Pten, Pi3K and PtdIns(3,4,5)P ₃ dynamics modulate pulsatile actin branching in Drosophila retina morphogenesis

Epithelial remodeling of the Drosophila retina depends on the pulsatile contraction and expansion of apical contacts between the cells that form its hexagonal lattice. Phosphoinositide PI(3,4,5)P ₃ (PIP ₃ ) accumulates around tricellular adherens junctions (tAJs) during contact expansion and dissipates during contraction, but with unknown function. Here we found that manipulations of Pten or Pi3K that either decreased or increased PIP ₃ resulted in shortened contacts and a disordered lattice, indicating a requirement for PIP ₃ dynamics and turnover. These phenotypes are caused by a loss of protrusive branched actin, resulting from impaired activity of the Rac1 Rho GTPase and the WAVE regulatory complex (WRC). We additionally found that during contact expansion, Pi3K moves into tAJs to promote the cyclical increase of PIP ₃ in a spatially and temporally precise manner. Thus, dynamic regulation of PIP ₃ by Pten and Pi3K controls the protrusive phase of junctional remodeling, which is essential for planar epithelial morphogenesis.