Fig 3. Knockdown of individual Septins result in class-independent wound repair phenotypes.

(A-G’) Confocal max projection images of wounds generated in embryos expressing an actin marker (sGMCA) in control (vermilion RNAi; A), Sep1 RNAi (B), Sep2² mutant (C), Pnut RNAi (D), Sep4 RNAi (E), Sep5² mutant (F), and Pnut+Sep4 RNAi (G). (A’-G’) Kymographs across the wound area depicted in A-G, respectively. Wound expansion is highlighted by yellow lines. Actin recruitment to the actomyosin ring is indicated by yellow arrows. Actomyosin ring disassembly (or lack thereof) is indicated by red arrowheads. Actin accumulation internal to the wound is indicated by blue arrows. Failure of the wound to close is indicated by blue arrowheads. Scale bars: 20μm. (H-N) Quantification of the wound area over time for knockdowns shown in (A-G), respectively. (O-R) Quantification of actin ring dynamics in Septin knockdowns. Quantification of fold wound expansion (O), Wound contraction rate (P), actin ring width (Q), actin ring intensity (R). Black line and error bars represent mean ± SEM. Red dotted line and square represent mean ± 95% CI from control. Kruskal-Wallis test (blue) and Mann-Whitney test (green): * p<0.05, ** p<0.01, *** p<0.001, **** p<0.0001, ns is not significant. Comparison to control is indicated by blue asterisks; comparisons of individual pairs are indicated by a line and green asterisks.