Rac GTPases control axon growth, guidance and branching

Julian Ng, Timothy Nardine, Matthew Harms, Julia Tzu, Ann Goldstein, Yan Sun, Georg Dietzl, Barry J. Dickson and Liqun Luo ()
Additional contact information
Julian Ng: Stanford University
Timothy Nardine: Stanford University
Matthew Harms: Stanford University
Julia Tzu: Stanford University
Ann Goldstein: Stanford University
Yan Sun: Research Institute of Molecular Pathology
Georg Dietzl: Research Institute of Molecular Pathology
Barry J. Dickson: Research Institute of Molecular Pathology
Liqun Luo: Stanford University

Nature, 2002, vol. 416, issue 6879, 442-447

Abstract: Abstract Growth, guidance and branching of axons are all essential processes for the precise wiring of the nervous system. Rho family GTPases transduce extracellular signals to regulate the actin cytoskeleton1. In particular, Rac has been implicated in axon growth and guidance2,3,4,5,6,7,8. Here we analyse the loss-of-function phenotypes of three Rac GTPases in Drosophila mushroom body neurons. We show that progressive loss of combined Rac1, Rac2 and Mtl activity leads first to defects in axon branching, then guidance, and finally growth. Expression of a Rac1 effector domain mutant that does not bind Pak rescues growth, partially rescues guidance, but does not rescue branching defects of Rac mutant neurons. Mosaic analysis reveals both cell autonomous and non-autonomous functions for Rac GTPases, the latter manifesting itself as a strong community effect in axon guidance and branching. These results demonstrate the central role of Rac GTPases in multiple aspects of axon development in vivo, and suggest that axon growth, guidance and branching could be controlled by differential activation of Rac signalling pathways.

Date: 2002
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DOI: 10.1038/416442a

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