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. 2016 May 1;129(9):1843–1854. doi: 10.1242/jcs.185447

Fig. 4.

Fig. 4.

Force-activated, E-cadherin-dependent cell stiffening requires Src, PI3K, myosin and ROCK. (A) Time sequence for measurements of the impact of inhibitors on ΔRMS Traction and adaptive stiffening. (B) The mean±s.e.m. change in the root mean square traction forces (ΔRMS Traction, Pa), after force-loading E-cadherin beads bound to cells treated with inhibitors of ROCK1 and ROCK2 (Y27632, n=12 cells), myosin II (Blebbistatin, n=9 cells), Src kinase (PP2, n=8 cells), or PI3K (LY294002, n=7 cells). Two independent experiments were performed. (C) The mean±s.e.m. percentage stiffness change, after 2 min of force-loading E-cadherin beads bound to cells treated with inhibitors of myosin II (blebbistatin, n=43 beads), ROCK1 (Y27632, n=33 beads), Src kinase (PP2, n=39 beads), PI3K (LY294002, n=22 beads; Wortmanin, n=47 beads). For the DMSO controls, n=50 beads, and more than 50 beads were analyzed in the PP3 controls. Two independent experiments were performed. *P<0.05 (Student's t-test).