Model illustrating temporal modulating of PI(4,5)P2-dependent actomyosin contractility during tissue morphogenesis. In each horizontal row, the left two cartoons correspond to optical cross section and the right two cartoons correspond to apical view at the level of the actomyosin network. (Top row) During the slow phase, PI(4,5)P2 (black) is required for the assembly and adhesion of the network to the plasma membrane. PI(4,5)P2 contractility is opposed by the presence of PI(3,4,5)P3 (light blue) and Bottleneck (dark blue). PI(3,4,5)P3 is required for keeping the network interconnected and organized in a matrix of dense actin bundles (red) with a relative low concentration of myosin-II. Bottleneck contributes to stabilizing the network by cross-linking actin filaments and by limiting the incorporation of myosin-II (green). During the fast phase, the decrease in PI(3,4,5)P3 levels and degradation of Bottleneck (Schejter and Wieschaus, 1993a) allow PI(4,5)P2-dependent contractility and basal closure. (Bottom row) An increase in PI(4,5)P2 or a decrease in PI(3,4,5)P3 levels during the slow phase causes premature contraction and formation of shortened cells with nuclei trapped in actomyosin rings recapitulating the bottleneck mutant phenotype.
