--- _id: '802' abstract: - lang: eng text: Glycoinositolphosphoceramides (GIPCs) are complex sphingolipids present at the plasma membrane of various eukaryotes with the important exception of mammals. In fungi, these glycosphingolipids commonly contain an alpha-mannose residue (Man) linked at position 2 of the inositol. However, several pathogenic fungi additionally synthesize zwitterionic GIPCs carrying an alpha-glucosamine residue (GlcN) at this position. In the human pathogen Aspergillus fumigatus, the GlcNalpha1,2IPC core (where IPC is inositolphosphoceramide) is elongated to Manalpha1,3Manalpha1,6GlcNalpha1,2IPC, which is the most abundant GIPC synthesized by this fungus. In this study, we identified an A. fumigatus N-acetylglucosaminyltransferase, named GntA, and demonstrate its involvement in the initiation of zwitterionic GIPC biosynthesis. Targeted deletion of the gene encoding GntA in A. fumigatus resulted in complete absence of zwitterionic GIPC; a phenotype that could be reverted by episomal expression of GntA in the mutant. The N-acetylhexosaminyltransferase activity of GntA was substantiated by production of N-acetylhexosamine-IPC in the yeast Saccharomyces cerevisiae upon GntA expression. Using an in vitro assay, GntA was furthermore shown to use UDP-N-acetylglucosamine as donor substrate to generate a glycolipid product resistant to saponification and to digestion by phosphatidylinositol-phospholipase C as expected for GlcNAcalpha1,2IPC. Finally, as the enzymes involved in mannosylation of IPC, GntA was localized to the Golgi apparatus, the site of IPC synthesis. author: - first_name: Jakob full_name: Engel, Jakob last_name: Engel - first_name: Philipp S full_name: Schmalhorst, Philipp S id: 309D50DA-F248-11E8-B48F-1D18A9856A87 last_name: Schmalhorst orcid: 0000-0002-5795-0133 - first_name: Anke full_name: Kruger, Anke last_name: Kruger - first_name: Christina full_name: Muller, Christina last_name: Muller - first_name: Falk full_name: Buettner, Falk last_name: Buettner - first_name: Françoise full_name: Routier, Françoise last_name: Routier citation: ama: Engel J, Schmalhorst PS, Kruger A, Muller C, Buettner F, Routier F. Characterization of an N-acetylglucosaminyltransferase involved in Aspergillus fumigatus zwitterionic glycoinositolphosphoceramide biosynthesis. Glycobiology. 2015;25(12):1423-1430. doi:10.1093/glycob/cwv059 apa: Engel, J., Schmalhorst, P. S., Kruger, A., Muller, C., Buettner, F., & Routier, F. (2015). Characterization of an N-acetylglucosaminyltransferase involved in Aspergillus fumigatus zwitterionic glycoinositolphosphoceramide biosynthesis. Glycobiology. Oxford University Press. https://doi.org/10.1093/glycob/cwv059 chicago: Engel, Jakob, Philipp S Schmalhorst, Anke Kruger, Christina Muller, Falk Buettner, and Françoise Routier. “Characterization of an N-Acetylglucosaminyltransferase Involved in Aspergillus Fumigatus Zwitterionic Glycoinositolphosphoceramide Biosynthesis.” Glycobiology. Oxford University Press, 2015. https://doi.org/10.1093/glycob/cwv059. ieee: J. Engel, P. S. Schmalhorst, A. Kruger, C. Muller, F. Buettner, and F. Routier, “Characterization of an N-acetylglucosaminyltransferase involved in Aspergillus fumigatus zwitterionic glycoinositolphosphoceramide biosynthesis,” Glycobiology, vol. 25, no. 12. Oxford University Press, pp. 1423–1430, 2015. ista: Engel J, Schmalhorst PS, Kruger A, Muller C, Buettner F, Routier F. 2015. Characterization of an N-acetylglucosaminyltransferase involved in Aspergillus fumigatus zwitterionic glycoinositolphosphoceramide biosynthesis. Glycobiology. 25(12), 1423–1430. mla: Engel, Jakob, et al. “Characterization of an N-Acetylglucosaminyltransferase Involved in Aspergillus Fumigatus Zwitterionic Glycoinositolphosphoceramide Biosynthesis.” Glycobiology, vol. 25, no. 12, Oxford University Press, 2015, pp. 1423–30, doi:10.1093/glycob/cwv059. short: J. Engel, P.S. Schmalhorst, A. Kruger, C. Muller, F. Buettner, F. Routier, Glycobiology 25 (2015) 1423–1430. date_created: 2018-12-11T11:48:35Z date_published: 2015-12-01T00:00:00Z date_updated: 2021-01-12T08:16:33Z day: '01' department: - _id: CaHe doi: 10.1093/glycob/cwv059 external_id: pmid: - '26306635' intvolume: ' 25' issue: '12' language: - iso: eng month: '12' oa_version: None page: 1423 - 1430 pmid: 1 publication: Glycobiology publication_status: published publisher: Oxford University Press publist_id: '6851' quality_controlled: '1' scopus_import: 1 status: public title: Characterization of an N-acetylglucosaminyltransferase involved in Aspergillus fumigatus zwitterionic glycoinositolphosphoceramide biosynthesis type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 25 year: '2015' ... --- _id: '1566' abstract: - lang: eng text: Deposits of misfolded proteins in the human brain are associated with the development of many neurodegenerative diseases. Recent studies show that these proteins have common traits even at the monomer level. Among them, a polyglutamine region that is present in huntingtin is known to exhibit a correlation between the length of the chain and the severity as well as the earliness of the onset of Huntington disease. Here, we apply bias exchange molecular dynamics to generate structures of polyglutamine expansions of several lengths and characterize the resulting independent conformations. We compare the properties of these conformations to those of the standard proteins, as well as to other homopolymeric tracts. We find that, similar to the previously studied polyvaline chains, the set of possible transient folds is much broader than the set of known-to-date folds, although the conformations have different structures. We show that the mechanical stability is not related to any simple geometrical characteristics of the structures. We demonstrate that long polyglutamine expansions result in higher mechanical stability than the shorter ones. They also have a longer life span and are substantially more prone to form knotted structures. The knotted region has an average length of 35 residues, similar to the typical threshold for most polyglutamine-related diseases. Similarly, changes in shape and mechanical stability appear once the total length of the peptide exceeds this threshold of 35 glutamine residues. We suggest that knotted conformers may also harm the cellular machinery and thus lead to disease. acknowledgement: 'We acknowledge the support by the EU Joint Programme in Neurodegenerative Diseases (JPND AC14/00037) project. The project is supported through the following funding organisations under the aegis of JPND—www.jpnd.eu: Ireland, HRB; Poland, National Science Centre; and Spain, ISCIII. ' article_number: e1004541 author: - first_name: Àngel full_name: Gómez Sicilia, Àngel last_name: Gómez Sicilia - first_name: Mateusz K full_name: Sikora, Mateusz K id: 2F74BCDE-F248-11E8-B48F-1D18A9856A87 last_name: Sikora - first_name: Marek full_name: Cieplak, Marek last_name: Cieplak - first_name: Mariano full_name: Carrión Vázquez, Mariano last_name: Carrión Vázquez citation: ama: Gómez Sicilia À, Sikora MK, Cieplak M, Carrión Vázquez M. An exploration of the universe of polyglutamine structures. PLoS Computational Biology. 2015;11(10). doi:10.1371/journal.pcbi.1004541 apa: Gómez Sicilia, À., Sikora, M. K., Cieplak, M., & Carrión Vázquez, M. (2015). An exploration of the universe of polyglutamine structures. PLoS Computational Biology. Public Library of Science. https://doi.org/10.1371/journal.pcbi.1004541 chicago: Gómez Sicilia, Àngel, Mateusz K Sikora, Marek Cieplak, and Mariano Carrión Vázquez. “An Exploration of the Universe of Polyglutamine Structures.” PLoS Computational Biology. Public Library of Science, 2015. https://doi.org/10.1371/journal.pcbi.1004541. ieee: À. Gómez Sicilia, M. K. Sikora, M. Cieplak, and M. Carrión Vázquez, “An exploration of the universe of polyglutamine structures,” PLoS Computational Biology, vol. 11, no. 10. Public Library of Science, 2015. ista: Gómez Sicilia À, Sikora MK, Cieplak M, Carrión Vázquez M. 2015. An exploration of the universe of polyglutamine structures. PLoS Computational Biology. 11(10), e1004541. mla: Gómez Sicilia, Àngel, et al. “An Exploration of the Universe of Polyglutamine Structures.” PLoS Computational Biology, vol. 11, no. 10, e1004541, Public Library of Science, 2015, doi:10.1371/journal.pcbi.1004541. short: À. Gómez Sicilia, M.K. Sikora, M. Cieplak, M. Carrión Vázquez, PLoS Computational Biology 11 (2015). date_created: 2018-12-11T11:52:45Z date_published: 2015-10-23T00:00:00Z date_updated: 2023-02-23T14:05:55Z day: '23' ddc: - '570' department: - _id: CaHe doi: 10.1371/journal.pcbi.1004541 file: - access_level: open_access checksum: 8b67d729be663bfc9af04bfd94459655 content_type: application/pdf creator: system date_created: 2018-12-12T10:16:21Z date_updated: 2020-07-14T12:45:02Z file_id: '5207' file_name: IST-2016-478-v1+1_journal.pcbi.1004541.pdf file_size: 1412511 relation: main_file file_date_updated: 2020-07-14T12:45:02Z has_accepted_license: '1' intvolume: ' 11' issue: '10' language: - iso: eng month: '10' oa: 1 oa_version: Published Version publication: PLoS Computational Biology publication_status: published publisher: Public Library of Science publist_id: '5605' pubrep_id: '478' quality_controlled: '1' related_material: record: - id: '9714' relation: research_data status: public scopus_import: 1 status: public title: An exploration of the universe of polyglutamine structures tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 11 year: '2015' ... --- _id: '9714' article_processing_charge: No author: - first_name: Àngel full_name: Gómez Sicilia, Àngel last_name: Gómez Sicilia - first_name: Mateusz K full_name: Sikora, Mateusz K id: 2F74BCDE-F248-11E8-B48F-1D18A9856A87 last_name: Sikora - first_name: Marek full_name: Cieplak, Marek last_name: Cieplak - first_name: Mariano full_name: Carrión Vázquez, Mariano last_name: Carrión Vázquez citation: ama: Gómez Sicilia À, Sikora MK, Cieplak M, Carrión Vázquez M. An exploration of the universe of polyglutamine structures - submission to PLOS journals. 