Co-operative Cdc42 and Rho signalling mediates ephrinB-triggered endothelial cell retraction

摘要: Cell repulsion responses to Eph receptor activation are linked rapid actin cytoskeletal reorganizations, which in turn partially mediated by Rho–ROCK (Rho kinase) signalling, driving actomyosin contractility. In the present study, we show that Rho alone is not sufficient for this response. Rather, Cdc42 (cell division cycle 42) and its effector MRCK (myotonic dystrophy kinase-related Cdc42-binding also critical ephrinB-induced cell retraction. Stimulation of endothelial cells with ephrinB2 triggers rapid, but transient, We that, although membrane retraction fully blocked blebbistatin (a myosin-II ATPase inhibitor), it only inhibiting suggesting there ROCK-independent signalling contractility downstream EphBs. find a combination either or inhibition ROCK completely abolishes Additionally, endocytosis ephrin–Eph complexes required initial retraction, essential subsequent Rac-mediated re-spreading cells. Our data reveal complex interplay Rho, Rac process EphB-mediated retraction–recovery responses.