v-Crk regulates membrane dynamics and Rac activation.
Cell migration is an integrated process that involves cell adhesion, protrusion and contraction. We recently used CAS (Crk-associated substrate, 130CAS)-deficient mouse embryo fibroblasts (MEFs) to examined contribution made to v-Crk to that process via its interaction with Rac1. v-Crk, the oncogene product of avian sarcoma virus CT10, directly affects membrane ruffle formation and is associated with Rac1 activation, even in the absence of CAS, a major substrate for Crk. In CAS-deficient MEFs, cell spreading and lamellipodium dynamics are delayed; moreover, Rac activation is significantly reduced and it is no longer targeted to the membrane. However, expression of v-Crk by CAS-deficient MEFs increased cell spreading and active lamellipodium protrusion and retraction. v-Crk expression appears to induce Rac1 activation and its targeting to the membrane, which directly affects membrane dynamics and, in turn, cell migration. It thus appears that v-Crk/Rac1 signaling contributes to the regulation of membrane dynamics and cell migration, and that v-Crk is an effector molecule for Rac1 activation that regulates cell motility.
Yeo
Myeong Gu
MG
Cell Dynamics Research Center and Bioimaging Research Center, Department of Life Science, Gwangju Institute of Science and Technology, Buk-gu, Gwangju, Korea.
Song
Woo Keun
WK
D000818:Animals; D002462:Cell Membrane / Q000378:metabolism*; D004789:Enzyme Activation; D050736:Oncogene Protein v-crk / Q000378:metabolism*; D015398:Signal Transduction; D020744:rac GTP-Binding Proteins / Q000378:metabolism*
D050736:Oncogene Protein v-crk; D020744:rac GTP-Binding Proteins