Figure 3

Rac and SCAR knockdowns exhibit different cell wound repair phenotypes. (A–I) Confocal projection images of wounds generated in embryos expressing an actin marker (sGMCA) in control (buffer only; A–C), NSC 23766 injected (potent Rac inhibitor; D–F), or SCAR RNAi knockdowns (G–I). Actin ring and halo are indicated in (A). (A’,D’,G’) Kymographs across the wound area in (A,D,G), respectively. Wound expansion is noted with yellow lines; actomyosin ring formation with red arrows; and actomyosin ring disassembly with yellow arrows. (B,E,H) XY projection image at 0–150 s post wounding showing cortical flow of actin to the wound edge. (C,F,I) Vector maps from PIV (Particle Image Velocimetry) analysis depicting actin flow from 60 to 90 s for (A,B,D,E,G,H) respectively. (J) Quantification of the wound area over time for control (buffer injected), NSC 23766 injected, and SCAR RNAi knockdowns. (K–N) Quantification of fold wound expansion (K), wound contraction rate (L), actin ring width (M), and actin ring intensity (N). Black line and error bars represent mean ± SEM. Red dotted line and square represent mean ± 95% CI from control. Kruskal–Wallis test (K–L) and Welch’s t-test (M–N) were performed with * is p < 0.05, ** is p < 0.01, *** is p < 0.001, **** is p < 0.0001, and ns is not significant. Scale bars: 20 μm.