The tricellular vertex-specific adhesion molecule Sidekick facilitates polarised cell intercalation during Drosophila axis extension

• Published in: bioRxiv
• Main Authors: Finegan, Tara M, Hervieux, Nathan, Nestor-Bergmann, Alexander, Fletcher, Alexander G, Blanchard, Guy B, Sanson, Benedicte
• Format: Paper
• Language: English
• Published: Cold Spring Harbor Cold Spring Harbor Laboratory Press 16.07.2019
• Subjects: Adherens junctions; Cell size; Drosophila; Embryos; Insects; Intercalation; Invertebrates; Mathematical models; Mechanical properties; Phenotypes; Visual system
• DOI: 10.1101/704932

In epithelia, tricellular vertices are emerging as important sites for the regulation of epithelial integrity and function. Compared to bicellular contacts, however, much less knowledge is available. In particular, resident proteins at tricellular vertices were identified only at occluding junctions, with none known at adherens junctions. 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 adherens junctions. Here, we survey a wide range of Drosophila epithelia and establish that Sdk is a resident protein at tricellular adherens junctions, the first of its kind. Clonal analysis suggests that pair-wise homophilic adhesion is necessary and sufficient for Sdk tricellular vertex 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 adherens junctions 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 strikingly abnormal in sdk mutants. Moreover, adhesion at apical vertices is compromised in rearranging cells, with holes forming and persisting throughout axis extension. Finally, we show that polarized cell intercalation is decreased and abnormal in sdk mutants. Mathematical modeling of the cell behaviours supports the conclusion that the T1 transitions of polarized cell intercalation are delayed in sdk mutants. We propose that this delay, in combination with a change in the mechanical properties of the converging and extending tissue, causes the striking cell shape phenotype of sdk mutant embryos.