2015. doi:10.1371/journal.pcbi.1004541.s001 apa: Gómez Sicilia, À., Sikora, M. K., Cieplak, M., & Carrión Vázquez, M. (2015). An exploration of the universe of polyglutamine structures - submission to PLOS journals. Public Library of Science . https://doi.org/10.1371/journal.pcbi.1004541.s001 chicago: Gómez Sicilia, Àngel, Mateusz K Sikora, Marek Cieplak, and Mariano Carrión Vázquez. “An Exploration of the Universe of Polyglutamine Structures - Submission to PLOS Journals.” Public Library of Science , 2015. https://doi.org/10.1371/journal.pcbi.1004541.s001. ieee: À. Gómez Sicilia, M. K. Sikora, M. Cieplak, and M. Carrión Vázquez, “An exploration of the universe of polyglutamine structures - submission to PLOS journals.” Public Library of Science , 2015. ista: Gómez Sicilia À, Sikora MK, Cieplak M, Carrión Vázquez M. 2015. An exploration of the universe of polyglutamine structures - submission to PLOS journals, Public Library of Science , 10.1371/journal.pcbi.1004541.s001. mla: Gómez Sicilia, Àngel, et al. An Exploration of the Universe of Polyglutamine Structures - Submission to PLOS Journals. Public Library of Science , 2015, doi:10.1371/journal.pcbi.1004541.s001. short: À. Gómez Sicilia, M.K. Sikora, M. Cieplak, M. Carrión Vázquez, (2015). date_created: 2021-07-23T12:05:28Z date_published: 2015-10-23T00:00:00Z date_updated: 2023-02-23T10:04:35Z day: '23' department: - _id: CaHe doi: 10.1371/journal.pcbi.1004541.s001 month: '10' oa_version: Published Version publisher: 'Public Library of Science ' related_material: record: - id: '1566' relation: used_in_publication status: public status: public title: An exploration of the universe of polyglutamine structures - submission to PLOS journals type: research_data_reference user_id: 6785fbc1-c503-11eb-8a32-93094b40e1cf year: '2015' ... --- _id: '1537' abstract: - lang: eng text: 3D amoeboid cell migration is central to many developmental and disease-related processes such as cancer metastasis. Here, we identify a unique prototypic amoeboid cell migration mode in early zebrafish embryos, termed stable-bleb migration. Stable-bleb cells display an invariant polarized balloon-like shape with exceptional migration speed and persistence. Progenitor cells can be reversibly transformed into stable-bleb cells irrespective of their primary fate and motile characteristics by increasing myosin II activity through biochemical or mechanical stimuli. Using a combination of theory and experiments, we show that, in stable-bleb cells, cortical contractility fluctuations trigger a stochastic switch into amoeboid motility, and a positive feedback between cortical flows and gradients in contractility maintains stable-bleb cell polarization. We further show that rearward cortical flows drive stable-bleb cell migration in various adhesive and non-adhesive environments, unraveling a highly versatile amoeboid migration phenotype. acknowledged_ssus: - _id: SSU acknowledgement: 'We would like to thank R. Hausschild and E. Papusheva for technical assistance and the service facilities at the IST Austria for continuous support. The caRhoA plasmid was a kind gift of T. Kudoh and A. Takesono. We thank M. Piel and E. Paluch for exchanging unpublished data. ' author: - first_name: Verena full_name: Ruprecht, Verena id: 4D71A03A-F248-11E8-B48F-1D18A9856A87 last_name: Ruprecht orcid: 0000-0003-4088-8633 - first_name: Stefan full_name: Wieser, Stefan id: 355AA5A0-F248-11E8-B48F-1D18A9856A87 last_name: Wieser orcid: 0000-0002-2670-2217 - first_name: Andrew full_name: Callan Jones, Andrew last_name: Callan Jones - first_name: Michael full_name: Smutny, Michael id: 3FE6E4E8-F248-11E8-B48F-1D18A9856A87 last_name: Smutny orcid: 0000-0002-5920-9090 - first_name: Hitoshi full_name: Morita, Hitoshi id: 4C6E54C6-F248-11E8-B48F-1D18A9856A87 last_name: Morita - first_name: Keisuke full_name: Sako, Keisuke id: 3BED66BE-F248-11E8-B48F-1D18A9856A87 last_name: Sako orcid: 0000-0002-6453-8075 - first_name: Vanessa full_name: Barone, Vanessa id: 419EECCC-F248-11E8-B48F-1D18A9856A87 last_name: Barone orcid: 0000-0003-2676-3367 - first_name: Monika full_name: Ritsch Marte, Monika last_name: Ritsch Marte - first_name: Michael K full_name: Sixt, Michael K id: 41E9FBEA-F248-11E8-B48F-1D18A9856A87 last_name: Sixt orcid: 0000-0002-6620-9179 - first_name: Raphaël full_name: Voituriez, Raphaël last_name: Voituriez - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 citation: ama: Ruprecht V, Wieser S, Callan Jones A, et al. Cortical contractility triggers a stochastic switch to fast amoeboid cell motility. Cell. 2015;160(4):673-685. doi:10.1016/j.cell.2015.01.008 apa: Ruprecht, V., Wieser, S., Callan Jones, A., Smutny, M., Morita, H., Sako, K., … Heisenberg, C.-P. J. (2015). Cortical contractility triggers a stochastic switch to fast amoeboid cell motility. Cell. Cell Press. https://doi.org/10.1016/j.cell.2015.01.008 chicago: Ruprecht, Verena, Stefan Wieser, Andrew Callan Jones, Michael Smutny, Hitoshi Morita, Keisuke Sako, Vanessa Barone, et al. “Cortical Contractility Triggers a Stochastic Switch to Fast Amoeboid Cell Motility.” Cell. Cell Press, 2015. https://doi.org/10.1016/j.cell.2015.01.008. ieee: V. Ruprecht et al., “Cortical contractility triggers a stochastic switch to fast amoeboid cell motility,” Cell, vol. 160, no. 4. Cell Press, pp. 673–685, 2015. ista: Ruprecht V, Wieser S, Callan Jones A, Smutny M, Morita H, Sako K, Barone V, Ritsch Marte M, Sixt MK, Voituriez R, Heisenberg C-PJ. 2015. Cortical contractility triggers a stochastic switch to fast amoeboid cell motility. Cell. 160(4), 673–685. mla: Ruprecht, Verena, et al. “Cortical Contractility Triggers a Stochastic Switch to Fast Amoeboid Cell Motility.” Cell, vol. 160, no. 4, Cell Press, 2015, pp. 673–85, doi:10.1016/j.cell.2015.01.008. short: V. Ruprecht, S. Wieser, A. Callan Jones, M. Smutny, H. Morita, K. Sako, V. Barone, M. Ritsch Marte, M.K. Sixt, R. Voituriez, C.-P.J. Heisenberg, Cell 160 (2015) 673–685. date_created: 2018-12-11T11:52:35Z date_published: 2015-02-12T00:00:00Z date_updated: 2023-09-07T12:05:08Z day: '12' ddc: - '570' department: - _id: CaHe - _id: MiSi doi: 10.1016/j.cell.2015.01.008 file: - access_level: open_access checksum: 228d3edf40627d897b3875088a0ac51f content_type: application/pdf creator: system date_created: 2018-12-12T10:13:21Z date_updated: 2020-07-14T12:45:01Z file_id: '5003' file_name: IST-2016-484-v1+1_1-s2.0-S0092867415000094-main.pdf file_size: 4362653 relation: main_file file_date_updated: 2020-07-14T12:45:01Z has_accepted_license: '1' intvolume: ' 160' issue: '4' language: - iso: eng month: '02' oa: 1 oa_version: Published Version page: 673 - 685 project: - _id: 2529486C-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: T 560-B17 name: Cell- and Tissue Mechanics in Zebrafish Germ Layer Formation - _id: 2527D5CC-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: I 812-B12 name: Cell Cortex and Germ Layer Formation in Zebrafish Gastrulation publication: Cell publication_status: published publisher: Cell Press publist_id: '5634' pubrep_id: '484' quality_controlled: '1' related_material: record: - id: '961' relation: dissertation_contains status: public scopus_import: 1 status: public title: Cortical contractility triggers a stochastic switch to fast amoeboid cell motility tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 160 year: '2015' ... --- _id: '10815' abstract: - lang: eng text: In the last several decades, developmental biology has clarified the molecular mechanisms of embryogenesis and organogenesis. In particular, it has demonstrated that the “tool-kit genes” essential for regulating developmental processes are not only highly conserved among species, but are also used as systems at various times and places in an organism to control distinct developmental events. Therefore, mutations in many of these tool-kit genes may cause congenital diseases involving morphological abnormalities. This link between genes and abnormal morphological phenotypes underscores the importance of understanding how cells behave and contribute to morphogenesis as a result of gene function. Recent improvements in live imaging and in quantitative analyses of cellular dynamics will advance our understanding of the cellular pathogenesis of congenital diseases associated with aberrant morphologies. In these studies, it is critical to select an appropriate model organism for the particular phenomenon of interest. acknowledgement: The authors thank all the members of the Division of Morphogenesis, National Institute for Basic Biology, for their contributions to the research, their encouragement, and helpful discussions, particularly Dr M. Suzuki for his critical reading of the manuscript. We also thank the Model Animal Research and Spectrography and Bioimaging Facilities, NIBB Core Research Facilities, for technical support. M.H. was supported by a research fellowship from the Japan Society for the Promotion of Science (JSPS). Our work introduced in this review was supported by a Grant-in-Aid for Scientific Research on Innovative Areas from the Ministry of Education, Culture, Sports, Science, and Technology (MEXT), Japan, to N.U. article_processing_charge: No article_type: original author: - first_name: Masakazu full_name: Hashimoto, Masakazu last_name: Hashimoto - first_name: Hitoshi full_name: Morita, Hitoshi id: 4C6E54C6-F248-11E8-B48F-1D18A9856A87 last_name: Morita - first_name: Naoto full_name: Ueno, Naoto last_name: Ueno citation: ama: Hashimoto M, Morita H, Ueno N. Molecular and cellular mechanisms of development underlying congenital diseases. Congenital Anomalies. 