ABSTRACT
Epithelial remodeling of the Drosophila retina depends on the generation of pulsatile contractile and protrusive forces that repeatedly contract and expand the apical contacts between the lattice cells (LCs) that form its hexagonal lattice. Phosphoinositide PI(3,4,5)P3 (PIP3) accumulates around tricellular adherens junctions (tAJs) when cell-cell contacts expand and dissipates when they contract, but its significance in this process is unknown. Here we found that manipulations of Pten or Pi3K that either decreased or increased PIP3 resulted in similar phenotypes characterized by shortened contacts and a disordered lattice, indicating a requirement for dynamics and turnover of PIP3. We further show that these phenotypes are caused by a loss of protrusive branched F-actin, the result of impaired activity of the Rac1 Rho GTPase and the WAVE regulatory complex (WRC). We additionally found that during contact expansion, Pi3K moves into tAJs where it is positioned to promote the cyclical increase of PIP3 in a spatially and temporally precise manner. Taken together, the results show that dynamic regulation of PIP3 by Pten and Pi3K is critical for the protrusive phase of junctional remodeling, which is essential for planar epithelial morphogenesis.
Competing Interest Statement
The authors have declared no competing interest.
