Cell signaling facilitates apical constriction by basolaterally recruiting Arp2/3 via Rac and WAVE.

Apical constriction is a critical cell shape change that drives cell internalization and tissue bending. How precisely localized actomyosin regulators drive apical constriction remains poorly understood. Caenorhabditis elegans gastrulation provides a valuable model to address this question. The Arp2/3 complex is essential in C. elegans gastrulation. To understand how Arp2/3 is locally regulated, we imaged embryos with endogenously tagged Arp2/3 and its nucleation-promoting factors (NPFs). The three NPFs-WAVE, WASP, and WASH-controlled Arp2/3 localization at distinct subcellular locations. We exploited this finding to study distinct populations of Arp2/3 and found that only WAVE depletion caused penetrant gastrulation defects. WAVE localized basolaterally with Arp2/3 and controlled F-actin levels near cell-cell contacts. WAVE and Arp2/3 localization depended on CED-10/Rac. Establishing ectopic cell contacts recruited WAVE and Arp2/3, identifying the contact as a symmetry-breaking cue for localization of these proteins. These results suggest that cell-cell signaling via Rac activates WAVE and Arp2/3 basolaterally and that basolateral Arp2/3 makes an important contribution to apical constriction.