hemocytes. First, Repo expression is repressed in the hemocyte anlagen by mesoderm-specific factors. Second, Repo ectopic activation in the procephalic mesoderm is sufficient to repress the expression of hemocyte-specific genes. Third, the lack of Repo triggers the expression of hemocyte markers in glia. Thus, a complex network of tissue-specific cues biases the potential of Glide/Gcm. These data allow us to revise the concept of fate determinants and help us understand the bases of cell specification. Both sexes were analyzed.SIGNIFICANCE STATEMENTDistinct cell types often require the same pioneer transcription factor, raising the issue of how does one factor trigger different fates. In Drosophila, glia and hemocytes provide a scavenger activity within and outside the nervous system, respectively. While they both require the Glide/Gcm transcription factor, glia originate from the ectoderm, hemocytes from the mesoderm. Here we show that tissue-specific factors inhibit the gliogenic potential of Glide/Gcm in the mesoderm by repressing the expression of the homeodomain protein Repo, a major glial-specific target of Glide/Gcm. Repo expression in turn inhibits the expression of hemocyte-specific genes in the nervous system. These cell-specific networks secure the establishment of the glial fate only in the nervous system and allow cell diversification. acknowledgement: This work was supported by INSERM, CNRS, UDS, Ligue Régionale contre le Cancer, Hôpital de Strasbourg, Association pour la Recherche sur le Cancer (ARC) and Agence Nationale de la Recherche (ANR) grants. P.B.C. was funded by the ANR and by the ARSEP (Fondation pour l'Aide à la Recherche sur la Sclérose en Plaques), and G.T. by governmental and ARC fellowships. This work was also supported by grants from the Ataxia UK (2491) and the NC3R (NC/L000199/1) awarded to M.F. The Institut de Génétique et de Biologie Moléculaire et Cellulaire was also supported by a French state fund through the ANR labex. D.E.S. was funded by Marie Curie Grant CIG 334077/IRTIM. We thank B. Altenhein, K. Brückner, M. Crozatier, L. Waltzer, M. Logan, E. Kurant, R. Reuter, E. Kurucz, J.L Dimarcq, J. Hoffmann, C. Goodman, the DHSB, and the BDSC for reagents and flies. We also thank all of the laboratory members for comments on the manuscript; C. Diebold, C. Delaporte, M. Pezze, the fly, and imaging and antibody facilities for technical assistance; and D. Dembele for help with statistics. In addition, we thank Alison Brewer for help with Luciferase assays. article_processing_charge: No article_type: original author: - first_name: Guillaume full_name: Trébuchet, Guillaume last_name: Trébuchet - first_name: Pierre B full_name: Cattenoz, Pierre B last_name: Cattenoz - first_name: János full_name: Zsámboki, János last_name: Zsámboki - first_name: David full_name: Mazaud, David last_name: Mazaud - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 - first_name: Manolis full_name: Fanto, Manolis last_name: Fanto - first_name: Angela full_name: Giangrande, Angela last_name: Giangrande citation: ama: Trébuchet G, Cattenoz PB, Zsámboki J, et al. The Repo homeodomain transcription factor suppresses hematopoiesis in Drosophila and preserves the glial fate. Journal of Neuroscience. 2019;39(2):238-255. doi:10.1523/JNEUROSCI.1059-18.2018 apa: Trébuchet, G., Cattenoz, P. B., Zsámboki, J., Mazaud, D., Siekhaus, D. E., Fanto, M., & Giangrande, A. (2019). The Repo homeodomain transcription factor suppresses hematopoiesis in Drosophila and preserves the glial fate. Journal of Neuroscience. Society for Neuroscience. https://doi.org/10.1523/JNEUROSCI.1059-18.2018 chicago: Trébuchet, Guillaume, Pierre B Cattenoz, János Zsámboki, David Mazaud, Daria E Siekhaus, Manolis Fanto, and Angela Giangrande. “The Repo Homeodomain Transcription Factor Suppresses Hematopoiesis in Drosophila and Preserves the Glial Fate.” Journal of Neuroscience. Society for Neuroscience, 2019. https://doi.org/10.1523/JNEUROSCI.1059-18.2018. ieee: G. Trébuchet et al., “The Repo homeodomain transcription factor suppresses hematopoiesis in Drosophila and preserves the glial fate,” Journal of Neuroscience, vol. 39, no. 2. Society for Neuroscience, pp. 238–255, 2019. ista: Trébuchet G, Cattenoz PB, Zsámboki J, Mazaud D, Siekhaus DE, Fanto M, Giangrande A. 2019. The Repo homeodomain transcription factor suppresses hematopoiesis in Drosophila and preserves the glial fate. Journal of Neuroscience. 39(2), 238–255. mla: Trébuchet, Guillaume, et al. “The Repo Homeodomain Transcription Factor Suppresses Hematopoiesis in Drosophila and Preserves the Glial Fate.” Journal of Neuroscience, vol. 39, no. 2, Society for Neuroscience, 2019, pp. 238–55, doi:10.1523/JNEUROSCI.1059-18.2018. short: G. Trébuchet, P.B. Cattenoz, J. Zsámboki, D. Mazaud, D.E. Siekhaus, M. Fanto, A. Giangrande, Journal of Neuroscience 39 (2019) 238–255. date_created: 2018-12-11T11:44:07Z date_published: 2019-01-09T00:00:00Z date_updated: 2023-09-19T10:10:55Z day: '09' ddc: - '570' department: - _id: DaSi doi: 10.1523/JNEUROSCI.1059-18.2018 ec_funded: 1 external_id: isi: - '000455189900006' pmid: - '30504274' file: - access_level: open_access checksum: 8f6925eb4cd1e8747d8ea25929c68de6 content_type: application/pdf creator: dernst date_created: 2020-10-02T09:33:28Z date_updated: 2020-10-02T09:33:28Z file_id: '8596' file_name: 2019_JournNeuroscience_Trebuchet.pdf file_size: 9455414 relation: main_file success: 1 file_date_updated: 2020-10-02T09:33:28Z has_accepted_license: '1' intvolume: ' 39' isi: 1 issue: '2' language: - iso: eng month: '01' oa: 1 oa_version: Published Version page: 238-255 pmid: 1 project: - _id: 2536F660-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '334077' name: Investigating the role of transporters in invasive migration through junctions publication: Journal of Neuroscience publication_status: published publisher: Society for Neuroscience publist_id: '8048' quality_controlled: '1' scopus_import: '1' status: public title: The Repo homeodomain transcription factor suppresses hematopoiesis in Drosophila and preserves the glial fate type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 39 year: '2019' ... --- _id: '6187' abstract: - lang: eng text: Aberrant display of the truncated core1 O-glycan T-antigen is a common feature of human cancer cells that correlates with metastasis. Here we show that T-antigen in Drosophila melanogaster macrophages is involved in their developmentally programmed tissue invasion. Higher macrophage T-antigen levels require an atypical major facilitator superfamily (MFS) member that we named Minerva which enables macrophage dissemination and invasion. We characterize for the first time the T and Tn glycoform O-glycoproteome of the Drosophila melanogaster embryo, and determine that Minerva increases the presence of T-antigen on proteins in pathways previously linked to cancer, most strongly on the sulfhydryl oxidase Qsox1 which we show is required for macrophage tissue entry. Minerva’s vertebrate ortholog, MFSD1, rescues the minerva mutant’s migration and T-antigen glycosylation defects. We thus identify a key conserved regulator that orchestrates O-glycosylation on a protein subset to activate a program governing migration steps important for both development and cancer metastasis. acknowledged_ssus: - _id: LifeSc article_number: e41801 article_processing_charge: No author: - first_name: Katarina full_name: Valosková, Katarina id: 46F146FC-F248-11E8-B48F-1D18A9856A87 last_name: Valosková - first_name: Julia full_name: Biebl, Julia id: 3CCBB46E-F248-11E8-B48F-1D18A9856A87 last_name: Biebl - first_name: Marko full_name: Roblek, Marko id: 3047D808-F248-11E8-B48F-1D18A9856A87 last_name: Roblek orcid: 0000-0001-9588-1389 - first_name: Shamsi full_name: Emtenani, Shamsi id: 49D32318-F248-11E8-B48F-1D18A9856A87 last_name: Emtenani orcid: 0000-0001-6981-6938 - first_name: Attila full_name: György, Attila id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87 last_name: György orcid: 0000-0002-1819-198X - first_name: Michaela full_name: Misova, Michaela id: 495A3C32-F248-11E8-B48F-1D18A9856A87 last_name: Misova orcid: 0000-0003-2427-6856 - first_name: Aparna full_name: Ratheesh, Aparna id: 2F064CFE-F248-11E8-B48F-1D18A9856A87 last_name: Ratheesh orcid: 0000-0001-7190-0776 - first_name: Patricia full_name: Rodrigues, Patricia id: 2CE4065A-F248-11E8-B48F-1D18A9856A87 last_name: Rodrigues - first_name: Katerina full_name: Shkarina, Katerina last_name: Shkarina - first_name: Ida Signe Bohse full_name: Larsen, Ida Signe Bohse last_name: Larsen - first_name: Sergey Y full_name: Vakhrushev, Sergey Y last_name: Vakhrushev - first_name: Henrik full_name: Clausen, Henrik last_name: Clausen - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 citation: ama: Valosková K, Bicher J, Roblek M, et al. A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion. eLife. 2019;8. doi:10.7554/elife.41801 apa: Valosková, K., Bicher, J., Roblek, M., Emtenani, S., György, A., Misova, M., … Siekhaus, D. E. (2019). A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion. ELife. eLife Sciences Publications. https://doi.org/10.7554/elife.41801 chicago: Valosková, Katarina, Julia Bicher, Marko Roblek, Shamsi Emtenani, Attila György, Michaela Misova, Aparna Ratheesh, et al. “A Conserved Major Facilitator Superfamily Member Orchestrates a Subset of O-Glycosylation to Aid Macrophage Tissue Invasion.” ELife. eLife Sciences Publications, 2019. https://doi.org/10.7554/elife.41801. ieee: K. Valosková et al., “A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion,” eLife, vol. 8. eLife Sciences Publications, 2019. ista: Valosková K, Bicher J, Roblek M, Emtenani S, György A, Misova M, Ratheesh A, Rodrigues P, Shkarina K, Larsen ISB, Vakhrushev SY, Clausen H, Siekhaus DE. 2019. A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion. eLife. 