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Significance Substrate rigidity has important roles for physiological processes, such as stem cell differentiation and cell growth. Although substrate rigidity clearly modulates gene expression, the mechanism of rigidity control of gene expression remains unknown. Our work reveals that four-and-a-half LIM domains (domain discovered in the proteins, Lin11, Isl-1, and Mec-3) 2 moves from adhesion sites to the nucleus on soft substrates through focal adhesion kinase activity and up-regulates p21 gene expression. Thus, we show a molecular pathway for inhibiting cell growth on soft substrates.

Matrix mechanics controls FHL2 movement to the nucleus to activate p21 expression