Loss of migfilin expression has no overt consequences on murine development and homeostasis

Abstract

Migfilin is a LIM-domain-containing protein of the zyxin family of adaptor proteins and is found at cell-matrix and cell-cell adhesion sites and in the nucleus. In vitro studies have suggested that migfilin promotes β1 integrin activity, regulates cell spreading and migration and induces cardiomyocyte differentiation. To test directly the function of migfilin in vivo, we generated a migfilin-null mouse strain. Here, we report that loss of migfilin expression permits normal development and normal postnatal aging. Fibroblasts and keratinocytes from migfilin-null mice display normal spreading and adhesion, and normal integrin expression and activation. The migration velocity and directionality of migfilin-null embryonic fibroblasts were normal, whereas the velocity of migfilin-null keratinocytes in wound scratch assays was slightly but significantly reduced. Our findings indicate that the roles of migfilin are functionally redundant during mouse development and tissue homeostasis.