The Rac1 GTPase CED-10 recruits WAVE and Arp2/3 at cell–cell contact and contributes to apical constriction. (A) Micrographs from time-lapse movies depicting localization of WAVE and Arp2/3 in control and ced-10 RNAi-treated embryos from a lateral view. Scale bar: 5 µm. The diagrams underneath each micrograph highlight the observed Arp2/3 localization in E and neighboring cells. (B) Violin plots reporting changes in WAVE and Arp2/3 localization at Ep-P₄ contacts, other cell–cell contacts, and the cytoplasm upon RNAi depletion of CED-10 (center dot, mean; vertical line, s.d.; outline, the distribution of the data; n = 11 embryos). (C) Micrographs from time-lapse DIC movies of wild-type and ced-10 RNAi-treated embryos with time on the left from MSa/p cell division. E-lineage cells are outlined and pseudocolored in green. Gastrulation defects (Ea or Ep cell dividing before being fully covered by neighboring cells) are indicated with white arrowheads. Scale bar: 5 µm. (D) Bar graph summarizing gastrulation defects caused by ced-10 RNAi. Statistical tests for experiments in B were chosen based on the normality and variance of the data: For WAVE (cytoplasm [control versus RNAi]), Mann–Whitney test; for WAVE (others), unpaired t test; for Arp2/3 (Ep-P4 contacts [control versus RNAi]), unpaired t test with Welch’s correction; For Arp2/3 (others), unpaired t test. Fisher’s exact test was used for categorical data in D. *P < 0.05, ***P < 0.001, ****P < 0.0001.