Src-FAK–dependent actomyosin remodeling is sufficient for E-cadherin relaxation, and dissociation of β-catenin is not required. (A) MDCK cells treated 4 h with or without HGF and stained with phalloidin, for pMLC and β-catenin. Arrowheads indicate fibers enriched in pMLC. Empty arrows indicate a cortex devoid of pMLC. Normalized intensity profiles of actin (phalloidin), pMLC, and contacts (β-catenin) of boxed regions shown on the right with same color code. (B) Stress fiber number per cell for conditions shown in panel a and Fig. S5 B (n = –HGF 99, +HGF 147, +HGF+PP1 68, +HGF+PF228 50 cells). (C) pMLC density at the cortex (C) or in stress fibers (S) for conditions shown in panel a and Fig. S5 B (n = C/S –HGF 40/45, +HGF 61/107, +HGF+PP1 26/20, and +HGF+PF228 35/33 cells). (D) Typical expression pattern and schematics of the β-catenin-less actin-binding E-α-TSMod chimera compared with EcadTSMod. (E) FRET index of E-α-TSMod in a wounded MDCK sheet. Top: Typical map. Bottom: FRET index of E-α-TSMod in leader (n = 135) and back (n = 245) cells of a wounded sheet. (F) FRET index of E-α-TSMod in cells with and without HGF (50 ng/ml). Top: Typical map. Bottom: FRET index change of E-α-TSMod 5 h after addition (n = 46 cells) or not (n = 45) of HGF (50 ng/ml). Bars, 20 µm. Two-tailed Mann–Whitney or Kruskal–Wallis tests. Values plotted are mean ± SEM.