Fig. 2.

CD98hc depletion impairs rigidity sensing. a Representative morphology of control or CD98hc-null dermal fibroblasts grown on FN-coated hydrogels of specified elastic modulus. Scale bar is 50 µm. Cell area is plotted as means with s.e.m. as error bars (n = 40–54 cells, ^**P < 0.01, ^****P < 0.0001 in a one-way ANOVA). b Loss of CD98hc in fibroblasts impairs RhoA activation upon substrate stiffening. c, d Loss of CD98hc impairs cell contractility (c) and rigidity sensing (d). Traction force microscopy was performed on subconfluent cells. Black and black hatched bar, control cells, gray and gray hatched bar, CD98hc-null cells (mean + s.e.m., n = 3, ^**P < 0.01 in a one-way ANOVA). Scale bar is 50 µm. e Loss of CD98hc impairs YAP/Taz activation by mechanical cues as measured by ANKRD1 and CTGF transcript quantification by RT-qPCR. Black bars, control cells and gray bars, CD98hc-null cells (mean + s.e.m., n = 3, ^****P < 0.0001 in a Student’s t test). f Forcing RhoA activation using CNF1 in CD98hc-null cells rescues YAP/Taz activation by mechanical cues. Means are plotted with s.e.m. as error bars. n = 2 **P < 0.01 in a Student’s t test