2014;54(1):1-7. doi:10.1111/cga.12039 apa: Hashimoto, M., Morita, H., & Ueno, N. (2014). Molecular and cellular mechanisms of development underlying congenital diseases. Congenital Anomalies. Wiley. https://doi.org/10.1111/cga.12039 chicago: Hashimoto, Masakazu, Hitoshi Morita, and Naoto Ueno. “Molecular and Cellular Mechanisms of Development Underlying Congenital Diseases.” Congenital Anomalies. Wiley, 2014. https://doi.org/10.1111/cga.12039. ieee: M. Hashimoto, H. Morita, and N. Ueno, “Molecular and cellular mechanisms of development underlying congenital diseases,” Congenital Anomalies, vol. 54, no. 1. Wiley, pp. 1–7, 2014. ista: Hashimoto M, Morita H, Ueno N. 2014. Molecular and cellular mechanisms of development underlying congenital diseases. Congenital Anomalies. 54(1), 1–7. mla: Hashimoto, Masakazu, et al. “Molecular and Cellular Mechanisms of Development Underlying Congenital Diseases.” Congenital Anomalies, vol. 54, no. 1, Wiley, 2014, pp. 1–7, doi:10.1111/cga.12039. short: M. Hashimoto, H. Morita, N. Ueno, Congenital Anomalies 54 (2014) 1–7. date_created: 2022-03-04T08:17:25Z date_published: 2014-02-01T00:00:00Z date_updated: 2022-03-04T08:26:05Z day: '01' department: - _id: CaHe doi: 10.1111/cga.12039 external_id: pmid: - '24666178' intvolume: ' 54' issue: '1' keyword: - Developmental Biology - Embryology - General Medicine - Pediatrics - Perinatology - and Child Health language: - iso: eng main_file_link: - open_access: '1' url: https://doi.org/10.1111/cga.12039 month: '02' oa: 1 oa_version: None page: 1-7 pmid: 1 publication: Congenital Anomalies publication_identifier: issn: - 0914-3505 publication_status: published publisher: Wiley quality_controlled: '1' scopus_import: '1' status: public title: Molecular and cellular mechanisms of development underlying congenital diseases type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 54 year: '2014' ... --- _id: '1891' abstract: - lang: eng text: We provide theoretical tests of a novel experimental technique to determine mechanostability of proteins based on stretching a mechanically protected protein by single-molecule force spectroscopy. This technique involves stretching a homogeneous or heterogeneous chain of reference proteins (single-molecule markers) in which one of them acts as host to the guest protein under study. The guest protein is grafted into the host through genetic engineering. It is expected that unraveling of the host precedes the unraveling of the guest removing ambiguities in the reading of the force-extension patterns of the guest protein. We study examples of such systems within a coarse-grained structure-based model. We consider systems with various ratios of mechanostability for the host and guest molecules and compare them to experimental results involving cohesin I as the guest molecule. For a comparison, we also study the force-displacement patterns in proteins that are linked in a serial fashion. We find that the mechanostability of the guest is similar to that of the isolated or serially linked protein. We also demonstrate that the ideal configuration of this strategy would be one in which the host is much more mechanostable than the single-molecule markers. We finally show that it is troublesome to use the highly stable cystine knot proteins as a host to graft a guest in stretching studies because this would involve a cleaving procedure. acknowledgement: Grant Nr. 2011/01/N/ST3/02475 author: - first_name: Mateusz full_name: Chwastyk, Mateusz last_name: Chwastyk - first_name: Albert full_name: Galera Prat, Albert last_name: Galera Prat - first_name: Mateusz K full_name: Sikora, Mateusz K id: 2F74BCDE-F248-11E8-B48F-1D18A9856A87 last_name: Sikora - first_name: Àngel full_name: Gómez Sicilia, Àngel last_name: Gómez Sicilia - first_name: Mariano full_name: Carrión Vázquez, Mariano last_name: Carrión Vázquez - first_name: Marek full_name: Cieplak, Marek last_name: Cieplak citation: ama: 'Chwastyk M, Galera Prat A, Sikora MK, Gómez Sicilia À, Carrión Vázquez M, Cieplak M. Theoretical tests of the mechanical protection strategy in protein nanomechanics. Proteins: Structure, Function and Bioinformatics. 2014;82(5):717-726. doi:10.1002/prot.24436' apa: 'Chwastyk, M., Galera Prat, A., Sikora, M. K., Gómez Sicilia, À., Carrión Vázquez, M., & Cieplak, M. (2014). Theoretical tests of the mechanical protection strategy in protein nanomechanics. Proteins: Structure, Function and Bioinformatics. Wiley-Blackwell. https://doi.org/10.1002/prot.24436' chicago: 'Chwastyk, Mateusz, Albert Galera Prat, Mateusz K Sikora, Àngel Gómez Sicilia, Mariano Carrión Vázquez, and Marek Cieplak. “Theoretical Tests of the Mechanical Protection Strategy in Protein Nanomechanics.” Proteins: Structure, Function and Bioinformatics. Wiley-Blackwell, 2014. https://doi.org/10.1002/prot.24436.' ieee: 'M. Chwastyk, A. Galera Prat, M. K. Sikora, À. Gómez Sicilia, M. Carrión Vázquez, and M. Cieplak, “Theoretical tests of the mechanical protection strategy in protein nanomechanics,” Proteins: Structure, Function and Bioinformatics, vol. 82, no. 5. Wiley-Blackwell, pp. 717–726, 2014.' ista: 'Chwastyk M, Galera Prat A, Sikora MK, Gómez Sicilia À, Carrión Vázquez M, Cieplak M. 2014. Theoretical tests of the mechanical protection strategy in protein nanomechanics. Proteins: Structure, Function and Bioinformatics. 82(5), 717–726.' mla: 'Chwastyk, Mateusz, et al. “Theoretical Tests of the Mechanical Protection Strategy in Protein Nanomechanics.” Proteins: Structure, Function and Bioinformatics, vol. 82, no. 5, Wiley-Blackwell, 2014, pp. 717–26, doi:10.1002/prot.24436.' short: 'M. Chwastyk, A. Galera Prat, M.K. Sikora, À. Gómez Sicilia, M. Carrión Vázquez, M. Cieplak, Proteins: Structure, Function and Bioinformatics 82 (2014) 717–726.' date_created: 2018-12-11T11:54:34Z date_published: 2014-05-01T00:00:00Z date_updated: 2021-01-12T06:53:52Z day: '01' department: - _id: CaHe doi: 10.1002/prot.24436 intvolume: ' 82' issue: '5' language: - iso: eng month: '05' oa_version: None page: 717 - 726 publication: 'Proteins: Structure, Function and Bioinformatics' publication_status: published publisher: Wiley-Blackwell publist_id: '5204' scopus_import: 1 status: public title: Theoretical tests of the mechanical protection strategy in protein nanomechanics type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 82 year: '2014' ... --- _id: '1900' abstract: - lang: eng text: Epithelial cell layers need to be tightly regulated to maintain their integrity and correct function. Cell integration into epithelial sheets is now shown to depend on the N-WASP-regulated stabilization of cortical F-actin, which generates distinct patterns of apical-lateral contractility at E-cadherin-based cell-cell junctions. author: - first_name: Martin full_name: Behrndt, Martin id: 3ECECA3A-F248-11E8-B48F-1D18A9856A87 last_name: Behrndt - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 citation: ama: Behrndt M, Heisenberg C-PJ. Lateral junction dynamics lead the way out. Nature Cell Biology. 2014;16(2):127-129. doi:10.1038/ncb2913 apa: Behrndt, M., & Heisenberg, C.-P. J. (2014). Lateral junction dynamics lead the way out. Nature Cell Biology. Nature Publishing Group. https://doi.org/10.1038/ncb2913 chicago: Behrndt, Martin, and Carl-Philipp J Heisenberg. “Lateral Junction Dynamics Lead the Way Out.” Nature Cell Biology. Nature Publishing Group, 2014. https://doi.org/10.1038/ncb2913. ieee: M. Behrndt and C.-P. J. Heisenberg, “Lateral junction dynamics lead the way out,” Nature Cell Biology, vol. 16, no. 2. Nature Publishing Group, pp. 127–129, 2014. ista: Behrndt M, Heisenberg C-PJ. 2014. Lateral junction dynamics lead the way out. Nature Cell Biology. 16(2), 127–129. mla: Behrndt, Martin, and Carl-Philipp J. Heisenberg. “Lateral Junction Dynamics Lead the Way Out.” Nature Cell Biology, vol. 16, no. 2, Nature Publishing Group, 2014, pp. 127–29, doi:10.1038/ncb2913. short: M. Behrndt, C.-P.J. Heisenberg, Nature Cell Biology 16 (2014) 127–129. date_created: 2018-12-11T11:54:37Z date_published: 2014-01-31T00:00:00Z date_updated: 2021-01-12T06:53:56Z day: '31' department: - _id: CaHe doi: 10.1038/ncb2913 intvolume: ' 16' issue: '2' language: - iso: eng month: '01' oa_version: None page: 127 - 129 publication: Nature Cell Biology publication_status: published publisher: Nature Publishing Group publist_id: '5195' quality_controlled: '1' scopus_import: 1 status: public title: Lateral junction dynamics lead the way out type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 16 year: '2014' ... --- _id: '1925' abstract: - lang: eng text: In the past decade carbon nanotubes (CNTs) have been widely studied as a potential drug-delivery system, especially with functionality for cellular targeting. Yet, little is known about the actual process of docking to cell receptors and transport dynamics after internalization. Here we performed single-particle studies of folic acid (FA) mediated CNT binding to human carcinoma cells and their transport inside the cytosol. In particular, we employed molecular recognition force spectroscopy, an atomic force microscopy based method, to visualize and quantify docking of FA functionalized CNTs to FA binding receptors in terms of binding probability and binding force. We then traced individual fluorescently labeled, FA functionalized CNTs after specific uptake, and created a dynamic 'roadmap' that clearly showed trajectories of directed diffusion and areas of nanotube confinement in the cytosol. Our results demonstrate the potential of a single-molecule approach for investigation of drug-delivery vehicles and their targeting capacity. acknowledgement: "This work was supported by EC grant Marie Curie RTN-CT-2006-035616, CARBIO 'Carbon nanotubes for biomedical applications' and Austrian FFG grant mnt-era.net 823980, 'IntelliTip'.