The G Protein Gα13 Is Required for Growth Factor-Induced Cell Migration

SummaryHeterotrimeric G proteins are critical cellular signal transducers. They are known to directly relay signals from seven-transmembrane G protein-coupled receptors (GPCRs) to downstream effectors. On the other hand, receptor tyrosine kinases (RTKs), a different family of membrane receptors, signal through docking sites in their carboxy-terminal tails created by autophosphorylated tyrosine residues. Here we show that a heterotrimeric G protein, Gα13, is essential for RTK-induced migration of mouse fibroblast and endothelial cells. Gα13 activity in cell migration is retained in a C-terminal mutant that is defective in GPCR coupling, suggesting that the migration function is independent of GPCR signaling. Thus, Gα13 appears to be a critical signal transducer for RTKs as well as GPCRs. This broader role of Gα13 in cell migration initiated by two types of receptors could provide a molecular basis for the vascular system defects exhibited by Gα13 knockout mice.