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dc.contributor.authorFinegan, Tara M.
dc.contributor.authorHervieux, Nathan
dc.contributor.authorNestor-Bergmann, Alexander
dc.contributor.authorFletcher, Alexander G.
dc.contributor.authorBlanchard, Guy B.
dc.contributor.authorSanson, Bénédicte
dc.date.accessioned2019-12-06T00:05:58Z
dc.date.available2019-12-06T00:05:58Z
dc.date.issued2019-12-05
dc.date.submitted2019-07-16
dc.identifier.issn1544-9173
dc.identifier.otherpbiology-d-19-02046
dc.identifier.urihttps://www.repository.cam.ac.uk/handle/1810/299550
dc.description.abstractIn epithelia, tricellular vertices are emerging as important sites for the regulation of epithelial integrity and function. Compared to bicellular contacts, however, much less is known. In particular, resident proteins at tricellular vertices were identified only at occluding junctions, with none known at adherens junctions (AJs). In a previous study, we discovered that in Drosophila embryos, the adhesion molecule Sidekick (Sdk), well-known in invertebrates and vertebrates for its role in the visual system, localises at tricellular vertices at the level of AJs. Here, we survey a wide range of Drosophila epithelia and establish that Sdk is a resident protein at tricellular AJs (tAJs), the first of its kind. Clonal analysis showed that two cells, rather than three cells, contributing Sdk are sufficient for tAJ localisation. Super-resolution imaging using structured illumination reveals that Sdk proteins form string-like structures at vertices. Postulating that Sdk may have a role in epithelia where AJs are actively remodelled, we analysed the phenotype of sdk null mutant embryos during Drosophila axis extension using quantitative methods. We find that apical cell shapes are abnormal in sdk mutants, suggesting a defect in tissue remodelling during convergence and extension. Moreover, adhesion at apical vertices is compromised in rearranging cells, with apical tears in the cortex forming and persisting throughout axis extension, especially at the centres of rosettes. Finally, we show that polarised cell intercalation is decreased in sdk mutants. Mathematical modelling of the cell behaviours supports the notion that the T1 transitions of polarised cell intercalation are delayed in sdk mutants, in particular in rosettes. We propose that this delay, in combination with a change in the mechanical properties of the converging and extending tissue, causes the abnormal apical cell shapes in sdk mutant embryos.
dc.languageen
dc.rightsAttribution 4.0 International (CC BY 4.0)en
dc.rights.urihttps://creativecommons.org/licenses/by/4.0/en
dc.subjectResearch Article
dc.subjectBiology and life sciences
dc.subjectResearch and analysis methods
dc.subjectMedicine and health sciences
dc.subjectPhysical sciences
dc.titleThe tricellular vertex-specific adhesion molecule Sidekick facilitates polarised cell intercalation during Drosophila axis extension
dc.typeArticle
dc.date.updated2019-12-06T00:05:57Z
dc.identifier.doi10.17863/CAM.46622
dcterms.dateAccepted2019-10-31
rioxxterms.versionofrecord10.1371/journal.pbio.3000522
rioxxterms.versionVoR
rioxxterms.licenseref.urihttp://creativecommons.org/licenses/by/4.0/
datacite.contributor.supervisoreditor: Tapon, Nicolas
dc.contributor.orcidFinegan, Tara M. [0000-0003-0801-9577]
dc.contributor.orcidHervieux, Nathan [0000-0001-7567-995X]
dc.contributor.orcidNestor-Bergmann, Alexander [0000-0002-0013-2607]
dc.contributor.orcidBlanchard, Guy B. [0000-0002-3689-0522]
dc.contributor.orcidSanson, Bénédicte [0000-0002-2782-4195]
dc.identifier.eissn1545-7885
datacite.issupplementedby.doi10.17863/CAM.44798


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Attribution 4.0 International (CC BY 4.0)
Except where otherwise noted, this item's licence is described as Attribution 4.0 International (CC BY 4.0)