\r\n" article_number: '125704' article_processing_charge: No article_type: original author: - first_name: Constanze full_name: Lamprecht, Constanze last_name: Lamprecht - first_name: Birgit full_name: Plochberger, Birgit last_name: Plochberger - first_name: Verena full_name: Ruprecht, Verena id: 4D71A03A-F248-11E8-B48F-1D18A9856A87 last_name: Ruprecht orcid: 0000-0003-4088-8633 - first_name: Stefan full_name: Wieser, Stefan id: 355AA5A0-F248-11E8-B48F-1D18A9856A87 last_name: Wieser orcid: 0000-0002-2670-2217 - first_name: Christian full_name: Rankl, Christian last_name: Rankl - first_name: Elena full_name: Heister, Elena last_name: Heister - first_name: Barbara full_name: Unterauer, Barbara last_name: Unterauer - first_name: Mario full_name: Brameshuber, Mario last_name: Brameshuber - first_name: Jürgen full_name: Danzberger, Jürgen last_name: Danzberger - first_name: Petar full_name: Lukanov, Petar last_name: Lukanov - first_name: Emmanuel full_name: Flahaut, Emmanuel last_name: Flahaut - first_name: Gerhard full_name: Schütz, Gerhard last_name: Schütz - first_name: Peter full_name: Hinterdorfer, Peter last_name: Hinterdorfer - first_name: Andreas full_name: Ebner, Andreas last_name: Ebner citation: ama: Lamprecht C, Plochberger B, Ruprecht V, et al. A single-molecule approach to explore binding uptake and transport of cancer cell targeting nanotubes. Nanotechnology. 2014;25(12). doi:10.1088/0957-4484/25/12/125704 apa: Lamprecht, C., Plochberger, B., Ruprecht, V., Wieser, S., Rankl, C., Heister, E., … Ebner, A. (2014). A single-molecule approach to explore binding uptake and transport of cancer cell targeting nanotubes. Nanotechnology. IOP Publishing. https://doi.org/10.1088/0957-4484/25/12/125704 chicago: Lamprecht, Constanze, Birgit Plochberger, Verena Ruprecht, Stefan Wieser, Christian Rankl, Elena Heister, Barbara Unterauer, et al. “A Single-Molecule Approach to Explore Binding Uptake and Transport of Cancer Cell Targeting Nanotubes.” Nanotechnology. IOP Publishing, 2014. https://doi.org/10.1088/0957-4484/25/12/125704. ieee: C. Lamprecht et al., “A single-molecule approach to explore binding uptake and transport of cancer cell targeting nanotubes,” Nanotechnology, vol. 25, no. 12. IOP Publishing, 2014. ista: Lamprecht C, Plochberger B, Ruprecht V, Wieser S, Rankl C, Heister E, Unterauer B, Brameshuber M, Danzberger J, Lukanov P, Flahaut E, Schütz G, Hinterdorfer P, Ebner A. 2014. A single-molecule approach to explore binding uptake and transport of cancer cell targeting nanotubes. Nanotechnology. 25(12), 125704. mla: Lamprecht, Constanze, et al. “A Single-Molecule Approach to Explore Binding Uptake and Transport of Cancer Cell Targeting Nanotubes.” Nanotechnology, vol. 25, no. 12, 125704, IOP Publishing, 2014, doi:10.1088/0957-4484/25/12/125704. short: C. Lamprecht, B. Plochberger, V. Ruprecht, S. Wieser, C. Rankl, E. Heister, B. Unterauer, M. Brameshuber, J. Danzberger, P. Lukanov, E. Flahaut, G. Schütz, P. Hinterdorfer, A. Ebner, Nanotechnology 25 (2014). date_created: 2018-12-11T11:54:45Z date_published: 2014-03-28T00:00:00Z date_updated: 2021-01-12T06:54:07Z day: '28' ddc: - '570' department: - _id: CaHe - _id: MiSi doi: 10.1088/0957-4484/25/12/125704 file: - access_level: open_access checksum: df4e03d225a19179e7790f6d87a12332 content_type: application/pdf creator: dernst date_created: 2020-05-15T09:21:19Z date_updated: 2020-07-14T12:45:21Z file_id: '7856' file_name: 2014_Nanotechnology_Lamprecht.pdf file_size: 3804152 relation: main_file file_date_updated: 2020-07-14T12:45:21Z has_accepted_license: '1' intvolume: ' 25' issue: '12' language: - iso: eng month: '03' oa: 1 oa_version: Submitted Version publication: Nanotechnology publication_status: published publisher: IOP Publishing publist_id: '5169' scopus_import: 1 status: public title: A single-molecule approach to explore binding uptake and transport of cancer cell targeting nanotubes type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 25 year: '2014' ... --- _id: '1923' abstract: - lang: eng text: We derive the equations for a thin, axisymmetric elastic shell subjected to an internal active stress giving rise to active tension and moments within the shell. We discuss the stability of a cylindrical elastic shell and its response to a localized change in internal active stress. This description is relevant to describe the cellular actomyosin cortex, a thin shell at the cell surface behaving elastically at a short timescale and subjected to active internal forces arising from myosin molecular motor activity. We show that the recent observations of cell deformation following detachment of adherent cells (Maître J-L et al 2012 Science 338 253-6) are well accounted for by this mechanical description. The actin cortex elastic and bending moduli can be obtained from a quantitative analysis of cell shapes observed in these experiments. Our approach thus provides a non-invasive, imaging-based method for the extraction of cellular physical parameters. article_number: '065005' author: - first_name: Hélène full_name: Berthoumieux, Hélène last_name: Berthoumieux - first_name: Jean-Léon full_name: Maître, Jean-Léon id: 48F1E0D8-F248-11E8-B48F-1D18A9856A87 last_name: Maître orcid: 0000-0002-3688-1474 - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 - first_name: Ewa full_name: Paluch, Ewa last_name: Paluch - first_name: Frank full_name: Julicher, Frank last_name: Julicher - first_name: Guillaume full_name: Salbreux, Guillaume last_name: Salbreux citation: ama: Berthoumieux H, Maître J-L, Heisenberg C-PJ, Paluch E, Julicher F, Salbreux G. Active elastic thin shell theory for cellular deformations. New Journal of Physics. 2014;16. doi:10.1088/1367-2630/16/6/065005 apa: Berthoumieux, H., Maître, J.-L., Heisenberg, C.-P. J., Paluch, E., Julicher, F., & Salbreux, G. (2014). Active elastic thin shell theory for cellular deformations. New Journal of Physics. IOP Publishing Ltd. https://doi.org/10.1088/1367-2630/16/6/065005 chicago: Berthoumieux, Hélène, Jean-Léon Maître, Carl-Philipp J Heisenberg, Ewa Paluch, Frank Julicher, and Guillaume Salbreux. “Active Elastic Thin Shell Theory for Cellular Deformations.” New Journal of Physics. IOP Publishing Ltd., 2014. https://doi.org/10.1088/1367-2630/16/6/065005. ieee: H. Berthoumieux, J.-L. Maître, C.-P. J. Heisenberg, E. Paluch, F. Julicher, and G. Salbreux, “Active elastic thin shell theory for cellular deformations,” New Journal of Physics, vol. 16. IOP Publishing Ltd., 2014. ista: Berthoumieux H, Maître J-L, Heisenberg C-PJ, Paluch E, Julicher F, Salbreux G. 2014. Active elastic thin shell theory for cellular deformations. New Journal of Physics. 16, 065005. mla: Berthoumieux, Hélène, et al. “Active Elastic Thin Shell Theory for Cellular Deformations.” New Journal of Physics, vol. 16, 065005, IOP Publishing Ltd., 2014, doi:10.1088/1367-2630/16/6/065005. short: H. Berthoumieux, J.-L. Maître, C.-P.J. Heisenberg, E. Paluch, F. Julicher, G. Salbreux, New Journal of Physics 16 (2014). date_created: 2018-12-11T11:54:44Z date_published: 2014-06-01T00:00:00Z date_updated: 2021-01-12T06:54:06Z day: '01' ddc: - '570' department: - _id: CaHe doi: 10.1088/1367-2630/16/6/065005 file: - access_level: open_access checksum: 8dbe81ec656bf1264d8889bda9b2b985 content_type: application/pdf creator: system date_created: 2018-12-12T10:16:16Z date_updated: 2020-07-14T12:45:21Z file_id: '5202' file_name: IST-2016-429-v1+1_document.pdf file_size: 941387 relation: main_file file_date_updated: 2020-07-14T12:45:21Z has_accepted_license: '1' intvolume: ' 16' language: - iso: eng month: '06' oa: 1 oa_version: Published Version publication: New Journal of Physics publication_status: published publisher: IOP Publishing Ltd. publist_id: '5171' pubrep_id: '429' quality_controlled: '1' scopus_import: 1 status: public title: Active elastic thin shell theory for cellular deformations tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 16 year: '2014' ... --- _id: '2248' abstract: - lang: eng text: 'Avian forelimb digit homology remains one of the standard themes in comparative biology and EvoDevo research. In order to resolve the apparent contradictions between embryological and paleontological evidence a variety of hypotheses have been presented in recent years. The proposals range from excluding birds from the dinosaur clade, to assignments of homology by different criteria, or even assuming a hexadactyl tetrapod limb ground state. At present two approaches prevail: the frame shift hypothesis and the pyramid reduction hypothesis. While the former postulates a homeotic shift of digit identities, the latter argues for a gradual bilateral reduction of phalanges and digits. Here we present a new model that integrates elements from both hypotheses with the existing experimental and fossil evidence. We start from the main feature common to both earlier concepts, the initiating ontogenetic event: reduction and loss of the anterior-most digit. It is proposed that a concerted mechanism of molecular regulation and developmental mechanics is capable of shifting the boundaries of hoxD expression in embryonic forelimb buds as well as changing the digit phenotypes. Based on a distinction between positional (topological) and compositional (phenotypic) homology criteria, we argue that the identity of the avian digits is II, III, IV, despite a partially altered phenotype. Finally, we introduce an alternative digit reduction scheme that reconciles the current fossil evidence with the presented molecular-morphogenetic model. Our approach identifies specific experiments that allow to test whether gene expression can be shifted and digit phenotypes can be altered by induced digit loss or digit gain.' author: - first_name: Daniel full_name: Capek, Daniel id: 31C42484-F248-11E8-B48F-1D18A9856A87 last_name: Capek orcid: 0000-0001-5199-9940 - first_name: Brian full_name: Metscher, Brian last_name: Metscher - first_name: Gerd full_name: Müller, Gerd last_name: Müller citation: ama: 'Capek D, Metscher B, Müller G. Thumbs down: A molecular-morphogenetic approach to avian digit homology. Journal of Experimental Zoology Part B: Molecular and Developmental Evolution. 