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Publication : Control of axonal branching and synapse formation by focal adhesion kinase.

First Author  Rico B Year  2004
Journal  Nat Neurosci Volume  7
Issue  10 Pages  1059-69
PubMed ID  15378065 Mgi Jnum  J:93215
Mgi Id  MGI:3056242 Doi  10.1038/nn1317
Citation  Rico B, et al. (2004) Control of axonal branching and synapse formation by focal adhesion kinase. Nat Neurosci 7(10):1059-1069
abstractText  The formation of neuronal networks in the central nervous system (CNS) requires precise control of axonal branch development and stabilization. Here we show that cell-specific ablation of the murine gene Ptk2 (more commonly known as fak), encoding focal adhesion kinase (FAK), increases the number of axonal terminals and synapses formed by neurons in vivo. Consistent with this, fak mutant neurons also form greater numbers of axonal branches in culture because they have increased branch formation and reduced branch retraction. Expression of wild-type FAK, but not that of several FAK variants that prevent interactions with regulators of Rho family GTPases including the p190 Rho guanine nuclear exchange factor (p190RhoGEF), rescues the axonal arborization phenotype observed in fak mutant neurons. In addition, expression of a mutant p190RhoGEF that cannot associate with FAK results in a phenotype very similar to that of neurons lacking FAK. Thus, FAK functions as a negative regulator of axonal branching and synapse formation, and it seems to exert its actions, in part, through Rho family GTPases.
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