Turku Centre for Biotechnology, Turku 20521, Finland.
J Cell Biol. 2011 Jul 25;194(2):291-306. doi: 10.1083/jcb.201012126. Epub 2011 Jul 18.
Integrin trafficking from and to the plasma membrane controls many aspects of cell behavior including cell motility, invasion, and cytokinesis. Recruitment of integrin cargo to the endocytic machinery is regulated by the small GTPase Rab21, but the detailed molecular mechanisms underlying integrin cargo recruitment are yet unknown. Here we identify an important role for p120RasGAP (RASA1) in the recycling of endocytosed α/β1-integrin heterodimers to the plasma membrane. Silencing of p120RasGAP attenuated integrin recycling and augmented cell motility. Mechanistically, p120RasGAP interacted with the cytoplasmic domain of integrin α-subunits via its GAP domain and competed with Rab21 for binding to endocytosed integrins. This in turn facilitated exit of the integrin from Rab21- and EEA1-positive endosomes to drive recycling. Our results assign an unexpected role for p120RasGAP in the regulation of integrin traffic in cancer cells and reveal a new concept of competitive binding of Rab GTPases and GAP proteins to receptors as a regulatory mechanism in trafficking.
整合素从质膜到质膜的转运控制着细胞行为的许多方面,包括细胞运动、侵袭和胞质分裂。整合素货物向胞内体机制的募集受小 GTP 酶 Rab21 调节,但整合素货物募集的详细分子机制尚不清楚。在这里,我们发现 p120RasGAP(RASA1)在再循环内化的α/β1-整合素异二聚体到质膜中起着重要作用。p120RasGAP 的沉默减弱了整合素的再循环,并增强了细胞运动。在机制上,p120RasGAP 通过其 GAP 结构域与整合素α亚基的细胞质结构域相互作用,并与 Rab21 竞争与内化的整合素结合。这反过来又促进了整合素从 Rab21 和 EEA1 阳性内涵体中逸出,从而驱动再循环。我们的结果为 p120RasGAP 在癌细胞中整合素运输的调节中赋予了一个意想不到的作用,并揭示了 Rab GTPases 和 GAP 蛋白与受体的竞争结合作为运输中的调节机制的新概念。