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First published online June 3, 2009
In this issue |
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Despite their high degree of similarity, the Rho GTPases Rac1 and Rac3 have opposing effects on neuronal morphology and differentiation – Rac1 induces cell spreading and neuritogenesis, but Rac 3 promotes cell rounding and prevents differentiation. On page 2127, John Collard and colleagues report new findings on the protein-protein interactions of Rac3 that help to explain these striking functional differences. Using a neuroblastoma cell line, the authors show that Rac3 (like Rac1) interacts with GIT1, a scaffolding protein that also acts as an Arf GTPase-activating protein (GAP) and has roles in cell adhesion and spreading. In contrast to Rac1, however, the Rac3-GIT1 interaction is not mediated by βPix (which interacts with GIT1). Moreover, Rac3 disrupts the interaction between GIT1 and the focal-adhesion protein paxillin (which is stimulated by Rac1). Notably, the authors show that Rac3-induced cell rounding results from the GIT1-dependent inactivation of the GTPase Arf6, and that expressing Arf6 or its activator ARNO restores spreading in Rac3-expressing cells. On the basis of their data, the authors propose that Rac1 and Rac3 oppose each other by differentially modulating GIT1 function. This work sheds light on the mechanism of neuronal differentiation.
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