--- - "\nAbstract\nAlterations in mechanical properties in the extracellular matrix are modulated by myofibroblasts and are required for progressive fibrotic diseases. Recently, we reported that fibroblasts depleted of SPIN90 showed enhanced differentiation into myofibroblasts via increased acetylation of microtubules in the soft matrix; the mechanisms of the underlying signaling network, however, remain unclear. In this study, we determine the effect of depletion of SPIN90 on FAK/ROCK signaling modules. Transcriptome analysis of \nSpin90 KO mouse embryonic fibroblasts (MEF) and fibroblasts activated by TGF‐β revealed that \nPostn is the most significantly upregulated gene. Knockdown of \nPostn by small interfering RNA suppressed cell adhesion and myofibroblastic differentiation and downregulated FAK activity in \nSpin90 KO MEF. Our results indicate that SPIN90 depletion activates FAK/ROCK signaling, induced by \nPostn expression, which is critical for myofibroblastic differentiation on soft matrices mimicking the mechanical environment of a normal tissue." - Journal of Cellular Physiology, EarlyView.