Finally, it was shown that polarised cell intercalation is decreased in sdk mutants. 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. Apical cell shapes were found to be abnormal in sdk mutants, suggesting a defect in tissue remodelling during convergence and extension. Postulating that Sdk may have a role in epithelia where AJs are actively remodelled, the phenotype of sdk null mutant embryos during Drosophila axis extension was analyzed using quantitative methods. Super-resolution imaging using structured illumination reveals that Sdk proteins form string-like structures at vertices. Clonal analysis showed that two cells, rather than three cells, contributing Sdk are sufficient for tAJ localisation. This study surveyed a wide range of Drosophila epithelia and establish that Sdk is a resident protein at tricellular AJs (tAJs), the first of its kind. A previous study 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. In particular, resident proteins at tricellular vertices were identified only at occluding junctions, with none known at adherens junctions (AJs). Compared to bicellular contacts, however, much less is known. In epithelia, tricellular vertices are emerging as important sites for the regulation of epithelial integrity and function. The tricellular vertex-specific adhesion molecule Sidekick facilitates polarised cell intercalation during Drosophila axis extension. M., Hervieux, N., Nestor-Bergmann, A., Fletcher, A. NCBI link: EntrezGene, Nucleotide, Proteinįinegan, T.
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