8, e41801. mla: Valosková, Katarina, et al. “A Conserved Major Facilitator Superfamily Member Orchestrates a Subset of O-Glycosylation to Aid Macrophage Tissue Invasion.” ELife, vol. 8, e41801, eLife Sciences Publications, 2019, doi:10.7554/elife.41801. short: K. Valosková, J. Bicher, M. Roblek, S. Emtenani, A. György, M. Misova, A. Ratheesh, P. Rodrigues, K. Shkarina, I.S.B. Larsen, S.Y. Vakhrushev, H. Clausen, D.E. Siekhaus, ELife 8 (2019). date_created: 2019-03-28T13:37:45Z date_published: 2019-03-26T00:00:00Z date_updated: 2024-03-27T23:30:29Z day: '26' ddc: - '570' department: - _id: DaSi doi: 10.7554/elife.41801 ec_funded: 1 external_id: isi: - '000462530200001' file: - access_level: open_access checksum: cc0d1a512559d52e7e7cb0e9b9854b40 content_type: application/pdf creator: dernst date_created: 2019-03-28T14:00:41Z date_updated: 2020-07-14T12:47:23Z file_id: '6188' file_name: 2019_eLife_Valoskova.pdf file_size: 4496017 relation: main_file file_date_updated: 2020-07-14T12:47:23Z has_accepted_license: '1' intvolume: ' 8' isi: 1 language: - iso: eng month: '03' oa: 1 oa_version: Published Version project: - _id: 253CDE40-B435-11E9-9278-68D0E5697425 grant_number: '24283' name: Examination of the role of a MFS transporter in the migration of Drosophila immune cells - _id: 253B6E48-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29638 name: The role of Drosophila TNF alpha in immune cell invasion - _id: 2536F660-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '334077' name: Investigating the role of transporters in invasive migration through junctions - _id: 25388084-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '329540' name: 'Breaking barriers: Investigating the junctional and mechanobiological changes underlying the ability of Drosophila immune cells to invade an epithelium' - _id: 2564DBCA-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '665385' name: International IST Doctoral Program publication: eLife publication_identifier: issn: - 2050-084X publication_status: published publisher: eLife Sciences Publications quality_controlled: '1' related_material: link: - description: News on IST Homepage relation: press_release url: https://ist.ac.at/en/news/new-gene-potentially-involved-in-metastasis-identified/ record: - id: '6530' relation: dissertation_contains - id: '8983' relation: dissertation_contains status: public - id: '6546' relation: dissertation_contains status: public scopus_import: '1' status: public title: A conserved major facilitator superfamily member orchestrates a subset of O-glycosylation to aid macrophage tissue invasion 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: 8 year: '2019' ... --- _id: '6546' abstract: - lang: eng text: "Invasive migration plays a crucial role not only during development and homeostasis but also in pathological states, such as tumor metastasis. Drosophila macrophage migration into the extended germband is an interesting system to study invasive migration. It carries similarities to immune cell transmigration and cancer cell invasion, therefore studying this process could also bring new understanding of invasion in higher organisms. In our work, we uncover a highly conserved member of the major facilitator family that plays a role in tissue invasion through regulation of glycosylation on a subgroup of proteins and/or by aiding the precise timing of DN-Cadherin downregulation. \r\n\r\nAberrant display of the truncated core1 O-glycan T-antigen is a common feature of human cancer cells that correlates with metastasis. Here we show that T-antigen in Drosophila melanogaster macrophages is involved in their developmentally programmed tissue invasion. Higher macrophage T-antigen levels require an atypical major facilitator superfamily (MFS) member that we named Minerva which enables macrophage dissemination and invasion. We characterize for the first time the T and Tn glycoform O-glycoproteome of the Drosophila melanogaster embryo, and determine that Minerva increases the presence of T-antigen on proteins in pathways previously linked to cancer, most strongly on the sulfhydryl oxidase Qsox1 which we show is required for macrophage tissue entry. Minerva’s vertebrate ortholog, MFSD1, rescues the minerva mutant’s migration and T-antigen glycosylation defects. We thus identify \r\na key conserved regulator that orchestrates O-glycosylation on a protein subset to activate \r\na program governing migration steps important for both development and cancer metastasis. \r\n" acknowledged_ssus: - _id: Bio alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Katarina full_name: Valosková, Katarina id: 46F146FC-F248-11E8-B48F-1D18A9856A87 last_name: Valosková citation: ama: Valosková K. The role of a highly conserved major facilitator superfamily member in Drosophila embryonic macrophage migration. 2019. doi:10.15479/AT:ISTA:6546 apa: Valosková, K. (2019). The role of a highly conserved major facilitator superfamily member in Drosophila embryonic macrophage migration. Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:6546 chicago: Valosková, Katarina. “The Role of a Highly Conserved Major Facilitator Superfamily Member in Drosophila Embryonic Macrophage Migration.” Institute of Science and Technology Austria, 2019. https://doi.org/10.15479/AT:ISTA:6546. ieee: K. Valosková, “The role of a highly conserved major facilitator superfamily member in Drosophila embryonic macrophage migration,” Institute of Science and Technology Austria, 2019. ista: Valosková K. 2019. The role of a highly conserved major facilitator superfamily member in Drosophila embryonic macrophage migration. Institute of Science and Technology Austria. mla: Valosková, Katarina. The Role of a Highly Conserved Major Facilitator Superfamily Member in Drosophila Embryonic Macrophage Migration. Institute of Science and Technology Austria, 2019, doi:10.15479/AT:ISTA:6546. short: K. Valosková, The Role of a Highly Conserved Major Facilitator Superfamily Member in Drosophila Embryonic Macrophage Migration, Institute of Science and Technology Austria, 2019. date_created: 2019-06-07T12:49:19Z date_published: 2019-06-07T00:00:00Z date_updated: 2023-09-19T10:15:54Z day: '07' ddc: - '570' degree_awarded: PhD department: - _id: DaSi doi: 10.15479/AT:ISTA:6546 file: - access_level: closed checksum: 68949c2d96210b45b981a23e9c9cd93c content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document creator: khribikova date_created: 2019-06-07T13:00:04Z date_updated: 2020-07-14T12:47:33Z embargo_to: open_access file_id: '6549' file_name: Katarina Valoskova_PhD thesis_final version.docx file_size: 14110626 relation: source_file - access_level: open_access checksum: 555329cd76e196c96f5278c480ee2e6e content_type: application/pdf creator: khribikova date_created: 2019-06-07T13:00:08Z date_updated: 2021-02-11T11:17:14Z embargo: 2020-06-07 file_id: '6550' file_name: Katarina Valoskova_PhD thesis_final version.pdf file_size: 10054156 relation: main_file file_date_updated: 2021-02-11T11:17:14Z has_accepted_license: '1' language: - iso: eng month: '06' oa: 1 oa_version: Published Version page: '141' project: - _id: 253CDE40-B435-11E9-9278-68D0E5697425 grant_number: '24283' name: Examination of the role of a MFS transporter in the migration of Drosophila immune cells publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria related_material: record: - id: '6187' relation: part_of_dissertation status: public - id: '544' relation: part_of_dissertation status: public status: public supervisor: - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 title: The role of a highly conserved major facilitator superfamily member in Drosophila embryonic macrophage migration type: dissertation user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 year: '2019' ... --- _id: '308' abstract: - lang: eng text: Migrating cells penetrate tissue barriers during development, inflammatory responses, and tumor metastasis. We study if migration in vivo in such three-dimensionally confined environments requires changes in the mechanical properties of the surrounding cells using embryonic Drosophila melanogaster hemocytes, also called macrophages, as a model. We find that macrophage invasion into the germband through transient separation of the apposing ectoderm and mesoderm requires cell deformations and reductions in apical tension in the ectoderm. Interestingly, the genetic pathway governing these mechanical shifts acts downstream of the only known tumor necrosis factor superfamily member in Drosophila, Eiger, and its receptor, Grindelwald. Eiger-Grindelwald signaling reduces levels of active Myosin in the germband ectodermal cortex through the localization of a Crumbs complex component, Patj (Pals-1-associated tight junction protein). We therefore elucidate a distinct molecular pathway that controls tissue tension and demonstrate the importance of such regulation for invasive migration in vivo. acknowledged_ssus: - _id: SSU article_processing_charge: No article_type: original author: - first_name: Aparna full_name: Ratheesh, Aparna id: 2F064CFE-F248-11E8-B48F-1D18A9856A87 last_name: Ratheesh orcid: 0000-0001-7190-0776 - first_name: Julia full_name: Biebl, Julia id: 3CCBB46E-F248-11E8-B48F-1D18A9856A87 last_name: Biebl - first_name: Michael full_name: Smutny, Michael last_name: Smutny - first_name: Jana full_name: Veselá, Jana id: 433253EE-F248-11E8-B48F-1D18A9856A87 last_name: Veselá - first_name: Ekaterina full_name: Papusheva, Ekaterina id: 41DB591E-F248-11E8-B48F-1D18A9856A87 last_name: Papusheva - first_name: Gabriel full_name: Krens, Gabriel id: 2B819732-F248-11E8-B48F-1D18A9856A87 last_name: Krens orcid: 0000-0003-4761-5996 - first_name: Walter full_name: Kaufmann, Walter id: 3F99E422-F248-11E8-B48F-1D18A9856A87 last_name: Kaufmann orcid: 0000-0001-9735-5315 - first_name: Attila full_name: György, Attila id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87 last_name: György orcid: 0000-0002-1819-198X - 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: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 citation: ama: Ratheesh A, Bicher J, Smutny M, et al. Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration. Developmental Cell. 2018;45(3):331-346. doi:10.1016/j.devcel.2018.04.002 apa: Ratheesh, A., Bicher, J., Smutny, M., Veselá, J., Papusheva, E., Krens, G., … Siekhaus, D. E. (2018). Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration. Developmental Cell. Elsevier. https://doi.org/10.1016/j.devcel.2018.04.002 chicago: Ratheesh, Aparna, Julia Bicher, Michael Smutny, Jana Veselá, Ekaterina Papusheva, Gabriel Krens, Walter Kaufmann, Attila György, Alessandra M Casano, and Daria E Siekhaus. “Drosophila TNF Modulates Tissue Tension in the Embryo to Facilitate Macrophage Invasive Migration.” Developmental Cell. Elsevier, 2018. https://doi.org/10.1016/j.devcel.2018.04.002. ieee: A. Ratheesh et al., “Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration,” Developmental Cell, vol. 45, no. 3. Elsevier, pp. 331–346, 2018. ista: Ratheesh A, Bicher J, Smutny M, Veselá J, Papusheva E, Krens G, Kaufmann W, György A, Casano AM, Siekhaus DE. 2018. Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration. Developmental Cell. 45(3), 331–346. mla: Ratheesh, Aparna, et al. “Drosophila TNF Modulates Tissue Tension in the Embryo to Facilitate Macrophage Invasive Migration.” Developmental Cell, vol. 45, no. 3, Elsevier, 2018, pp. 331–46, doi:10.1016/j.devcel.2018.04.002. short: A. Ratheesh, J. Bicher, M. Smutny, J. Veselá, E. Papusheva, G. Krens, W. Kaufmann, A. György, A.M. Casano, D.E. Siekhaus, Developmental Cell 45 (2018) 331–346. date_created: 2018-12-11T11:45:44Z date_published: 2018-05-07T00:00:00Z date_updated: 2023-09-11T13:22:13Z day: '07' department: - _id: DaSi - _id: CaHe - _id: Bio - _id: EM-Fac - _id: MiSi doi: 10.1016/j.devcel.2018.04.002 ec_funded: 1 external_id: isi: - '000432461400009' pmid: - '29738712' intvolume: ' 45' isi: 1 issue: '3' language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1016/j.devcel.2018.04.002 month: '05' oa: 1 oa_version: Published Version page: 331 - 346 pmid: 1 project: - _id: 253B6E48-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29638 name: Drosophila TNFa´s Funktion in Immunzellen - _id: 2536F660-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '334077' name: Investigating the role of transporters in invasive migration through junctions publication: Developmental Cell publication_status: published publisher: Elsevier quality_controlled: '1' related_material: link: - description: News on IST Homepage relation: press_release url: https://ist.ac.at/en/news/cells-change-tension-to-make-tissue-barriers-easier-to-get-through/ scopus_import: '1' status: public title: Drosophila TNF modulates tissue tension in the embryo to facilitate macrophage invasive migration type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 45 year: '2018' ... --- _id: '620' abstract: - lang: eng text: Clathrin-mediated endocytosis requires the coordinated assembly of various endocytic proteins and lipids at the plasma membrane. Accumulating evidence demonstrates a crucial role for phosphatidylinositol-4,5-bisphosphate (PtdIns(4,5)P2) in endocytosis, but specific roles for PtdIns(4)P other than as the biosynthetic precursor of PtdIns(4,5)P2 have not been clarified. In this study we investigated the role of PtdIns(4)P or PtdIns(4,5)P2 in receptor-mediated endocytosis through the construction of temperature-sensitive (ts) mutants for the PI 4-kinases Stt4p and Pik1p and the PtdIns(4) 5-kinase Mss4p. Quantitative analyses of endocytosis revealed that both the stt4(ts)pik1(ts) and mss4(ts) mutants have a severe defect in endocytic internalization. Live-cell imaging of endocytic protein dynamics in stt4(ts)pik1(ts) and mss4(ts) mutants revealed that PtdIns(4)P is required for the recruitment of the alpha-factor receptor Ste2p to clathrin-coated pits whereas PtdIns(4,5)P2 is required for membrane internalization. We also found that the localization to endocytic sites of the ENTH/ANTH domain-bearing clathrin adaptors, Ent1p/Ent2p and Yap1801p/Yap1802p, is significantly impaired in the stt4(ts)pik1(ts) mutant, but not in the mss4(ts) mutant. These results suggest distinct roles in successive steps for PtdIns(4)P and PtdIns(4,5)P2 during receptor-mediated endocytosis. article_number: jcs207696 article_processing_charge: No author: - first_name: Wataru full_name: Yamamoto, Wataru last_name: Yamamoto - first_name: Suguru full_name: Wada, Suguru last_name: Wada - first_name: Makoto full_name: Nagano, Makoto last_name: Nagano - first_name: Kaito full_name: Aoshima, Kaito last_name: Aoshima - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 - first_name: Junko full_name: Toshima, Junko last_name: Toshima - first_name: Jiro full_name: Toshima, Jiro last_name: Toshima citation: ama: Yamamoto W, Wada S, Nagano M, et al. Distinct roles for plasma membrane PtdIns 4 P and PtdIns 4 5 P2 during yeast receptor mediated endocytosis. Journal of Cell Science. 2018;131(1). doi:10.1242/jcs.207696 apa: Yamamoto, W., Wada, S., Nagano, M., Aoshima, K., Siekhaus, D. E., Toshima, J., & Toshima, J. (2018). Distinct roles for plasma membrane PtdIns 4 P and PtdIns 4 5 P2 during yeast receptor mediated endocytosis. Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.207696 chicago: Yamamoto, Wataru, Suguru Wada, Makoto Nagano, Kaito Aoshima, Daria E Siekhaus, Junko Toshima, and Jiro Toshima. “Distinct Roles for Plasma Membrane PtdIns 4 P and PtdIns 4 5 P2 during Yeast Receptor Mediated Endocytosis.” Journal of Cell Science. Company of Biologists, 2018. https://doi.org/10.1242/jcs.207696. ieee: W. Yamamoto et al., “Distinct roles for plasma membrane PtdIns 4 P and PtdIns 4 5 P2 during yeast receptor mediated endocytosis,” Journal of Cell Science, vol. 131, no. 1. Company of Biologists, 2018. ista: Yamamoto W, Wada S, Nagano M, Aoshima K, Siekhaus DE, Toshima J, Toshima J. 2018. Distinct roles for plasma membrane PtdIns 4 P and PtdIns 4 5 P2 during yeast receptor mediated endocytosis. Journal of Cell Science. 131(1), jcs207696. mla: Yamamoto, Wataru, et al. “Distinct Roles for Plasma Membrane PtdIns 4 P and PtdIns 4 5 P2 during Yeast Receptor Mediated Endocytosis.” Journal of Cell Science, vol. 131, no. 1, jcs207696, Company of Biologists, 2018, doi:10.1242/jcs.207696. short: W. Yamamoto, S. Wada, M. Nagano, K. Aoshima, D.E. Siekhaus, J. Toshima, J. Toshima, Journal of Cell Science 131 (2018). date_created: 2018-12-11T11:47:32Z date_published: 2018-01-04T00:00:00Z date_updated: 2023-09-11T12:57:13Z day: '04' department: - _id: DaSi doi: 10.1242/jcs.207696 external_id: isi: - '000424786900012' pmid: - '29192062' intvolume: ' 131' isi: 1 issue: '1' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pubmed/29192062 month: '01' oa: 1 oa_version: Published Version pmid: 1 publication: Journal of Cell Science publication_status: published publisher: Company of Biologists publist_id: '7184' quality_controlled: '1' scopus_import: '1' status: public title: Distinct roles for plasma membrane PtdIns 4 P and PtdIns 4 5 P2 during yeast receptor mediated endocytosis type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 131 year: '2018' ... --- _id: '192' abstract: - lang: eng text: The phytohormone auxin is the information carrier in a plethora of developmental and physiological processes in plants(1). It has been firmly established that canonical, nuclear auxin signalling acts through regulation of gene transcription(2). Here, we combined microfluidics, live imaging, genetic engineering and computational modelling to reanalyse the classical case of root growth inhibition(3) by auxin. We show that Arabidopsis roots react to addition and removal of auxin by extremely rapid adaptation of growth rate. This process requires intracellular auxin perception but not transcriptional reprogramming. The formation of the canonical TIR1/AFB-Aux/IAA co-receptor complex is required for the growth regulation, hinting to a novel, non-transcriptional branch of this signalling pathway. Our results challenge the current understanding of root growth regulation by auxin and suggest another, presumably non-transcriptional, signalling output of the canonical auxin pathway. article_processing_charge: No article_type: original author: - first_name: Matyas full_name: Fendrych, Matyas id: 43905548-F248-11E8-B48F-1D18A9856A87 last_name: Fendrych orcid: 0000-0002-9767-8699 - first_name: Maria full_name: Akhmanova, Maria id: 3425EC26-F248-11E8-B48F-1D18A9856A87 last_name: Akhmanova orcid: 0000-0003-1522-3162 - first_name: Jack full_name: Merrin, Jack id: 4515C308-F248-11E8-B48F-1D18A9856A87 last_name: Merrin orcid: 0000-0001-5145-4609 - first_name: Matous full_name: Glanc, Matous last_name: Glanc - first_name: Shinya full_name: Hagihara, Shinya last_name: Hagihara - first_name: Koji full_name: Takahashi, Koji last_name: Takahashi - first_name: Naoyuki full_name: Uchida, Naoyuki last_name: Uchida - first_name: Keiko U full_name: Torii, Keiko U last_name: Torii - first_name: Jirí full_name: Friml, Jirí id: 4159519E-F248-11E8-B48F-1D18A9856A87 last_name: Friml orcid: 0000-0002-8302-7596 citation: ama: Fendrych M, Akhmanova M, Merrin J, et al. Rapid and reversible root growth inhibition by TIR1 auxin signalling. Nature Plants. 