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XB-ART-41285
Mol Cell Neurosci June 1, 2010; 44 (2): 118-28.

Balanced Vav2 GEF activity regulates neurite outgrowth and branching in vitro and in vivo.

Moon MS , Gomez TM .


Abstract
We have investigated the role of Vav2, a reported Rac1/Cdc42 GEF, on the development of Xenopus spinal neurons in vitro and in vivo. Both gain and loss of Vav2 function inhibited the rate neurite extension on laminin (LN), while only GFP-Vav2 over-expression enhanced process formation and branching. Vav2 over-expression protected neurons from RhoA-mediated growth cone collapse, similar to constitutively active Rac1, suggesting that Vav2 activates Rac1 in spinal neurons. Enhanced branching on LN required both Vav2 GEF activity and N-terminal tyrosine residues, but protection from RhoA-mediated collapse only required GEF activity. Interestingly, wild-type spinal neurons exhibited increased branching on the cell adhesion molecule L1, which required Vav2 GEF function, but not N-terminal tyrosine residues. Finally, we find that Vav2 differentially affects the Rohon-Beard peripheral and central process extension but promotes neurite branching of commissural interneurons near the ventral midline. Together, we suggest that balanced Vav2 activity is necessary for optimal neurite outgrowth and promotes branching by targeting GEF activity to branch points.

PubMed ID: 20298788
PMC ID: PMC2862809
Article link: Mol Cell Neurosci
Grant support: [+]
Genes referenced: cdc42 rac1 rhoa vav2
Morpholinos: vav2 MO1

References [+] :
Abe, Vav2 is an activator of Cdc42, Rac1, and RhoA. 2000, Pubmed


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