p130(Cas) (Cas) is an adaptor molecule which becomes tyrosine phosphorylated by v-Src- or v-Crk-triggered transformation and several physiological stimuli, such as cell attachment to fibronectin. We previously generated mice lacking Cas and demonstrated that Cas functions as an assembling molecule of actin filaments. To further explore Cas role in cellular function, we established Cas-deficient and Cas-re-expressing fibroblasts and compared their behaviors in response to several biological stimuli. We found that Cas-deficient fibroblasts showed significant defects in cell movement after mechanical wounding and in cell migration toward fibronectin as compared with Cas-re-expressing cells. In addition, when plated on fibronectin-coated dishes, Cas-deficient cells exhibited a significant delay in cell spreading as compared with Cas-re-expressing cells albeit that protein-tyrosine phosphorylation was similarly induced. These results demonstrated that Cas functions as a molecule promoting cell movement, cell migration, and cell spreading and suggest that Cas would be implicated in various physiological and pathological processes, such as would healing, chemotaxis, and tumor invasion.
Copyright 1999 Academic Press.