2014;322(1):1-12. doi:10.1002/jez.b.22545' apa: 'Capek, D., Metscher, B., & Müller, G. (2014). Thumbs down: A molecular-morphogenetic approach to avian digit homology. Journal of Experimental Zoology Part B: Molecular and Developmental Evolution. Wiley-Blackwell. https://doi.org/10.1002/jez.b.22545' chicago: 'Capek, Daniel, Brian Metscher, and Gerd Müller. “Thumbs down: A Molecular-Morphogenetic Approach to Avian Digit Homology.” Journal of Experimental Zoology Part B: Molecular and Developmental Evolution. Wiley-Blackwell, 2014. https://doi.org/10.1002/jez.b.22545.' ieee: 'D. Capek, B. Metscher, and G. Müller, “Thumbs down: A molecular-morphogenetic approach to avian digit homology,” Journal of Experimental Zoology Part B: Molecular and Developmental Evolution, vol. 322, no. 1. Wiley-Blackwell, pp. 1–12, 2014.' ista: 'Capek D, Metscher B, Müller G. 2014. Thumbs down: A molecular-morphogenetic approach to avian digit homology. Journal of Experimental Zoology Part B: Molecular and Developmental Evolution. 322(1), 1–12.' mla: 'Capek, Daniel, et al. “Thumbs down: A Molecular-Morphogenetic Approach to Avian Digit Homology.” Journal of Experimental Zoology Part B: Molecular and Developmental Evolution, vol. 322, no. 1, Wiley-Blackwell, 2014, pp. 1–12, doi:10.1002/jez.b.22545.' short: 'D. Capek, B. Metscher, G. Müller, Journal of Experimental Zoology Part B: Molecular and Developmental Evolution 322 (2014) 1–12.' date_created: 2018-12-11T11:56:33Z date_published: 2014-01-01T00:00:00Z date_updated: 2021-01-12T06:56:16Z day: '01' department: - _id: CaHe doi: 10.1002/jez.b.22545 intvolume: ' 322' issue: '1' language: - iso: eng month: '01' oa_version: None page: 1 - 12 publication: 'Journal of Experimental Zoology Part B: Molecular and Developmental Evolution' publication_identifier: issn: - '15525007' publication_status: published publisher: Wiley-Blackwell publist_id: '4701' quality_controlled: '1' scopus_import: 1 status: public title: 'Thumbs down: A molecular-morphogenetic approach to avian digit homology' type: journal_article user_id: 4435EBFC-F248-11E8-B48F-1D18A9856A87 volume: 322 year: '2014' ... --- _id: '6178' abstract: - lang: eng text: Mechanically coupled cells can generate forces driving cell and tissue morphogenesis during development. Visualization and measuring of these forces is of major importance to better understand the complexity of the biomechanic processes that shape cells and tissues. Here, we describe how UV laser ablation can be utilized to quantitatively assess mechanical tension in different tissues of the developing zebrafish and in cultures of primary germ layer progenitor cells ex vivo. article_processing_charge: No author: - first_name: Michael full_name: Smutny, Michael id: 3FE6E4E8-F248-11E8-B48F-1D18A9856A87 last_name: Smutny orcid: 0000-0002-5920-9090 - first_name: Martin full_name: Behrndt, Martin id: 3ECECA3A-F248-11E8-B48F-1D18A9856A87 last_name: Behrndt - first_name: Pedro full_name: Campinho, Pedro id: 3AFBBC42-F248-11E8-B48F-1D18A9856A87 last_name: Campinho orcid: 0000-0002-8526-5416 - first_name: Verena full_name: Ruprecht, Verena id: 4D71A03A-F248-11E8-B48F-1D18A9856A87 last_name: Ruprecht orcid: 0000-0003-4088-8633 - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 citation: ama: 'Smutny M, Behrndt M, Campinho P, Ruprecht V, Heisenberg C-PJ. UV laser ablation to measure cell and tissue-generated forces in the zebrafish embryo in vivo and ex vivo. In: Nelson C, ed. Tissue Morphogenesis. Vol 1189. Methods in Molecular Biology. New York, NY: Springer; 2014:219-235. doi:10.1007/978-1-4939-1164-6_15' apa: 'Smutny, M., Behrndt, M., Campinho, P., Ruprecht, V., & Heisenberg, C.-P. J. (2014). UV laser ablation to measure cell and tissue-generated forces in the zebrafish embryo in vivo and ex vivo. In C. Nelson (Ed.), Tissue Morphogenesis (Vol. 1189, pp. 219–235). New York, NY: Springer. https://doi.org/10.1007/978-1-4939-1164-6_15' chicago: 'Smutny, Michael, Martin Behrndt, Pedro Campinho, Verena Ruprecht, and Carl-Philipp J Heisenberg. “UV Laser Ablation to Measure Cell and Tissue-Generated Forces in the Zebrafish Embryo in Vivo and Ex Vivo.” In Tissue Morphogenesis, edited by Celeste Nelson, 1189:219–35. Methods in Molecular Biology. New York, NY: Springer, 2014. https://doi.org/10.1007/978-1-4939-1164-6_15.' ieee: 'M. Smutny, M. Behrndt, P. Campinho, V. Ruprecht, and C.-P. J. Heisenberg, “UV laser ablation to measure cell and tissue-generated forces in the zebrafish embryo in vivo and ex vivo,” in Tissue Morphogenesis, vol. 1189, C. Nelson, Ed. New York, NY: Springer, 2014, pp. 219–235.' ista: 'Smutny M, Behrndt M, Campinho P, Ruprecht V, Heisenberg C-PJ. 2014.UV laser ablation to measure cell and tissue-generated forces in the zebrafish embryo in vivo and ex vivo. In: Tissue Morphogenesis. vol. 1189, 219–235.' mla: Smutny, Michael, et al. “UV Laser Ablation to Measure Cell and Tissue-Generated Forces in the Zebrafish Embryo in Vivo and Ex Vivo.” Tissue Morphogenesis, edited by Celeste Nelson, vol. 1189, Springer, 2014, pp. 219–35, doi:10.1007/978-1-4939-1164-6_15. short: M. Smutny, M. Behrndt, P. Campinho, V. Ruprecht, C.-P.J. Heisenberg, in:, C. Nelson (Ed.), Tissue Morphogenesis, Springer, New York, NY, 2014, pp. 219–235. date_created: 2019-03-26T08:55:59Z date_published: 2014-08-22T00:00:00Z date_updated: 2023-09-05T14:12:00Z day: '22' department: - _id: CaHe doi: 10.1007/978-1-4939-1164-6_15 editor: - first_name: Celeste full_name: Nelson, Celeste last_name: Nelson external_id: pmid: - '25245697' intvolume: ' 1189' language: - iso: eng month: '08' oa_version: None page: 219-235 place: New York, NY pmid: 1 publication: Tissue Morphogenesis publication_identifier: eissn: - 1940-6029 isbn: - '9781493911639' - '9781493911646' issn: - 1064-3745 publication_status: published publisher: Springer quality_controlled: '1' series_title: Methods in Molecular Biology status: public title: UV laser ablation to measure cell and tissue-generated forces in the zebrafish embryo in vivo and ex vivo type: book_chapter user_id: c635000d-4b10-11ee-a964-aac5a93f6ac1 volume: 1189 year: '2014' ... --- _id: '1912' abstract: - lang: eng text: Kupffer's vesicle (KV) is the zebrafish organ of laterality, patterning the embryo along its left-right (LR) axis. Regional differences in cell shape within the lumen-lining KV epithelium are essential for its LR patterning function. However, the processes by which KV cells acquire their characteristic shapes are largely unknown. Here, we show that the notochord induces regional differences in cell shape within KV by triggering extracellular matrix (ECM) accumulation adjacent to anterior-dorsal (AD) regions of KV. This localized ECM deposition restricts apical expansion of lumen-lining epithelial cells in AD regions of KV during lumen growth. Our study provides mechanistic insight into the processes by which KV translates global embryonic patterning into regional cell shape differences required for its LR symmetry-breaking function. acknowledgement: We are grateful to members of the C.-P.H. lab, M. Concha, D. Siekhaus, and J. Vermot for comments on the manuscript and to M. Furutani-Seiki for sharing reagents. This work was supported by the Institute of Science and Technology Austria and an Alexander von Humboldt Foundation fellowship to J.C. article_processing_charge: No author: - first_name: Julien full_name: Compagnon, Julien id: 2E3E0988-F248-11E8-B48F-1D18A9856A87 last_name: Compagnon - first_name: Vanessa full_name: Barone, Vanessa id: 419EECCC-F248-11E8-B48F-1D18A9856A87 last_name: Barone orcid: 0000-0003-2676-3367 - first_name: Srivarsha full_name: Rajshekar, Srivarsha last_name: Rajshekar - first_name: Rita full_name: Kottmeier, Rita last_name: Kottmeier - first_name: Kornelija full_name: Pranjic-Ferscha, Kornelija id: 4362B3C2-F248-11E8-B48F-1D18A9856A87 last_name: Pranjic-Ferscha - first_name: Martin full_name: Behrndt, Martin id: 3ECECA3A-F248-11E8-B48F-1D18A9856A87 last_name: Behrndt - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 citation: ama: Compagnon J, Barone V, Rajshekar S, et al. The notochord breaks bilateral symmetry by controlling cell shapes in the Zebrafish laterality organ. Developmental Cell. 2014;31(6):774-783. doi:10.1016/j.devcel.2014.11.003 apa: Compagnon, J., Barone, V., Rajshekar, S., Kottmeier, R., Pranjic-Ferscha, K., Behrndt, M., & Heisenberg, C.-P. J. (2014). The notochord breaks bilateral symmetry by controlling cell shapes in the Zebrafish laterality organ. Developmental Cell. Cell Press. https://doi.org/10.1016/j.devcel.2014.11.003 chicago: Compagnon, Julien, Vanessa Barone, Srivarsha Rajshekar, Rita Kottmeier, Kornelija Pranjic-Ferscha, Martin Behrndt, and Carl-Philipp J Heisenberg. “The Notochord Breaks Bilateral Symmetry by Controlling Cell Shapes in the Zebrafish Laterality Organ.” Developmental Cell. Cell Press, 2014. https://doi.org/10.1016/j.devcel.2014.11.003. ieee: J. Compagnon et al., “The notochord breaks bilateral symmetry by controlling cell shapes in the Zebrafish laterality organ,” Developmental Cell, vol. 31, no. 6. Cell Press, pp. 774–783, 2014. ista: Compagnon J, Barone V, Rajshekar S, Kottmeier R, Pranjic-Ferscha K, Behrndt M, Heisenberg C-PJ. 2014. The notochord breaks bilateral symmetry by controlling cell shapes in the Zebrafish laterality organ. Developmental Cell. 31(6), 774–783. mla: Compagnon, Julien, et al. “The Notochord Breaks Bilateral Symmetry by Controlling Cell Shapes in the Zebrafish Laterality Organ.” Developmental Cell, vol. 31, no. 6, Cell Press, 2014, pp. 774–83, doi:10.1016/j.devcel.2014.11.003. short: J. Compagnon, V. Barone, S. Rajshekar, R. Kottmeier, K. Pranjic-Ferscha, M. Behrndt, C.