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J Biol Chem, Vol. 273, Issue 25, 15453-15457, June 19, 1998

Activation of G1 Progression, JNK Mitogen-activated Protein Kinase, and Actin Filament Assembly by the Exchange Factor FGD1

Koh-ichi NagataDagger , Mariette DriessensDagger , Nathalie LamarcheDagger , Jerome L. Gorskiparallel , and Alan Hall**

From the Dagger  Medical Research Council Laboratory for Molecular Cell Biology, Cancer Research Campaign Oncogene and Signal Transduction Group and the ** Department of Biochemistry, University College London, Gower Street, London WC1E 6BT, United Kingdom and the parallel  Departments of Human Genetics and Pediatrics, University of Michigan, Ann Arbor, Michigan 48109-0680

Cdc42 has been shown to control bifurcating pathways leading to filopodia formation/G1 cell cycle progression and to JNK mitogen-activated protein kinase activation. To dissect these pathways further, the cellular effects induced by a Cdc42 guanine nucleotide exchange factor, FGD1, have been examined. All exchange factors acting on the Rho GTPase family have juxtaposed Dbl homology (DH) and pleckstrin homology (PH) domains. We report here that FGD1 triggers G1 cell cycle progression and filopodia formation in Swiss 3T3 fibroblasts as well as JNK mitogen-activated protein kinase activation in COS cell transfection assays. FGD1-induced filopodia formation is Cdc42-dependent, and both the DH and PH domains are essential. Although expression of the FGD1 DH domain alone does not activate Cdc42 and induce filopodia, it does trigger both the JNK cascade in COS cells and G1 progression in quiescent Swiss 3T3 cells. We conclude that FGD1 can trigger G1 progression independently of actin polymerization or integrin adhesion complex assembly. Furthermore, since FGD1 activates JNK and G1 progression in a Cdc42-independent manner, it must have additional, as yet unidentified, targets.

Copyright © 1998 by The American Society for Biochemistry and Molecular Biology, Inc.


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