2018;4(7):453-459. doi:10.1038/s41477-018-0190-1 apa: Fendrych, M., Akhmanova, M., Merrin, J., Glanc, M., Hagihara, S., Takahashi, K., … Friml, J. (2018). Rapid and reversible root growth inhibition by TIR1 auxin signalling. Nature Plants. Springer Nature. https://doi.org/10.1038/s41477-018-0190-1 chicago: Fendrych, Matyas, Maria Akhmanova, Jack Merrin, Matous Glanc, Shinya Hagihara, Koji Takahashi, Naoyuki Uchida, Keiko U Torii, and Jiří Friml. “Rapid and Reversible Root Growth Inhibition by TIR1 Auxin Signalling.” Nature Plants. Springer Nature, 2018. https://doi.org/10.1038/s41477-018-0190-1. ieee: M. Fendrych et al., “Rapid and reversible root growth inhibition by TIR1 auxin signalling,” Nature Plants, vol. 4, no. 7. Springer Nature, pp. 453–459, 2018. ista: Fendrych M, Akhmanova M, Merrin J, Glanc M, Hagihara S, Takahashi K, Uchida N, Torii KU, Friml J. 2018. Rapid and reversible root growth inhibition by TIR1 auxin signalling. Nature Plants. 4(7), 453–459. mla: Fendrych, Matyas, et al. “Rapid and Reversible Root Growth Inhibition by TIR1 Auxin Signalling.” Nature Plants, vol. 4, no. 7, Springer Nature, 2018, pp. 453–59, doi:10.1038/s41477-018-0190-1. short: M. Fendrych, M. Akhmanova, J. Merrin, M. Glanc, S. Hagihara, K. Takahashi, N. Uchida, K.U. Torii, J. Friml, Nature Plants 4 (2018) 453–459. date_created: 2018-12-11T11:45:07Z date_published: 2018-06-25T00:00:00Z date_updated: 2023-09-15T12:11:03Z day: '25' department: - _id: JiFr - _id: DaSi - _id: NanoFab doi: 10.1038/s41477-018-0190-1 external_id: isi: - '000443221200017' pmid: - '29942048' intvolume: ' 4' isi: 1 issue: '7' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pubmed/29942048 month: '06' oa: 1 oa_version: Submitted Version page: 453 - 459 pmid: 1 publication: Nature Plants publication_status: published publisher: Springer Nature publist_id: '7728' quality_controlled: '1' related_material: link: - description: News on IST Homepage relation: press_release url: https://ist.ac.at/en/news/new-mechanism-for-the-plant-hormone-auxin-discovered/ scopus_import: '1' status: public title: Rapid and reversible root growth inhibition by TIR1 auxin signalling type: journal_article user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 4 year: '2018' ... --- _id: '14' abstract: - lang: eng text: The intercellular transport of auxin is driven by PIN-formed (PIN) auxin efflux carriers. PINs are localized at the plasma membrane (PM) and on constitutively recycling endomembrane vesicles. Therefore, PINs can mediate auxin transport either by direct translocation across the PM or by pumping auxin into secretory vesicles (SVs), leading to its secretory release upon fusion with the PM. Which of these two mechanisms dominates is a matter of debate. Here, we addressed the issue with a mathematical modeling approach. We demonstrate that the efficiency of secretory transport depends on SV size, half-life of PINs on the PM, pH, exocytosis frequency and PIN density. 3D structured illumination microscopy (SIM) was used to determine PIN density on the PM. Combining this data with published values of the other parameters, we show that the transport activity of PINs in SVs would have to be at least 1000× greater than on the PM in order to produce a comparable macroscopic auxin transport. If both transport mechanisms operated simultaneously and PINs were equally active on SVs and PM, the contribution of secretion to the total auxin flux would be negligible. In conclusion, while secretory vesicle-mediated transport of auxin is an intriguing and theoretically possible model, it is unlikely to be a major mechanism of auxin transport inplanta. acknowledgement: 'European Research Council (ERC): 742985 to Jiri Friml; M.A. was supported by the Austrian Science Fund (FWF) (M2379-B28); AJ was supported by the Austria Science Fund (FWF): I03630 to Jiri Friml.' article_processing_charge: No article_type: original author: - first_name: Sander full_name: Hille, Sander last_name: Hille - first_name: Maria full_name: Akhmanova, Maria id: 3425EC26-F248-11E8-B48F-1D18A9856A87 last_name: Akhmanova orcid: 0000-0003-1522-3162 - first_name: Matous full_name: Glanc, Matous id: 1AE1EA24-02D0-11E9-9BAA-DAF4881429F2 last_name: Glanc orcid: 0000-0003-0619-7783 - first_name: Alexander J full_name: Johnson, Alexander J id: 46A62C3A-F248-11E8-B48F-1D18A9856A87 last_name: Johnson orcid: 0000-0002-2739-8843 - first_name: Jirí full_name: Friml, Jirí id: 4159519E-F248-11E8-B48F-1D18A9856A87 last_name: Friml orcid: 0000-0002-8302-7596 citation: ama: 'Hille S, Akhmanova M, Glanc M, Johnson AJ, Friml J. Relative contribution of PIN-containing secretory vesicles and plasma membrane PINs to the directed auxin transport: Theoretical estimation. International Journal of Molecular Sciences. 2018;19(11). doi:10.3390/ijms19113566' apa: 'Hille, S., Akhmanova, M., Glanc, M., Johnson, A. J., & Friml, J. (2018). Relative contribution of PIN-containing secretory vesicles and plasma membrane PINs to the directed auxin transport: Theoretical estimation. International Journal of Molecular Sciences. MDPI. https://doi.org/10.3390/ijms19113566' chicago: 'Hille, Sander, Maria Akhmanova, Matous Glanc, Alexander J Johnson, and Jiří Friml. “Relative Contribution of PIN-Containing Secretory Vesicles and Plasma Membrane PINs to the Directed Auxin Transport: Theoretical Estimation.” International Journal of Molecular Sciences. MDPI, 2018. https://doi.org/10.3390/ijms19113566.' ieee: 'S. Hille, M. Akhmanova, M. Glanc, A. J. Johnson, and J. Friml, “Relative contribution of PIN-containing secretory vesicles and plasma membrane PINs to the directed auxin transport: Theoretical estimation,” International Journal of Molecular Sciences, vol. 19, no. 11. MDPI, 2018.' ista: 'Hille S, Akhmanova M, Glanc M, Johnson AJ, Friml J. 2018. Relative contribution of PIN-containing secretory vesicles and plasma membrane PINs to the directed auxin transport: Theoretical estimation. International Journal of Molecular Sciences. 19(11).' mla: 'Hille, Sander, et al. “Relative Contribution of PIN-Containing Secretory Vesicles and Plasma Membrane PINs to the Directed Auxin Transport: Theoretical Estimation.” International Journal of Molecular Sciences, vol. 19, no. 11, MDPI, 2018, doi:10.3390/ijms19113566.' short: S. Hille, M. Akhmanova, M. Glanc, A.J. Johnson, J. Friml, International Journal of Molecular Sciences 19 (2018). date_created: 2018-12-11T11:44:09Z date_published: 2018-11-12T00:00:00Z date_updated: 2023-09-18T08:09:32Z day: '12' ddc: - '580' department: - _id: DaSi - _id: JiFr doi: 10.3390/ijms19113566 ec_funded: 1 external_id: isi: - '000451528500282' file: - access_level: open_access checksum: e4b59c2599b0ca26ebf5b8434bcde94a content_type: application/pdf creator: dernst date_created: 2018-12-17T16:04:11Z date_updated: 2020-07-14T12:44:50Z file_id: '5719' file_name: 2018_IJMS_Hille.pdf file_size: 2200593 relation: main_file file_date_updated: 2020-07-14T12:44:50Z has_accepted_license: '1' intvolume: ' 19' isi: 1 issue: '11' language: - iso: eng month: '11' oa: 1 oa_version: Published Version project: - _id: 261099A6-B435-11E9-9278-68D0E5697425 call_identifier: H2020 grant_number: '742985' name: Tracing Evolution of Auxin Transport and Polarity in Plants - _id: 26538374-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: I03630 name: Molecular mechanisms of endocytic cargo recognition in plants publication: International Journal of Molecular Sciences publication_identifier: eissn: - 1422-0067 publication_status: published publisher: MDPI publist_id: '8042' quality_controlled: '1' scopus_import: '1' status: public title: 'Relative contribution of PIN-containing secretory vesicles and plasma membrane PINs to the directed auxin transport: Theoretical estimation' 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: 19 year: '2018' ... --- _id: '9' abstract: - lang: eng text: 'Immune cells migrating to the sites of infection navigate through diverse tissue architectures and switch their migratory mechanisms upon demand. However, little is known about systemic regulators that could allow the acquisition of these mechanisms. We performed a genetic screen in Drosophila melanogaster to identify regulators of germband invasion by embryonic macrophages into the confined space between the ectoderm and mesoderm. We have found that bZIP circadian transcription factors (TFs) Kayak (dFos) and Vrille (dNFIL3) have opposite effects on macrophage germband infiltration: Kayak facilitated and Vrille inhibited it. These TFs are enriched in the macrophages during migration and genetically interact to control it. Kayak sets a less coordinated mode of migration of the macrophage group and increases the probability and length of Levy walks. Intriguingly, the motility of kayak mutant macrophages was also strongly affected during initial germband invasion but not along another less confined route. Inhibiting Rho1 signaling within the tail ectoderm partially rescued the Kayak mutant phenotype, strongly suggesting that migrating macrophages have to overcome a barrier imposed by the stiffness of the ectoderm. Also, Kayak appeared to be important for the maintenance of the round cell shape and the rear edge translocation of the macrophages invading the germband. Complementary to this, the cortical actin cytoskeleton of Kayak- deficient macrophages was strongly affected. RNA sequencing revealed the filamin Cheerio and tetraspanin TM4SF to be downstream of Kayak. Chromatin immunoprecipitation and immunostaining revealed that the formin Diaphanous is another downstream target of Kayak. Immunostaining revealed that the formin Diaphanous is another downstream target of Kayak. Indeed, Cheerio, TM4SF and Diaphanous are required within macrophages for germband invasion, and expression of constitutively active Diaphanous in macrophages was able to rescue the kayak mutant phenotype. Moreover, Cher and Diaphanous are also reduced in the macrophages overexpressing Vrille. We hypothesize that Kayak, through its targets, increases actin polymerization and cortical tension in macrophages and thus allows extra force generation necessary for macrophage dissemination and migration through confined stiff tissues, while Vrille counterbalances it.' alternative_title: - ISTA Thesis article_processing_charge: No author: - first_name: Vera full_name: Belyaeva, Vera id: 47F080FE-F248-11E8-B48F-1D18A9856A87 last_name: Belyaeva citation: ama: Belyaeva V. Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo . 2018. doi:10.15479/AT:ISTA:th1064 apa: Belyaeva, V. (2018). Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo . Institute of Science and Technology Austria. https://doi.org/10.15479/AT:ISTA:th1064 chicago: Belyaeva, Vera. “Transcriptional Regulation of Macrophage Migration in the Drosophila Melanogaster Embryo .” Institute of Science and Technology Austria, 2018. https://doi.org/10.15479/AT:ISTA:th1064. ieee: V. Belyaeva, “Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo ,” Institute of Science and Technology Austria, 2018. ista: Belyaeva V. 2018. Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo . Institute of Science and Technology Austria. mla: Belyaeva, Vera. Transcriptional Regulation of Macrophage Migration in the Drosophila Melanogaster Embryo . Institute of Science and Technology Austria, 2018, doi:10.15479/AT:ISTA:th1064. short: V. Belyaeva, Transcriptional Regulation of Macrophage Migration in the Drosophila Melanogaster Embryo , Institute of Science and Technology Austria, 2018. date_created: 2018-12-11T11:44:08Z date_published: 2018-07-01T00:00:00Z date_updated: 2023-09-07T12:43:10Z day: '01' ddc: - '570' degree_awarded: PhD department: - _id: DaSi doi: 10.15479/AT:ISTA:th1064 file: - access_level: closed checksum: d27b2465cb70d0c9678a0381b9b6ced1 content_type: application/vnd.openxmlformats-officedocument.wordprocessingml.document creator: dernst date_created: 2019-04-08T14:13:12Z date_updated: 2020-07-14T12:48:14Z embargo_to: open_access file_id: '6243' file_name: 2018_Thesis_Belyaeva_source.docx file_size: 102737483 relation: source_file - access_level: open_access checksum: a2939b61bde2de7b8ced77bbae0eaaed content_type: application/pdf creator: dernst date_created: 2019-04-08T14:14:08Z date_updated: 2021-02-11T11:17:16Z embargo: 2019-11-19 file_id: '6244' file_name: 2018_Thesis_Belyaeva.pdf file_size: 88077843 relation: main_file file_date_updated: 2021-02-11T11:17:16Z has_accepted_license: '1' language: - iso: eng month: '07' oa: 1 oa_version: Published Version page: '96' publication_identifier: issn: - 2663-337X publication_status: published publisher: Institute of Science and Technology Austria publist_id: '8047' pubrep_id: '1064' status: public supervisor: - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 title: 'Transcriptional regulation of macrophage migration in the Drosophila melanogaster embryo ' type: dissertation user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 year: '2018' ... --- _id: '544' abstract: - lang: eng text: Drosophila melanogaster plasmatocytes, the phagocytic cells among hemocytes, are essential for immune responses, but also play key roles from early development to death through their interactions with other cell types. They regulate homeostasis and signaling during development, stem cell proliferation, metabolism, cancer, wound responses and aging, displaying intriguing molecular and functional conservation with vertebrate macrophages. Given the relative ease of genetics in Drosophila compared to vertebrates, tools permitting visualization and genetic manipulation of plasmatocytes and surrounding tissues independently at all stages would greatly aid in fully understanding these processes, but are lacking. Here we describe a comprehensive set of transgenic lines that allow this. These include extremely brightly fluorescing mCherry-based lines that allow GAL4-independent visualization of plasmatocyte nuclei, cytoplasm or actin cytoskeleton from embryonic Stage 8 through adulthood in both live and fixed samples even as heterozygotes, greatly facilitating screening. These lines allow live visualization and tracking of embryonic plasmatocytes, as well as larval plasmatocytes residing at the body wall or flowing with the surrounding hemolymph. With confocal imaging, interactions of plasmatocytes and inner tissues can be seen in live or fixed embryos, larvae and adults. They permit efficient GAL4-independent FACS analysis/sorting of plasmatocytes throughout life. To facilitate genetic analysis of reciprocal signaling, we have also made a plasmatocyte-expressing QF2 line that in combination with extant GAL4 drivers allows independent genetic manipulation of both plasmatocytes and surrounding tissues, and a GAL80 line that blocks GAL4 drivers from affecting plasmatocytes, both of which function from the early embryo to the adult. acknowledged_ssus: - _id: LifeSc acknowledgement: ' A. Ratheesh also by Marie Curie IIF GA-2012-32950BB:DICJI, Marko Roblek by the provincial government of Lower Austria, K. Valoskova and S. Wachner by DOC Fellowships from the Austrian Academy of Sciences, ' article_processing_charge: No author: - first_name: Attila full_name: György, Attila id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87 last_name: György orcid: 0000-0002-1819-198X - first_name: Marko full_name: Roblek, Marko id: 3047D808-F248-11E8-B48F-1D18A9856A87 last_name: Roblek orcid: 0000-0001-9588-1389 - first_name: Aparna full_name: Ratheesh, Aparna id: 2F064CFE-F248-11E8-B48F-1D18A9856A87 last_name: Ratheesh orcid: 0000-0001-7190-0776 - first_name: Katarina full_name: Valosková, Katarina id: 46F146FC-F248-11E8-B48F-1D18A9856A87 last_name: Valosková - first_name: Vera full_name: Belyaeva, Vera id: 47F080FE-F248-11E8-B48F-1D18A9856A87 last_name: Belyaeva - first_name: Stephanie full_name: Wachner, Stephanie id: 2A95E7B0-F248-11E8-B48F-1D18A9856A87 last_name: Wachner - first_name: Yutaka full_name: Matsubayashi, Yutaka last_name: Matsubayashi - first_name: Besaiz full_name: Sanchez Sanchez, Besaiz last_name: Sanchez Sanchez - first_name: Brian full_name: Stramer, Brian last_name: Stramer - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 citation: ama: 'György A, Roblek M, Ratheesh A, et al. Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues. G3: Genes, Genomes, Genetics. 2018;8(3):845-857. doi:10.1534/g3.117.300452' apa: 'György, A., Roblek, M., Ratheesh, A., Valosková, K., Belyaeva, V., Wachner, S., … Siekhaus, D. E. (2018). Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues. G3: Genes, Genomes, Genetics. Genetics Society of America. https://doi.org/10.1534/g3.117.300452' chicago: 'György, Attila, Marko Roblek, Aparna Ratheesh, Katarina Valosková, Vera Belyaeva, Stephanie Wachner, Yutaka Matsubayashi, Besaiz Sanchez Sanchez, Brian Stramer, and Daria E Siekhaus. “Tools Allowing Independent Visualization and Genetic Manipulation of Drosophila Melanogaster Macrophages and Surrounding Tissues.” G3: Genes, Genomes, Genetics. Genetics Society of America, 2018. https://doi.org/10.1534/g3.117.300452.' ieee: 'A. György et al., “Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues,” G3: Genes, Genomes, Genetics, vol. 8, no. 3. Genetics Society of America, pp. 845–857, 2018.' ista: 'György A, Roblek M, Ratheesh A, Valosková K, Belyaeva V, Wachner S, Matsubayashi Y, Sanchez Sanchez B, Stramer B, Siekhaus DE. 2018. Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues. G3: Genes, Genomes, Genetics. 8(3), 845–857.' mla: 'György, Attila, et al. “Tools Allowing Independent Visualization and Genetic Manipulation of Drosophila Melanogaster Macrophages and Surrounding Tissues.” G3: Genes, Genomes, Genetics, vol. 8, no. 3, Genetics Society of America, 2018, pp. 845–57, doi:10.1534/g3.117.300452.' short: 'A. György, M. Roblek, A. Ratheesh, K. Valosková, V. Belyaeva, S. Wachner, Y. Matsubayashi, B. Sanchez Sanchez, B. Stramer, D.E. Siekhaus, G3: Genes, Genomes, Genetics 8 (2018) 845–857.' date_created: 2018-12-11T11:47:05Z date_published: 2018-03-01T00:00:00Z date_updated: 2024-03-27T23:30:29Z day: '01' ddc: - '570' department: - _id: DaSi doi: 10.1534/g3.117.300452 ec_funded: 1 external_id: isi: - '000426693300011' file: - access_level: open_access checksum: 7d9d28b915159078a4ca7add568010e8 content_type: application/pdf creator: system date_created: 2018-12-12T10:11:48Z date_updated: 2020-07-14T12:46:56Z file_id: '4905' file_name: IST-2018-990-v1+1_2018_Gyoergy_Tools_allowing.pdf file_size: 2251222 relation: main_file file_date_updated: 2020-07-14T12:46:56Z has_accepted_license: '1' intvolume: ' 8' isi: 1 issue: '3' language: - iso: eng month: '03' oa: 1 oa_version: Published Version page: 845 - 857 project: - _id: 253B6E48-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29638 name: Drosophila TNFa´s Funktion in Immunzellen - _id: 253B6E48-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: P29638 name: The role of Drosophila TNF alpha in immune cell invasion - _id: 2637E9C0-B435-11E9-9278-68D0E5697425 grant_number: 'LSC16-021 ' name: Investigating the role of the novel major superfamily facilitator transporter family member MFSD1 in metastasis - _id: 2536F660-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '334077' name: Investigating the role of transporters in invasive migration through junctions publication: 'G3: Genes, Genomes, Genetics' publication_status: published publisher: Genetics Society of America publist_id: '7271' pubrep_id: '990' quality_controlled: '1' related_material: record: - id: '6530' relation: research_paper - id: '6543' relation: research_paper - id: '11193' relation: dissertation_contains status: public - id: '6546' relation: dissertation_contains status: public scopus_import: '1' status: public title: Tools allowing independent visualization and genetic manipulation