-P.J. Heisenberg, Developmental Cell 31 (2014) 774–783. date_created: 2018-12-11T11:54:41Z date_published: 2014-12-22T00:00:00Z date_updated: 2023-09-07T12:05:08Z day: '22' department: - _id: CaHe doi: 10.1016/j.devcel.2014.11.003 external_id: pmid: - '25535919' intvolume: ' 31' issue: '6' language: - iso: eng main_file_link: - open_access: '1' url: https://www.ncbi.nlm.nih.gov/pubmed/25535919 month: '12' oa: 1 oa_version: Published Version page: 774 - 783 pmid: 1 publication: Developmental Cell publication_status: published publisher: Cell Press publist_id: '5182' quality_controlled: '1' related_material: record: - id: '961' relation: dissertation_contains status: public scopus_import: '1' status: public title: The notochord breaks bilateral symmetry by controlling cell shapes in the Zebrafish laterality organ type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 31 year: '2014' ... --- _id: '1403' abstract: - lang: eng text: A variety of developmental and disease related processes depend on epithelial cell sheet spreading. In order to gain insight into the biophysical mechanism(s) underlying the tissue morphogenesis we studied the spreading of an epithelium during the early development of the zebrafish embryo. In zebrafish epiboly the enveloping cell layer (EVL), a simple squamous epithelium, spreads over the yolk cell to completely engulf it at the end of gastrulation. Previous studies have proposed that an actomyosin ring forming within the yolk syncytial layer (YSL) acts as purse string that through constriction along its circumference pulls on the margin of the EVL. Direct biophysical evidence for this hypothesis has however been missing. The aim of the thesis was to understand how the actomyosin ring may generate pulling forces onto the EVL and what cellular mechanism(s) may facilitate the spreading of the epithelium. Using laser ablation to measure cortical tension within the actomyosin ring we found an anisotropic tension distribution, which was highest along the circumference of the ring. However the low degree of anisotropy was incompatible with the actomyosin ring functioning as a purse string only. Additionally, we observed retrograde cortical flow from vegetal parts of the ring into the EVL margin. Interpreting the experimental data using a theoretical distribution that models the tissues as active viscous gels led us to proposen that the actomyosin ring has a twofold contribution to EVL epiboly. It not only acts as a purse string through constriction along its circumference, but in addition constriction along the width of the ring generates pulling forces through friction-resisted cortical flow. Moreover, when rendering the purse string mechanism unproductive EVL epiboly proceeded normally indicating that the flow-friction mechanism is sufficient to drive the process. Aiming to understand what cellular mechanism(s) may facilitate the spreading of the epithelium we found that tension-oriented EVL cell divisions limit tissue anisotropy by releasing tension along the division axis and promote epithelial spreading. Notably, EVL cells undergo ectopic cell fusion in conditions in which oriented-cell division is impaired or the epithelium is mechanically challenged. Taken together our study of EVL epiboly suggests a novel mechanism of force generation for actomyosin rings through friction-resisted cortical flow and highlights the importance of tension-oriented cell divisions in epithelial morphogenesis. acknowledged_ssus: - _id: SSU alternative_title: - IST Austria Thesis author: - first_name: Martin full_name: Behrndt, Martin id: 3ECECA3A-F248-11E8-B48F-1D18A9856A87 last_name: Behrndt citation: ama: Behrndt M. Forces driving epithelial spreading in zebrafish epiboly. 2014. apa: Behrndt, M. (2014). Forces driving epithelial spreading in zebrafish epiboly. IST Austria. chicago: Behrndt, Martin. “Forces Driving Epithelial Spreading in Zebrafish Epiboly.” IST Austria, 2014. ieee: M. Behrndt, “Forces driving epithelial spreading in zebrafish epiboly,” IST Austria, 2014. ista: Behrndt M. 2014. Forces driving epithelial spreading in zebrafish epiboly. IST Austria. mla: Behrndt, Martin. Forces Driving Epithelial Spreading in Zebrafish Epiboly. IST Austria, 2014. short: M. Behrndt, Forces Driving Epithelial Spreading in Zebrafish Epiboly, IST Austria, 2014. date_created: 2018-12-11T11:51:49Z date_published: 2014-08-01T00:00:00Z date_updated: 2023-10-17T12:16:58Z day: '01' department: - _id: CaHe language: - iso: eng month: '08' oa_version: None page: '91' publication_status: published publisher: IST Austria publist_id: '5804' related_material: record: - id: '2282' relation: part_of_dissertation status: public - id: '2950' relation: part_of_dissertation status: public - id: '3373' relation: part_of_dissertation status: public status: public supervisor: - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 title: Forces driving epithelial spreading in zebrafish epiboly type: dissertation user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 year: '2014' ... --- _id: '2278' abstract: - lang: eng text: It is firmly established that interactions between neurons and glia are fundamental across species for the correct establishment of a functional brain. Here, we found that the glia of the Drosophila larval brain display an essential non-autonomous role during the development of the optic lobe. The optic lobe develops from neuroepithelial cells that proliferate by dividing symmetrically until they switch to asymmetric/differentiative divisions that generate neuroblasts. The proneural gene lethal of scute (l9sc) is transiently activated by the epidermal growth factor receptor (EGFR)-Ras signal transduction pathway at the leading edge of a proneural wave that sweeps from medial to lateral neuroepithelium, promoting this switch. This process is tightly regulated by the tissue-autonomous function within the neuroepithelium of multiple signaling pathways, including EGFR-Ras and Notch. This study shows that the Notch ligand Serrate (Ser) is expressed in the glia and it forms a complex in vivo with Notch and Canoe, which colocalize at the adherens junctions of neuroepithelial cells. This complex is crucial for interactions between glia and neuroepithelial cells during optic lobe development. Ser is tissue-autonomously required in the glia where it activates Notch to regulate its proliferation, and non-autonomously in the neuroepithelium where Ser induces Notch signaling to avoid the premature activation of the EGFR-Ras pathway and hence of L9sc. Interestingly, different Notch activity reporters showed very different expression patterns in the glia and in the neuroepithelium, suggesting the existence of tissue-specific factors that promote the expression of particular Notch target genes or/and a reporter response dependent on different thresholds of Notch signaling. author: - first_name: Raquel full_name: Pérez Gómez, Raquel last_name: Pérez Gómez - first_name: Jana full_name: Slovakova, Jana id: 30F3F2F0-F248-11E8-B48F-1D18A9856A87 last_name: Slovakova - first_name: Noemí full_name: Rives Quinto, Noemí last_name: Rives Quinto - first_name: Alena full_name: Krejčí, Alena last_name: Krejčí - first_name: Ana full_name: Carmena, Ana last_name: Carmena citation: ama: Pérez Gómez R, Slovakova J, Rives Quinto N, Krejčí A, Carmena A. A serrate-notch-canoe complex mediates essential interactions between glia and neuroepithelial cells during Drosophila optic lobe development. Journal of Cell Science. 2013;126(21):4873-4884. doi:10.1242/jcs.125617 apa: Pérez Gómez, R., Slovakova, J., Rives Quinto, N., Krejčí, A., & Carmena, A. (2013). A serrate-notch-canoe complex mediates essential interactions between glia and neuroepithelial cells during Drosophila optic lobe development. Journal of Cell Science. Company of Biologists. https://doi.org/10.1242/jcs.125617 chicago: Pérez Gómez, Raquel, Jana Slovakova, Noemí Rives Quinto, Alena Krejčí, and Ana Carmena. “A Serrate-Notch-Canoe Complex Mediates Essential Interactions between Glia and Neuroepithelial Cells during Drosophila Optic Lobe Development.” Journal of Cell Science. Company of Biologists, 2013. https://doi.org/10.1242/jcs.125617. ieee: R. Pérez Gómez, J. Slovakova, N. Rives Quinto, A. Krejčí, and A. Carmena, “A serrate-notch-canoe complex mediates essential interactions between glia and neuroepithelial cells during Drosophila optic lobe development,” Journal of Cell Science, vol. 126, no. 21. Company of Biologists, pp. 4873–4884, 2013. ista: Pérez Gómez R, Slovakova J, Rives Quinto N, Krejčí A, Carmena A. 2013. A serrate-notch-canoe complex mediates essential interactions between glia and neuroepithelial cells during Drosophila optic lobe development. Journal of Cell Science. 