G-Protein Gα 13 Functions with Abl Kinase to Regulate Actin Cytoskeletal Reorganization

摘要

Abstract Heterotrimeric G-proteins are essential cellular signal transducers. One of the G-proteins, Gα 13 , is critical for actin cytoskeletal reorganization, cell migration, cell proliferation, and apoptosis. Previously, we have shown that Gα 13 is essential for both G-protein-coupled receptor and receptor tyrosine kinase-induced actin cytoskeletal reorganization such as dynamic dorsal ruffle turnover and cell migration. However, the mechanism by which Gα 13 signals to actin cytoskeletal reorganization is not completely understood. Here we show that Gα 13 directly interacts with Abl tyrosine kinase, which is a critical regulator of actin cytoskeleton. This interaction is critical for Gα 13 -induced dorsal ruffle turnover, endothelial cell remodeling, and cell migration. Our data uncover a new molecular signaling pathway by which Gα 13 controls actin cytoskeletal reorganization. Graphical abstract Display Omitted Highlights ? Signaling mechanism by which G-protein Gα 13 regulates actin cytoskeletal reorganization was investigated. ? Gα 13 and Abl tyrosine kinase directly interact. ? Gα 13 and Abl regulate the dynamic dorsal ruffle turnover. ? This interaction between Gα 13 and Abl is critical for actin cytoskeletal reorganization.