of Drosophila melanogaster macrophages and surrounding tissues 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: 8 year: '2018' ... --- _id: '751' abstract: - lang: eng text: The basement membrane (BM) is a thin layer of extracellular matrix (ECM) beneath nearly all epithelial cell types that is critical for cellular and tissue function. It is composed of numerous components conserved among all bilaterians [1]; however, it is unknown how all of these components are generated and subsequently constructed to form a fully mature BM in the living animal. Although BM formation is thought to simply involve a process of self-assembly [2], this concept suffers from a number of logistical issues when considering its construction in vivo. First, incorporation of BM components appears to be hierarchical [3-5], yet it is unclear whether their production during embryogenesis must also be regulated in a temporal fashion. Second, many BM proteins are produced not only by the cells residing on the BM but also by surrounding cell types [6-9], and it is unclear how large, possibly insoluble protein complexes [10] are delivered into the matrix. Here we exploit our ability to live image and genetically dissect de novo BM formation during Drosophila development. This reveals that there is a temporal hierarchy of BM protein production that is essential for proper component incorporation. Furthermore, we show that BM components require secretion by migrating macrophages (hemocytes) during their developmental dispersal, which is critical for embryogenesis. Indeed, hemocyte migration is essential to deliver a subset of ECM components evenly throughout the embryo. This reveals that de novo BM construction requires a combination of both production and distribution logistics allowing for the timely delivery of core components. article_processing_charge: No author: - first_name: Yutaka full_name: Matsubayashi, Yutaka last_name: Matsubayashi - first_name: Adam full_name: Louani, Adam last_name: Louani - first_name: Anca full_name: Dragu, Anca last_name: Dragu - first_name: Besaiz full_name: Sanchez Sanchez, Besaiz last_name: Sanchez Sanchez - first_name: Eduardo full_name: Serna Morales, Eduardo last_name: Serna Morales - first_name: Lawrence full_name: Yolland, Lawrence last_name: Yolland - first_name: Attila full_name: György, Attila id: 3BCEDBE0-F248-11E8-B48F-1D18A9856A87 last_name: György orcid: 0000-0002-1819-198X - first_name: Gema full_name: Vizcay, Gema last_name: Vizcay - first_name: Roland full_name: Fleck, Roland last_name: Fleck - first_name: John full_name: Heddleston, John last_name: Heddleston - first_name: Teng full_name: Chew, Teng last_name: Chew - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 - first_name: Brian full_name: Stramer, Brian last_name: Stramer citation: ama: Matsubayashi Y, Louani A, Dragu A, et al. A moving source of matrix components is essential for De Novo basement membrane formation. Current Biology. 2017;27(22):3526-3534e.4. doi:10.1016/j.cub.2017.10.001 apa: Matsubayashi, Y., Louani, A., Dragu, A., Sanchez Sanchez, B., Serna Morales, E., Yolland, L., … Stramer, B. (2017). A moving source of matrix components is essential for De Novo basement membrane formation. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2017.10.001 chicago: Matsubayashi, Yutaka, Adam Louani, Anca Dragu, Besaiz Sanchez Sanchez, Eduardo Serna Morales, Lawrence Yolland, Attila György, et al. “A Moving Source of Matrix Components Is Essential for De Novo Basement Membrane Formation.” Current Biology. Cell Press, 2017. https://doi.org/10.1016/j.cub.2017.10.001. ieee: Y. Matsubayashi et al., “A moving source of matrix components is essential for De Novo basement membrane formation,” Current Biology, vol. 27, no. 22. Cell Press, p. 3526–3534e.4, 2017. ista: Matsubayashi Y, Louani A, Dragu A, Sanchez Sanchez B, Serna Morales E, Yolland L, György A, Vizcay G, Fleck R, Heddleston J, Chew T, Siekhaus DE, Stramer B. 2017. A moving source of matrix components is essential for De Novo basement membrane formation. Current Biology. 27(22), 3526–3534e.4. mla: Matsubayashi, Yutaka, et al. “A Moving Source of Matrix Components Is Essential for De Novo Basement Membrane Formation.” Current Biology, vol. 27, no. 22, Cell Press, 2017, p. 3526–3534e.4, doi:10.1016/j.cub.2017.10.001. short: Y. Matsubayashi, A. Louani, A. Dragu, B. Sanchez Sanchez, E. Serna Morales, L. Yolland, A. György, G. Vizcay, R. Fleck, J. Heddleston, T. Chew, D.E. Siekhaus, B. Stramer, Current Biology 27 (2017) 3526–3534e.4. date_created: 2018-12-11T11:48:18Z date_published: 2017-11-09T00:00:00Z date_updated: 2023-09-27T12:25:31Z day: '09' ddc: - '570' - '576' department: - _id: DaSi doi: 10.1016/j.cub.2017.10.001 external_id: isi: - '000415815800031' file: - access_level: open_access checksum: 264cf6c6c3551486ba5ea786850e000a content_type: application/pdf creator: system date_created: 2018-12-12T10:09:45Z date_updated: 2020-07-14T12:47:59Z file_id: '4770' file_name: IST-2017-875-v1+1_1-s2.0-S0960982217312691-main.pdf file_size: 4770657 relation: main_file file_date_updated: 2020-07-14T12:47:59Z has_accepted_license: '1' intvolume: ' 27' isi: 1 issue: '22' language: - iso: eng month: '11' oa: 1 oa_version: Published Version page: 3526 - 3534e.4 publication: Current Biology publication_identifier: issn: - '09609822' publication_status: published publisher: Cell Press publist_id: '6905' pubrep_id: '875' quality_controlled: '1' scopus_import: '1' status: public title: A moving source of matrix components is essential for De Novo basement membrane formation 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: 27 year: '2017' ... --- _id: '1476' abstract: - lang: eng text: The dynamic assembly and disassembly of actin filaments is essential for the formation and transport of vesicles during endocytosis. In yeast, two types of actin structures, namely cortical patches and cytoplasmic cables, play a direct role in endocytosis, but how their interaction is regulated remains unclear. Here, we show that Srv2/CAP, an evolutionarily conserved actin regulator, is required for efficient endocytosis owing to its role in the formation of the actin patches that aid initial vesicle invagination and of the actin cables that these move along. Deletion of the SRV2 gene resulted in the appearance of aberrant fragmented actin cables that frequently moved past actin patches, the sites of endocytosis. We find that the C-terminal CARP domain of Srv2p is vitally important for the proper assembly of actin patches and cables; we also demonstrate that the N-terminal helical folded domain of Srv2 is required for its localization to actin patches, specifically to the ADP-actin rich region through an interaction with cofilin. These results demonstrate the in vivo roles of Srv2p in the regulation of the actin cytoskeleton during clathrin-mediated endocytosis acknowledgement: We are grateful to Anthony Bretscher (Cornell University, NY) for providing the bni1-12 bnr1Δ (Y4135) strain. J.Y.T. was supported by a Japan Society for the Promotion of Science (JSPS) KAKENHI grant [grant number 26440067]; the Takeda Science Foundation; and the Novartis Foundation (Japan). J.T. was supported by a JSPS KAKENHI grant [grant number 25440054]; the Takeda Science Foundation; and the Kurata Memorial Hitachi Science and Technology Foundation. D.E.S. was supported by the European Union [grant number PCIG12-GA-2012-334077]. author: - first_name: Junko full_name: Toshima, Junko last_name: Toshima - first_name: Chika full_name: Horikomi, Chika last_name: Horikomi - first_name: Asuka full_name: Okada, Asuka last_name: Okada - first_name: Makiko full_name: Hatori, Makiko last_name: Hatori - first_name: Makoto full_name: Nagano, Makoto last_name: Nagano - first_name: Atsushi full_name: Masuda, Atsushi last_name: Masuda - first_name: Wataru full_name: Yamamoto, Wataru last_name: Yamamoto - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 - first_name: Jiro full_name: Toshima, Jiro last_name: Toshima citation: ama: Toshima J, Horikomi C, Okada A, et al. Srv2/CAP is required for polarized actin cable assembly and patch internalization during clathrin-mediated endocytosis. Journal of Cell Science. 2016;129(2):367-379. doi:10.1242/jcs.176651 apa: Toshima, J., Horikomi, C., Okada, A., Hatori, M., Nagano, M., Masuda, A., … Toshima, J. (2016). Srv2/CAP is required for polarized actin cable assembly and patch internalization during clathrin-mediated endocytosis. Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.176651 chicago: Toshima, Junko, Chika Horikomi, Asuka Okada, Makiko Hatori, Makoto Nagano, Atsushi Masuda, Wataru Yamamoto, Daria E Siekhaus, and Jiro Toshima. “Srv2/CAP Is Required for Polarized Actin Cable Assembly and Patch Internalization during Clathrin-Mediated Endocytosis.” Journal of Cell Science. Company of Biologists, 2016. https://doi.org/10.1242/jcs.176651. ieee: J. Toshima et al., “Srv2/CAP is required for polarized actin cable assembly and patch internalization during clathrin-mediated endocytosis,” Journal of Cell Science, vol. 129, no. 2. Company of Biologists, pp. 367–379, 2016. ista: Toshima J, Horikomi C, Okada A, Hatori M, Nagano M, Masuda A, Yamamoto W, Siekhaus DE, Toshima J. 2016. Srv2/CAP is required for polarized actin cable assembly and patch internalization during clathrin-mediated endocytosis. Journal of Cell Science. 