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Published online January 22, 2007
doi:10.1083/jcb.200609021
The Journal of Cell Biology, Vol. 176, No. 3, 277-282
The Rockefeller University Press, 0021-9525 $30.00
© 2007 Grove et al.
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Report

 FAK is required for axonal sorting by Schwann cells

Matthew Grove1, Noboru H. Komiyama2, Klaus-Armin Nave3, Seth G. Grant2, Diane L. Sherman1, and Peter J. Brophy1

1 Centre for Neuroscience Research, University of Edinburgh, Edinburgh EH9 1QH, Scotland, UK
2 Wellcome Trust Sanger Institute, Hinxton CB10 1SA, England, UK
3 Department of Neurogenetics, Max-Planck-Institute of Experimental Medicine, 37075 Göttingen, Germany

Correspondence to Peter J. Brophy: Peter.Brophy{at}ed.ac.uk

Signaling by laminins and axonal neuregulin has been implicated in regulating axon sorting by myelin-forming Schwann cells. However, the signal transduction mechanisms are unknown. Focal adhesion kinase (FAK) has been linked to {alpha}6ß1 integrin and ErbB receptor signaling, and we show that myelination by Schwann cells lacking FAK is severely impaired. Mutant Schwann cells could interdigitate between axon bundles, indicating that FAK signaling was not required for process extension. However, Schwann cell FAK was required to stimulate cell proliferation, suggesting that amyelination was caused by insufficient Schwann cells. ErbB2 receptor and AKT were robustly phosphorylated in mutant Schwann cells, indicating that neuregulin signaling from axons was unimpaired. These findings demonstrate the vital relationship between axon defasciculation and Schwann cell number and show the importance of FAK in regulating cell proliferation in the developing nervous system.

Abbreviations used in this paper: CNS, central nervous system; E, embryonic day; ES, embryonic stem; P, postnatal day; PNS, peripheral nervous system.


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