126(21), 4873–4884. mla: Pérez Gómez, Raquel, et al. “A Serrate-Notch-Canoe Complex Mediates Essential Interactions between Glia and Neuroepithelial Cells during Drosophila Optic Lobe Development.” Journal of Cell Science, vol. 126, no. 21, Company of Biologists, 2013, pp. 4873–84, doi:10.1242/jcs.125617. short: R. Pérez Gómez, J. Slovakova, N. Rives Quinto, A. Krejčí, A. Carmena, Journal of Cell Science 126 (2013) 4873–4884. date_created: 2018-12-11T11:56:43Z date_published: 2013-11-01T00:00:00Z date_updated: 2021-01-12T06:56:29Z day: '01' department: - _id: CaHe doi: 10.1242/jcs.125617 intvolume: ' 126' issue: '21' language: - iso: eng month: '11' oa_version: None page: 4873 - 4884 publication: Journal of Cell Science publication_status: published publisher: Company of Biologists publist_id: '4658' quality_controlled: '1' scopus_import: 1 status: public title: A serrate-notch-canoe complex mediates essential interactions between glia and neuroepithelial cells during Drosophila optic lobe development type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 126 year: '2013' ... --- _id: '2282' abstract: - lang: eng text: Epithelial spreading is a common and fundamental aspect of various developmental and disease-related processes such as epithelial closure and wound healing. A key challenge for epithelial tissues undergoing spreading is to increase their surface area without disrupting epithelial integrity. Here we show that orienting cell divisions by tension constitutes an efficient mechanism by which the enveloping cell layer (EVL) releases anisotropic tension while undergoing spreading during zebrafish epiboly. The control of EVL cell-division orientation by tension involves cell elongation and requires myosin II activity to align the mitotic spindle with the main tension axis. We also found that in the absence of tension-oriented cell divisions and in the presence of increased tissue tension, EVL cells undergo ectopic fusions, suggesting that the reduction of tension anisotropy by oriented cell divisions is required to prevent EVL cells from fusing. We conclude that cell-division orientation by tension constitutes a key mechanism for limiting tension anisotropy and thus promoting tissue spreading during EVL epiboly. acknowledged_ssus: - _id: PreCl - _id: Bio acknowledgement: 'This work was supported by the IST Austria and MPI-CBG ' author: - first_name: Pedro full_name: Campinho, Pedro id: 3AFBBC42-F248-11E8-B48F-1D18A9856A87 last_name: Campinho orcid: 0000-0002-8526-5416 - first_name: Martin full_name: Behrndt, Martin id: 3ECECA3A-F248-11E8-B48F-1D18A9856A87 last_name: Behrndt - first_name: Jonas full_name: Ranft, Jonas last_name: Ranft - first_name: Thomas full_name: Risler, Thomas last_name: Risler - first_name: Nicolas full_name: Minc, Nicolas last_name: Minc - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 citation: ama: Campinho P, Behrndt M, Ranft J, Risler T, Minc N, Heisenberg C-PJ. Tension-oriented cell divisions limit anisotropic tissue tension in epithelial spreading during zebrafish epiboly. Nature Cell Biology. 2013;15:1405-1414. doi:10.1038/ncb2869 apa: Campinho, P., Behrndt, M., Ranft, J., Risler, T., Minc, N., & Heisenberg, C.-P. J. (2013). Tension-oriented cell divisions limit anisotropic tissue tension in epithelial spreading during zebrafish epiboly. Nature Cell Biology. Nature Publishing Group. https://doi.org/10.1038/ncb2869 chicago: Campinho, Pedro, Martin Behrndt, Jonas Ranft, Thomas Risler, Nicolas Minc, and Carl-Philipp J Heisenberg. “Tension-Oriented Cell Divisions Limit Anisotropic Tissue Tension in Epithelial Spreading during Zebrafish Epiboly.” Nature Cell Biology. Nature Publishing Group, 2013. https://doi.org/10.1038/ncb2869. ieee: P. Campinho, M. Behrndt, J. Ranft, T. Risler, N. Minc, and C.-P. J. Heisenberg, “Tension-oriented cell divisions limit anisotropic tissue tension in epithelial spreading during zebrafish epiboly,” Nature Cell Biology, vol. 15. Nature Publishing Group, pp. 1405–1414, 2013. ista: Campinho P, Behrndt M, Ranft J, Risler T, Minc N, Heisenberg C-PJ. 2013. Tension-oriented cell divisions limit anisotropic tissue tension in epithelial spreading during zebrafish epiboly. Nature Cell Biology. 15, 1405–1414. mla: Campinho, Pedro, et al. “Tension-Oriented Cell Divisions Limit Anisotropic Tissue Tension in Epithelial Spreading during Zebrafish Epiboly.” Nature Cell Biology, vol. 15, Nature Publishing Group, 2013, pp. 1405–14, doi:10.1038/ncb2869. short: P. Campinho, M. Behrndt, J. Ranft, T. Risler, N. Minc, C.-P.J. Heisenberg, Nature Cell Biology 15 (2013) 1405–1414. date_created: 2018-12-11T11:56:45Z date_published: 2013-11-10T00:00:00Z date_updated: 2023-02-21T17:02:44Z day: '10' department: - _id: CaHe doi: 10.1038/ncb2869 intvolume: ' 15' language: - iso: eng main_file_link: - open_access: '1' url: http://hal.upmc.fr/hal-00983313/ month: '11' oa: 1 oa_version: Submitted Version page: 1405 - 1414 project: - _id: 252ABD0A-B435-11E9-9278-68D0E5697425 call_identifier: FWF grant_number: I 930-B20 name: Control of Epithelial Cell Layer Spreading in Zebrafish publication: Nature Cell Biology publication_status: published publisher: Nature Publishing Group publist_id: '4652' quality_controlled: '1' related_material: record: - id: '1403' relation: dissertation_contains status: public scopus_import: 1 status: public title: Tension-oriented cell divisions limit anisotropic tissue tension in epithelial spreading during zebrafish epiboly type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 15 year: '2013' ... --- _id: '2286' abstract: - lang: eng text: The spatiotemporal control of cell divisions is a key factor in epithelial morphogenesis and patterning. Mao et al (2013) now describe how differential rates of proliferation within the Drosophila wing disc epithelium give rise to anisotropic tissue tension in peripheral/proximal regions of the disc. Such global tissue tension anisotropy in turn determines the orientation of cell divisions by controlling epithelial cell elongation. author: - first_name: Pedro full_name: Campinho, Pedro id: 3AFBBC42-F248-11E8-B48F-1D18A9856A87 last_name: Campinho orcid: 0000-0002-8526-5416 - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 citation: ama: Campinho P, Heisenberg C-PJ. The force and effect of cell proliferation. EMBO Journal. 2013;32(21):2783-2784. doi:10.1038/emboj.2013.225 apa: Campinho, P., & Heisenberg, C.-P. J. (2013). The force and effect of cell proliferation. EMBO Journal. Wiley-Blackwell. https://doi.org/10.1038/emboj.2013.225 chicago: Campinho, Pedro, and Carl-Philipp J Heisenberg. “The Force and Effect of Cell Proliferation.” EMBO Journal. Wiley-Blackwell, 2013. https://doi.org/10.1038/emboj.2013.225. ieee: P. Campinho and C.-P. J. Heisenberg, “The force and effect of cell proliferation,” EMBO Journal, vol. 32, no. 21. Wiley-Blackwell, pp. 2783–2784, 2013. ista: Campinho P, Heisenberg C-PJ. 2013. The force and effect of cell proliferation. EMBO Journal. 32(21), 2783–2784. mla: Campinho, Pedro, and Carl-Philipp J. Heisenberg. “The Force and Effect of Cell Proliferation.” EMBO Journal, vol. 32, no. 21, Wiley-Blackwell, 2013, pp. 2783–84, doi:10.1038/emboj.2013.225. short: P. Campinho, C.-P.J. Heisenberg, EMBO Journal 32 (2013) 2783–2784. date_created: 2018-12-11T11:56:46Z date_published: 2013-10-04T00:00:00Z date_updated: 2021-01-12T06:56:32Z day: '04' department: - _id: CaHe doi: 10.1038/emboj.2013.225 external_id: pmid: - '24097062' intvolume: ' 32' issue: '21' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3817470/ month: '10' oa: 1 oa_version: Submitted Version page: 2783 - 2784 pmid: 1 publication: EMBO Journal publication_status: published publisher: Wiley-Blackwell publist_id: '4645' quality_controlled: '1' scopus_import: 1 status: public title: The force and effect of cell proliferation type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 32 year: '2013' ... --- _id: '2469' abstract: - lang: eng text: Cadherins are transmembrane proteins that mediate cell–cell adhesion in animals. By regulating contact formation and stability, cadherins play a crucial role in tissue morphogenesis and homeostasis. Here, we review the three major unctions of cadherins in cell–cell contact formation and stability. Two of those functions lead to a decrease in interfacial ension at the forming cell–cell contact, thereby promoting contact expansion — first, by providing adhesion tension that lowers interfacial tension at the cell–cell contact, and second, by signaling to the actomyosin cytoskeleton in order to reduce cortex tension and thus interfacial tension at the contact. The third function of cadherins in cell–cell contact formation is to stabilize the contact by resisting mechanical forces that pull on the contact. author: - first_name: Jean-Léon full_name: Maître, Jean-Léon id: 48F1E0D8-F248-11E8-B48F-1D18A9856A87 last_name: Maître orcid: 0000-0002-3688-1474 - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 citation: ama: Maître J-L, Heisenberg C-PJ. Three functions of cadherins in cell adhesion. Current Biology. 2013;23(14):R626-R633. doi:10.1016/j.cub.2013.06.019 apa: Maître, J.-L., & Heisenberg, C.-P. J. (2013). Three functions of cadherins in cell adhesion. Current Biology. Cell Press. https://doi.org/10.1016/j.cub.2013.06.019 chicago: Maître, Jean-Léon, and Carl-Philipp J Heisenberg. “Three Functions of Cadherins in Cell Adhesion.” Current Biology. Cell Press, 2013. https://doi.org/10.1016/j.cub.2013.06.019. ieee: J.-L. Maître and C.-P. J. Heisenberg, “Three functions of cadherins in cell adhesion,” Current Biology, vol. 23, no. 14. Cell Press, pp. R626–R633, 2013. ista: Maître J-L, Heisenberg C-PJ. 2013. Three functions of cadherins in cell adhesion. Current Biology. 23(14), R626–R633. mla: Maître, Jean-Léon, and Carl-Philipp J. Heisenberg. “Three Functions of Cadherins in Cell Adhesion.” Current Biology, vol. 23, no. 14, Cell Press, 2013, pp. R626–33, doi:10.1016/j.cub.2013.06.019. short: J.-L. Maître, C.-P.J. Heisenberg, Current Biology 23 (2013) R626–R633. date_created: 2018-12-11T11:57:51Z date_published: 2013-07-22T00:00:00Z date_updated: 2021-01-12T06:57:40Z day: '22' ddc: - '570' department: - _id: CaHe doi: 10.1016/j.cub.2013.06.019 external_id: pmid: - '23885883' file: - access_level: open_access checksum: 6a424b2f007b41d4955a9135793b2162 content_type: application/pdf creator: dernst date_created: 2019-01-24T15:40:22Z date_updated: 2020-07-14T12:45:41Z file_id: '5881' file_name: 2013_CurrentBiology_Maitre.pdf file_size: 247320 relation: main_file file_date_updated: 2020-07-14T12:45:41Z has_accepted_license: '1' intvolume: ' 23' issue: '14' language: - iso: eng month: '07' oa: 1 oa_version: Published Version page: R626 - R633 pmid: 1 publication: Current Biology publication_status: published publisher: Cell Press publist_id: '4433' quality_controlled: '1' scopus_import: 1 status: public title: Three functions of cadherins in cell adhesion tmp: image: /images/cc_by.png legal_code_url: https://creativecommons.org/licenses/by/4.0/legalcode name: Creative Commons Attribution 4.0 International Public License (CC-BY 4.0) short: CC BY (4.0) type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 23 year: '2013' ... --- _id: '2833' abstract: - lang: eng text: During development, mechanical forces cause changes in size, shape, number, position, and gene expression of cells. They are therefore integral to any morphogenetic processes. Force generation by actin-myosin networks and force transmission through adhesive complexes are two self-organizing phenomena driving tissue morphogenesis. Coordination and integration of forces by long-range force transmission and mechanosensing of cells within tissues produce large-scale tissue shape changes. Extrinsic mechanical forces also control tissue patterning by modulating cell fate specification and differentiation. Thus, the interplay between tissue mechanics and biochemical signaling orchestrates tissue morphogenesis and patterning in development. acknowledgement: C.