Fig. 3
α1-helix and βH are critical for the formation of multicellular structures and wound healing. a Epithelial sheet disruption assay of R2/7 cells expressing α-catenin variants. Representative αEcat monolayers before and after mechanical stress treatment are shown. b Plots showing total cell monolayer fragments after mechanical stress treatment. Mechanical disruption caused αEcatFL cell monolayers to fragment, whereas αEcat-H1 monolayers remained intact with only few fragments forming at a low calcium concentration. Data are presented as mean ± standard deviation (SD) (N = 3). Significance by ANOVA; ****P < 0.0001. c Confocal images of R2/7 cells expressing αEcat variants at the wound fronts. Close-up views of inset boxes are shown. Scale bar, 20 μm. d Scratch wound healing assays with R2/7 cells expressing αEcat-WT or αEcat-H1. The areas of wound healing after 15 hrs are shown in red. Scale bar = 50 μm. e Plots showing changes in total wound closure area and the wound closure percentage over time. Data are presented as mean ± SD (>35 fields of view (FOV); > 5 biological replicates (BR)). Significance by ANOVA; ****P < 0.0001. f Plots showing changes in the persistence, but not the velocity, of αEcat mutant cells at the wound front compared to αEcatFL cells. Data are presented as mean ± SD (>35 FOV; > 5 BR). Significance by ANOVA; **P < 0.01