129(2), 367–379. mla: Toshima, Junko, et al. “Srv2/CAP Is Required for Polarized Actin Cable Assembly and Patch Internalization during Clathrin-Mediated Endocytosis.” Journal of Cell Science, vol. 129, no. 2, Company of Biologists, 2016, pp. 367–79, doi:10.1242/jcs.176651. short: J. Toshima, C. Horikomi, A. Okada, M. Hatori, M. Nagano, A. Masuda, W. Yamamoto, D.E. Siekhaus, J. Toshima, Journal of Cell Science 129 (2016) 367–379. date_created: 2018-12-11T11:52:14Z date_published: 2016-01-15T00:00:00Z date_updated: 2021-01-12T06:51:00Z day: '15' ddc: - '570' - '576' department: - _id: DaSi doi: 10.1242/jcs.176651 ec_funded: 1 file: - access_level: open_access checksum: 2da0a09149a9ed956cdf79a95c17f08a content_type: application/pdf creator: system date_created: 2018-12-12T10:11:08Z date_updated: 2020-07-14T12:44:56Z file_id: '4861' file_name: IST-2017-767-v1+1_367.full.pdf file_size: 7176912 relation: main_file file_date_updated: 2020-07-14T12:44:56Z has_accepted_license: '1' intvolume: ' 129' issue: '2' language: - iso: eng month: '01' oa: 1 oa_version: Published Version page: 367 - 379 project: - _id: 2536F660-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '334077' name: Investigating the role of transporters in invasive migration through junctions publication: Journal of Cell Science publication_status: published publisher: Company of Biologists publist_id: '5720' pubrep_id: '767' quality_controlled: '1' scopus_import: 1 status: public title: Srv2/CAP is required for polarized actin cable assembly and patch internalization during clathrin-mediated endocytosis type: journal_article user_id: 3E5EF7F0-F248-11E8-B48F-1D18A9856A87 volume: 129 year: '2016' ... --- _id: '1475' abstract: - lang: eng text: The actin cytoskeleton plays important roles in the formation and internalization of endocytic vesicles. In yeast, endocytic vesicles move towards early endosomes along actin cables, however, the molecular machinery regulating interaction between endocytic vesicles and actin cables is poorly understood. The Eps15-like protein Pan1p plays a key role in actin-mediated endocytosis and is negatively regulated by Ark1 and Prk1 kinases. Here we show that pan1 mutated to prevent phosphorylation at all 18 threonines, pan1-18TA, displayed almost the same endocytic defect as ark1Δ prk1Δ cells, and contained abnormal actin concentrations including several endocytic compartments. Early endosomes were highly localized in the actin concentrations and displayed movement along actin cables. The dephosphorylated form of Pan1p also caused stable associations between endocytic vesicles and actin cables, and between endocytic vesicles and endosomes. Thus Pan1 phosphorylation is part of a novel mechanism that regulates endocytic compartment interactions with each other and with actin cables. article_number: e10276 author: - first_name: Junko full_name: Toshima, Junko last_name: Toshima - first_name: Eri full_name: Furuya, Eri last_name: Furuya - first_name: Makoto full_name: Nagano, Makoto last_name: Nagano - first_name: Chisa full_name: Kanno, Chisa last_name: Kanno - first_name: Yuta full_name: Sakamoto, Yuta last_name: Sakamoto - first_name: Masashi full_name: Ebihara, Masashi last_name: Ebihara - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 - first_name: Jiro full_name: Toshima, Jiro last_name: Toshima citation: ama: Toshima J, Furuya E, Nagano M, et al. Yeast Eps15-like endocytic protein Pan1p regulates the interaction between endocytic vesicles, endosomes and the actin cytoskeleton. eLife. 2016;5(February 2016). doi:10.7554/eLife.10276 apa: Toshima, J., Furuya, E., Nagano, M., Kanno, C., Sakamoto, Y., Ebihara, M., … Toshima, J. (2016). Yeast Eps15-like endocytic protein Pan1p regulates the interaction between endocytic vesicles, endosomes and the actin cytoskeleton. ELife. eLife Sciences Publications. https://doi.org/10.7554/eLife.10276 chicago: Toshima, Junko, Eri Furuya, Makoto Nagano, Chisa Kanno, Yuta Sakamoto, Masashi Ebihara, Daria E Siekhaus, and Jiro Toshima. “Yeast Eps15-like Endocytic Protein Pan1p Regulates the Interaction between Endocytic Vesicles, Endosomes and the Actin Cytoskeleton.” ELife. eLife Sciences Publications, 2016. https://doi.org/10.7554/eLife.10276. ieee: J. Toshima et al., “Yeast Eps15-like endocytic protein Pan1p regulates the interaction between endocytic vesicles, endosomes and the actin cytoskeleton,” eLife, vol. 5, no. February 2016. eLife Sciences Publications, 2016. ista: Toshima J, Furuya E, Nagano M, Kanno C, Sakamoto Y, Ebihara M, Siekhaus DE, Toshima J. 2016. Yeast Eps15-like endocytic protein Pan1p regulates the interaction between endocytic vesicles, endosomes and the actin cytoskeleton. eLife. 5(February 2016), e10276. mla: Toshima, Junko, et al. “Yeast Eps15-like Endocytic Protein Pan1p Regulates the Interaction between Endocytic Vesicles, Endosomes and the Actin Cytoskeleton.” ELife, vol. 5, no. February 2016, e10276, eLife Sciences Publications, 2016, doi:10.7554/eLife.10276. short: J. Toshima, E. Furuya, M. Nagano, C. Kanno, Y. Sakamoto, M. Ebihara, D.E. Siekhaus, J. Toshima, ELife 5 (2016). date_created: 2018-12-11T11:52:14Z date_published: 2016-02-25T00:00:00Z date_updated: 2021-01-12T06:50:59Z day: '25' ddc: - '570' department: - _id: DaSi doi: 10.7554/eLife.10276 ec_funded: 1 file: - access_level: open_access checksum: d1cc44870580756ba8badd8e41adfdb5 content_type: application/pdf creator: system date_created: 2018-12-12T10:10:08Z date_updated: 2020-07-14T12:44:56Z file_id: '4793' file_name: IST-2016-529-v1+1_elife-10276-v1.pdf file_size: 5198001 relation: main_file file_date_updated: 2020-07-14T12:44:56Z has_accepted_license: '1' intvolume: ' 5' issue: February 2016 language: - iso: eng month: '02' oa: 1 oa_version: Published Version project: - _id: 2536F660-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '334077' name: Investigating the role of transporters in invasive migration through junctions publication: eLife publication_status: published publisher: eLife Sciences Publications publist_id: '5721' pubrep_id: '529' quality_controlled: '1' scopus_import: 1 status: public title: Yeast Eps15-like endocytic protein Pan1p regulates the interaction between endocytic vesicles, endosomes and the actin cytoskeleton 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: 5 year: '2016' ... --- _id: '1712' abstract: - lang: eng text: The majority of immune cells in Drosophila melanogaster are plasmatocytes; they carry out similar functions to vertebrate macrophages, influencing development as well as protecting against infection and cancer. Plasmatocytes, sometimes referred to with the broader term of hemocytes, migrate widely during embryonic development and cycle in the larvae between sessile and circulating positions. Here we discuss the similarities of plasmatocyte developmental migration and its functions to that of vertebrate macrophages, considering the recent controversy regarding the functions of Drosophila PDGF/VEGF related ligands. We also examine recent findings on the significance of adhesion for plasmatocyte migration in the embryo, as well as proliferation, trans-differentiation, and tumor responses in the larva. We spotlight parallels throughout to vertebrate immune responses. author: - first_name: Aparna full_name: Ratheesh, Aparna id: 2F064CFE-F248-11E8-B48F-1D18A9856A87 last_name: Ratheesh - first_name: Vera full_name: Belyaeva, Vera id: 47F080FE-F248-11E8-B48F-1D18A9856A87 last_name: Belyaeva - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 citation: ama: Ratheesh A, Belyaeva V, Siekhaus DE. Drosophila immune cell migration and adhesion during embryonic development and larval immune responses. Current Opinion in Cell Biology. 2015;36(10):71-79. doi:10.1016/j.ceb.2015.07.003 apa: Ratheesh, A., Belyaeva, V., & Siekhaus, D. E. (2015). Drosophila immune cell migration and adhesion during embryonic development and larval immune responses. Current Opinion in Cell Biology. Elsevier. https://doi.org/10.1016/j.ceb.2015.07.003 chicago: Ratheesh, Aparna, Vera Belyaeva, and Daria E Siekhaus. “Drosophila Immune Cell Migration and Adhesion during Embryonic Development and Larval Immune Responses.” Current Opinion in Cell Biology. Elsevier, 2015. https://doi.org/10.1016/j.ceb.2015.07.003. ieee: A. Ratheesh, V. Belyaeva, and D. E. Siekhaus, “Drosophila immune cell migration and adhesion during embryonic development and larval immune responses,” Current Opinion in Cell Biology, vol. 36, no. 10. Elsevier, pp. 71–79, 2015. ista: Ratheesh A, Belyaeva V, Siekhaus DE. 2015. Drosophila immune cell migration and adhesion during embryonic development and larval immune responses. Current Opinion in Cell Biology. 36(10), 71–79. mla: Ratheesh, Aparna, et al. “Drosophila Immune Cell Migration and Adhesion during Embryonic Development and Larval Immune Responses.” Current Opinion in Cell Biology, vol. 36, no. 10, Elsevier, 2015, pp. 71–79, doi:10.1016/j.ceb.2015.07.003. short: A. Ratheesh, V. Belyaeva, D.E. Siekhaus, Current Opinion in Cell Biology 36 (2015) 71–79. date_created: 2018-12-11T11:53:36Z date_published: 2015-10-01T00:00:00Z date_updated: 2021-01-12T06:52:41Z day: '01' ddc: - '573' department: - _id: DaSi doi: 10.1016/j.ceb.2015.07.003 ec_funded: 1 file: - access_level: open_access checksum: bbb1ee39ca52929aefe4f48752b166ee content_type: application/pdf creator: system date_created: 2018-12-12T10:14:44Z date_updated: 2020-07-14T12:45:13Z file_id: '5098' file_name: IST-2015-346-v1+1_Current_Opinion_Review_Ratheesh_et_al_2015.pdf file_size: 1023680 relation: main_file file_date_updated: 2020-07-14T12:45:13Z has_accepted_license: '1' intvolume: ' 36' issue: '10' language: - iso: eng license: https://creativecommons.org/licenses/by-nc-nd/4.0/ month: '10' oa: 1 oa_version: Published Version page: 71 - 79 project: - _id: 2536F660-B435-11E9-9278-68D0E5697425 call_identifier: FP7 grant_number: '334077' name: Investigating the role of transporters in invasive migration through junctions publication: Current Opinion in Cell Biology publication_status: published publisher: Elsevier publist_id: '5421' pubrep_id: '346' quality_controlled: '1' scopus_import: 1 status: public title: Drosophila