-P.H. is supported by the Institute of Science and Technology Austria and grants from the Deutsche Forschungsgemeinschaft (DFG) and Fonds zur Förderung der wissenschaftlichen Forschung (FWF). author: - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 - first_name: Yohanns full_name: Bellaïche, Yohanns last_name: Bellaïche citation: ama: Heisenberg C-PJ, Bellaïche Y. Forces in tissue morphogenesis and patterning. Cell. 2013;153(5):948-962. doi:10.1016/j.cell.2013.05.008 apa: Heisenberg, C.-P. J., & Bellaïche, Y. (2013). Forces in tissue morphogenesis and patterning. Cell. Cell Press. https://doi.org/10.1016/j.cell.2013.05.008 chicago: Heisenberg, Carl-Philipp J, and Yohanns Bellaïche. “Forces in Tissue Morphogenesis and Patterning.” Cell. Cell Press, 2013. https://doi.org/10.1016/j.cell.2013.05.008. ieee: C.-P. J. Heisenberg and Y. Bellaïche, “Forces in tissue morphogenesis and patterning,” Cell, vol. 153, no. 5. Cell Press, pp. 948–962, 2013. ista: Heisenberg C-PJ, Bellaïche Y. 2013. Forces in tissue morphogenesis and patterning. Cell. 153(5), 948–962. mla: Heisenberg, Carl-Philipp J., and Yohanns Bellaïche. “Forces in Tissue Morphogenesis and Patterning.” Cell, vol. 153, no. 5, Cell Press, 2013, pp. 948–62, doi:10.1016/j.cell.2013.05.008. short: C.-P.J. Heisenberg, Y. Bellaïche, Cell 153 (2013) 948–962. date_created: 2018-12-11T11:59:50Z date_published: 2013-05-23T00:00:00Z date_updated: 2021-01-12T07:00:04Z day: '23' department: - _id: CaHe doi: 10.1016/j.cell.2013.05.008 intvolume: ' 153' issue: '5' language: - iso: eng month: '05' oa_version: None page: 948 - 962 publication: Cell publication_status: published publisher: Cell Press publist_id: '3966' quality_controlled: '1' scopus_import: 1 status: public title: Forces in tissue morphogenesis and patterning type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 153 year: '2013' ... --- _id: '2841' abstract: - lang: eng text: In zebrafish early development, blastoderm cells undergo extensive radial intercalations, triggering the spreading of the blastoderm over the yolk cell and thereby initiating embryonic body axis formation. Now reporting in Developmental Cell, Song et al. (2013) demonstrate a critical function for EGF-dependent E-cadherin endocytosis in promoting blastoderm cell intercalations. author: - first_name: Hitoshi full_name: Morita, Hitoshi id: 4C6E54C6-F248-11E8-B48F-1D18A9856A87 last_name: Morita - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 citation: ama: 'Morita H, Heisenberg C-PJ. Holding on and letting go: Cadherin turnover in cell intercalation. Developmental Cell. 2013;24(6):567-569. doi:10.1016/j.devcel.2013.03.007' apa: 'Morita, H., & Heisenberg, C.-P. J. (2013). Holding on and letting go: Cadherin turnover in cell intercalation. Developmental Cell. Cell Press. https://doi.org/10.1016/j.devcel.2013.03.007' chicago: 'Morita, Hitoshi, and Carl-Philipp J Heisenberg. “Holding on and Letting Go: Cadherin Turnover in Cell Intercalation.” Developmental Cell. Cell Press, 2013. https://doi.org/10.1016/j.devcel.2013.03.007.' ieee: 'H. Morita and C.-P. J. Heisenberg, “Holding on and letting go: Cadherin turnover in cell intercalation,” Developmental Cell, vol. 24, no. 6. Cell Press, pp. 567–569, 2013.' ista: 'Morita H, Heisenberg C-PJ. 2013. Holding on and letting go: Cadherin turnover in cell intercalation. Developmental Cell. 24(6), 567–569.' mla: 'Morita, Hitoshi, and Carl-Philipp J. Heisenberg. “Holding on and Letting Go: Cadherin Turnover in Cell Intercalation.” Developmental Cell, vol. 24, no. 6, Cell Press, 2013, pp. 567–69, doi:10.1016/j.devcel.2013.03.007.' short: H. Morita, C.-P.J. Heisenberg, Developmental Cell 24 (2013) 567–569. date_created: 2018-12-11T11:59:52Z date_published: 2013-05-25T00:00:00Z date_updated: 2021-01-12T07:00:09Z day: '25' department: - _id: CaHe doi: 10.1016/j.devcel.2013.03.007 intvolume: ' 24' issue: '6' language: - iso: eng month: '05' oa_version: None page: 567 - 569 publication: Developmental Cell publication_status: published publisher: Cell Press publist_id: '3956' quality_controlled: '1' scopus_import: 1 status: public title: 'Holding on and letting go: Cadherin turnover in cell intercalation' type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 24 year: '2013' ... --- _id: '2862' abstract: - lang: eng text: Motile cilia perform crucial functions during embryonic development and throughout adult life. Development of organs containing motile cilia involves regulation of cilia formation (ciliogenesis) and formation of a luminal space (lumenogenesis) in which cilia generate fluid flows. Control of ciliogenesis and lumenogenesis is not yet fully understood, and it remains unclear whether these processes are coupled. In the zebrafish embryo, lethal giant larvae 2 (lgl2) is expressed prominently in ciliated organs. Lgl proteins are involved in establishing cell polarity and have been implicated in vesicle trafficking. Here, we identified a role for Lgl2 in development of ciliated epithelia in Kupffer's vesicle, which directs left-right asymmetry of the embryo; the otic vesicles, which give rise to the inner ear; and the pronephric ducts of the kidney. Using Kupffer's vesicle as a model ciliated organ, we found that depletion of Lgl2 disrupted lumen formation and reduced cilia number and length. Immunofluorescence and time-lapse imaging of Kupffer's vesicle morphogenesis in Lgl2-deficient embryos suggested cell adhesion defects and revealed loss of the adherens junction component E-cadherin at lateral membranes. Genetic interaction experiments indicate that Lgl2 interacts with Rab11a to regulate E-cadherin and mediate lumen formation that is uncoupled from cilia formation. These results uncover new roles and interactions for Lgl2 that are crucial for both lumenogenesis and ciliogenesis and indicate that these processes are genetically separable in zebrafish. acknowledgement: Deposited in PMC for release after 12 months. We thank members of the Amack lab for helpful discussions and Mahendra Sonawane for donating reagents. author: - first_name: Hwee full_name: Tay, Hwee last_name: Tay - first_name: Sabrina full_name: Schulze, Sabrina last_name: Schulze - first_name: Julien full_name: Compagnon, Julien id: 2E3E0988-F248-11E8-B48F-1D18A9856A87 last_name: Compagnon - first_name: Fiona full_name: Foley, Fiona last_name: Foley - first_name: Carl-Philipp J full_name: Heisenberg, Carl-Philipp J id: 39427864-F248-11E8-B48F-1D18A9856A87 last_name: Heisenberg orcid: 0000-0002-0912-4566 - first_name: H Joseph full_name: Yost, H Joseph last_name: Yost - first_name: Salim full_name: Abdelilah Seyfried, Salim last_name: Abdelilah Seyfried - first_name: Jeffrey full_name: Amack, Jeffrey last_name: Amack citation: ama: Tay H, Schulze S, Compagnon J, et al. Lethal giant larvae 2 regulates development of the ciliated organ Kupffer’s vesicle. Development. 2013;140(7):1550-1559. doi:10.1242/dev.087130 apa: Tay, H., Schulze, S., Compagnon, J., Foley, F., Heisenberg, C.-P. J., Yost, H. J., … Amack, J. (2013). Lethal giant larvae 2 regulates development of the ciliated organ Kupffer’s vesicle. Development. Company of Biologists. https://doi.org/10.1242/dev.087130 chicago: Tay, Hwee, Sabrina Schulze, Julien Compagnon, Fiona Foley, Carl-Philipp J Heisenberg, H Joseph Yost, Salim Abdelilah Seyfried, and Jeffrey Amack. “Lethal Giant Larvae 2 Regulates Development of the Ciliated Organ Kupffer’s Vesicle.” Development. Company of Biologists, 2013. https://doi.org/10.1242/dev.087130. ieee: H. Tay et al., “Lethal giant larvae 2 regulates development of the ciliated organ Kupffer’s vesicle,” Development, vol. 140, no. 7. Company of Biologists, pp. 1550–1559, 2013. ista: Tay H, Schulze S, Compagnon J, Foley F, Heisenberg C-PJ, Yost HJ, Abdelilah Seyfried S, Amack J. 2013. Lethal giant larvae 2 regulates development of the ciliated organ Kupffer’s vesicle. Development. 140(7), 1550–1559. mla: Tay, Hwee, et al. “Lethal Giant Larvae 2 Regulates Development of the Ciliated Organ Kupffer’s Vesicle.” Development, vol. 140, no. 7, Company of Biologists, 2013, pp. 1550–59, doi:10.1242/dev.087130. short: H. Tay, S. Schulze, J. Compagnon, F. Foley, C.-P.J. Heisenberg, H.J. Yost, S. Abdelilah Seyfried, J. Amack, Development 140 (2013) 1550–1559. date_created: 2018-12-11T11:59:59Z date_published: 2013-04-01T00:00:00Z date_updated: 2021-01-12T07:00:20Z day: '01' department: - _id: CaHe doi: 10.1242/dev.087130 external_id: pmid: - '23482490' intvolume: ' 140' issue: '7' language: - iso: eng main_file_link: - open_access: '1' url: http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3596994/ month: '04' oa: 1 oa_version: Submitted Version page: 1550 - 1559 pmid: 1 publication: Development publication_status: published publisher: Company of Biologists publist_id: '3927' quality_controlled: '1' scopus_import: 1 status: public title: Lethal giant larvae 2 regulates development of the ciliated organ Kupffer’s vesicle type: journal_article user_id: 2DF688A6-F248-11E8-B48F-1D18A9856A87 volume: 140 year: '2013' ...