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Published 5 December 2005. doi:10.1083/jcb.200507061
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 171, Number 5, 857-869
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Article

Ral GTPases regulate neurite branching through GAP-43 and the exocyst complex



Giovanna Lalli and Alan Hall

Medical Research Council Laboratory for Molecular Cell Biology and Cell Biology Unit and Department of Biochemistry and Molecular Biology, University College London, London WC1E 6BT, England, UK

Correspondence to Alan Hall: alan.hall{at}ucl.ac.uk

Neurite branching is essential for the establishment of appropriate neuronal connections during development and regeneration. We identify the small GTPase Ral as a mediator of neurite branching. Active Ral promotes neurite branching in cortical and sympathetic neurons, whereas Ral inhibition decreases laminin-induced branching. In addition, depletion of endogenous Ral by RNA interference decreases branching in cortical neurons. The two Ral isoforms, RalA and -B, promote branching through distinct pathways, involving the exocyst complex and phospholipase D, respectively. Finally, Ral-dependent branching is mediated by protein kinase C–dependent phosphorylation of 43-kD growth-associated protein, a crucial molecule involved in pathfinding, plasticity, and regeneration. These findings highlight an important role for Ral in the regulation of neuronal morphology.

Abbreviations used in this paper: cGAP-43, chick GAP-43; EGFP-F, farnesylated EGFP; GAP-43, 43-kD growth-associated protein; GEF, guanine nucleotide exchange factor; PLD, phospholipase D; RNAi, RNA interference; SCG, superior cervical ganglia; siRNA, small interfering RNA.


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