immune cell migration and adhesion during embryonic development and larval immune responses 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: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 36 year: '2015' ... --- _id: '2025' abstract: - lang: eng text: Small GTP-binding proteins of the Ras superfamily play diverse roles in intracellular trafficking. Among them, the Rab, Arf, and Rho families function in successive steps of vesicle transport, in forming vesicles from donor membranes, directing vesicle trafficking toward target membranes and docking vesicles onto target membranes. These proteins act as molecular switches that are controlled by a cycle of GTP binding and hydrolysis regulated by guanine nucleotide exchange factors (GEFs) and GTPase-activating proteins (GAPs). In this study we explored the role of GAPs in the regulation of the endocytic pathway using fluorescently labeled yeast mating pheromone α-factor. Among 25 non-essential GAP mutants, we found that deletion of the GLO3 gene, encoding Arf-GAP protein, caused defective internalization of fluorescently labeled α-factor. Quantitative analysis revealed that glo3Δ cells show defective α-factor binding to the cell surface. Interestingly, Ste2p, the α-factor receptor, was mis-localized from the plasma membrane to the vacuole in glo3Δ cells. Domain deletion mutants of Glo3p revealed that a GAP-independent function, as well as the GAP activity, of Glo3p is important for both α-factor binding and Ste2p localization at the cell surface. Additionally, we found that deletion of the GLO3 gene affects the size and number of Arf1p-residing Golgi compartments and causes a defect in transport from the TGN to the plasma membrane. Furthermore, we demonstrated that glo3Δ cells were defective in the late endosome-to-TGN transport pathway, but not in the early endosome-to-TGN transport pathway. These findings suggest novel roles for Arf-GAP Glo3p in endocytic recycling of cell surface proteins. author: - first_name: Daiki full_name: Kawada, Daiki last_name: Kawada - first_name: Hiromu full_name: Kobayashi, Hiromu last_name: Kobayashi - first_name: Tsuyoshi full_name: Tomita, Tsuyoshi last_name: Tomita - first_name: Eisuke full_name: Nakata, Eisuke last_name: Nakata - first_name: Makoto full_name: Nagano, Makoto last_name: Nagano - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 - first_name: Junko full_name: Toshima, Junko last_name: Toshima - first_name: Jiro full_name: Toshimaa, Jiro last_name: Toshimaa citation: ama: Kawada D, Kobayashi H, Tomita T, et al. The yeast Arf-GAP Glo3p is required for the endocytic recycling of cell surface proteins. Biochimica et Biophysica Acta - Molecular Cell Research. 2015;1853(1):144-156. doi:10.1016/j.bbamcr.2014.10.009 apa: Kawada, D., Kobayashi, H., Tomita, T., Nakata, E., Nagano, M., Siekhaus, D. E., … Toshimaa, J. (2015). The yeast Arf-GAP Glo3p is required for the endocytic recycling of cell surface proteins. Biochimica et Biophysica Acta - Molecular Cell Research. Elsevier. https://doi.org/10.1016/j.bbamcr.2014.10.009 chicago: Kawada, Daiki, Hiromu Kobayashi, Tsuyoshi Tomita, Eisuke Nakata, Makoto Nagano, Daria E Siekhaus, Junko Toshima, and Jiro Toshimaa. “The Yeast Arf-GAP Glo3p Is Required for the Endocytic Recycling of Cell Surface Proteins.” Biochimica et Biophysica Acta - Molecular Cell Research. Elsevier, 2015. https://doi.org/10.1016/j.bbamcr.2014.10.009. ieee: D. Kawada et al., “The yeast Arf-GAP Glo3p is required for the endocytic recycling of cell surface proteins,” Biochimica et Biophysica Acta - Molecular Cell Research, vol. 1853, no. 1. Elsevier, pp. 144–156, 2015. ista: Kawada D, Kobayashi H, Tomita T, Nakata E, Nagano M, Siekhaus DE, Toshima J, Toshimaa J. 2015. The yeast Arf-GAP Glo3p is required for the endocytic recycling of cell surface proteins. Biochimica et Biophysica Acta - Molecular Cell Research. 1853(1), 144–156. mla: Kawada, Daiki, et al. “The Yeast Arf-GAP Glo3p Is Required for the Endocytic Recycling of Cell Surface Proteins.” Biochimica et Biophysica Acta - Molecular Cell Research, vol. 1853, no. 1, Elsevier, 2015, pp. 144–56, doi:10.1016/j.bbamcr.2014.10.009. short: D. Kawada, H. Kobayashi, T. Tomita, E. Nakata, M. Nagano, D.E. Siekhaus, J. Toshima, J. Toshimaa, Biochimica et Biophysica Acta - Molecular Cell Research 1853 (2015) 144–156. date_created: 2018-12-11T11:55:17Z date_published: 2015-01-01T00:00:00Z date_updated: 2021-01-12T06:54:48Z day: '01' ddc: - '570' department: - _id: DaSi doi: 10.1016/j.bbamcr.2014.10.009 file: - access_level: open_access checksum: 5bb328edebb6a91337cadd7d63f961b7 content_type: application/pdf creator: system date_created: 2018-12-12T10:12:18Z date_updated: 2020-07-14T12:45:25Z file_id: '4936' file_name: IST-2016-615-v1+1_BBAMCR.pdf file_size: 926685 relation: main_file file_date_updated: 2020-07-14T12:45:25Z has_accepted_license: '1' intvolume: ' 1853' issue: '1' language: - iso: eng month: '01' oa: 1 oa_version: Submitted Version page: 144 - 156 publication: Biochimica et Biophysica Acta - Molecular Cell Research publication_status: published publisher: Elsevier publist_id: '5047' pubrep_id: '615' quality_controlled: '1' scopus_import: 1 status: public title: The yeast Arf-GAP Glo3p is required for the endocytic recycling of cell surface proteins 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: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 1853 year: '2015' ... --- _id: '2024' abstract: - lang: eng text: 'The yeast Rab5 homologue, Vps21p, is known to be involved both in the vacuolar protein sorting (VPS) pathway from the trans-Golgi network to the vacuole, and in the endocytic pathway from the plasma membrane to the vacuole. However, the intracellular location at which these two pathways converge remains unclear. In addition, the endocytic pathway is not completely blocked in yeast cells lacking all Rab5 genes, suggesting the existence of an unidentified route that bypasses the Rab5-dependent endocytic pathway. Here we show that convergence of the endocytic and VPS pathways occurs upstream of the requirement for Vps21p in these pathways. We also identify a previously unidentified endocytic pathway mediated by the AP-3 complex. Importantly, the AP-3-mediated pathway appears mostly intact in Rab5-disrupted cells, and thus works as an alternative route to the vacuole/lysosome. We propose that the endocytic traffic branches into two routes to reach the vacuole: a Rab5-dependent VPS pathway and a Rab5-independent AP-3-mediated pathway.' article_number: '3498' author: - first_name: Junko full_name: Toshima, Junko last_name: Toshima - first_name: Show full_name: Nishinoaki, Show last_name: Nishinoaki - first_name: Yoshifumi full_name: Sato, Yoshifumi last_name: Sato - first_name: Wataru full_name: Yamamoto, Wataru last_name: Yamamoto - first_name: Daiki full_name: Furukawa, Daiki last_name: Furukawa - first_name: Daria E full_name: Siekhaus, Daria E id: 3D224B9E-F248-11E8-B48F-1D18A9856A87 last_name: Siekhaus orcid: 0000-0001-8323-8353 - first_name: Akira full_name: Sawaguchi, Akira last_name: Sawaguchi - first_name: Jiro full_name: Toshima, Jiro last_name: Toshima citation: ama: Toshima J, Nishinoaki S, Sato Y, et al. Bifurcation of the endocytic pathway into Rab5-dependent and -independent transport to the vacuole. Nature Communications. 2014;5. doi:10.1038/ncomms4498 apa: Toshima, J., Nishinoaki, S., Sato, Y., Yamamoto, W., Furukawa, D., Siekhaus, D. E., … Toshima, J. (2014). Bifurcation of the endocytic pathway into Rab5-dependent and -independent transport to the vacuole. Nature Communications. Nature Publishing Group. https://doi.org/10.1038/ncomms4498 chicago: Toshima, Junko, Show Nishinoaki, Yoshifumi Sato, Wataru Yamamoto, Daiki Furukawa, Daria E Siekhaus, Akira Sawaguchi, and Jiro Toshima. “Bifurcation of the Endocytic Pathway into Rab5-Dependent and -Independent Transport to the Vacuole.” Nature Communications. Nature Publishing Group, 2014. https://doi.org/10.1038/ncomms4498. ieee: J. Toshima et al., “Bifurcation of the endocytic pathway into Rab5-dependent and -independent transport to the vacuole,” Nature Communications, vol. 5. Nature Publishing Group, 2014. ista: Toshima J, Nishinoaki S, Sato Y, Yamamoto W, Furukawa D, Siekhaus DE, Sawaguchi A, Toshima J. 2014. Bifurcation of the endocytic pathway into Rab5-dependent and -independent transport to the vacuole. Nature Communications. 5, 3498. mla: Toshima, Junko, et al. “Bifurcation of the Endocytic Pathway into Rab5-Dependent and -Independent Transport to the Vacuole.” Nature Communications, vol. 5, 3498, Nature Publishing Group, 2014, doi:10.1038/ncomms4498. short: J. Toshima, S. Nishinoaki, Y. Sato, W. Yamamoto, D. Furukawa, D.E. Siekhaus, A. Sawaguchi, J. Toshima, Nature Communications 5 (2014). date_created: 2018-12-11T11:55:16Z date_published: 2014-03-25T00:00:00Z date_updated: 2021-01-12T06:54:48Z day: '25' ddc: - '570' department: - _id: DaSi doi: 10.1038/ncomms4498 file: - access_level: open_access checksum: 614fb6579c86d1f95bdd95eeb9ab01b0 content_type: application/pdf creator: system date_created: 2018-12-12T10:11:11Z date_updated: 2020-07-14T12:45:25Z file_id: '4864' file_name: IST-2016-616-v1+1_DaSi_Bifurcation_Postprint.pdf file_size: 4803515 relation: main_file file_date_updated: 2020-07-14T12:45:25Z has_accepted_license: '1' intvolume: ' 5' language: - iso: eng month: '03' oa: 1 oa_version: Submitted Version publication: Nature Communications publication_status: published publisher: Nature Publishing Group publist_id: '5048' pubrep_id: '616' quality_controlled: '1' scopus_import: 1 status: public title: Bifurcation of the endocytic pathway into Rab5-dependent and -independent transport to the vacuole type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 5 year: '2014' ...