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Published online 7 February 2005. doi:10.1083/jcb.200411158
The Rockefeller University Press, 0021-9525 $8.00
JCB, Volume 168, Number 4, 655-666
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Article

Coordinate control of axon defasciculation and myelination by laminin-2 and -8



Dongren Yang1, Jesse Bierman1, Yukie S. Tarumi1, Yong-Ping Zhong1, Reshma Rangwala3, Thomas M. Proctor1, Yuko Miyagoe-Suzuki4, Shin'ichi Takeda4, Jeffrey H. Miner5, Larry S. Sherman3, Bruce G. Gold1,2, and Bruce L. Patton1

1 Center for Research on Occupational and Environmental Toxicology, Oregon Health and Science University, Portland, OR 97239
2 Department of Neurology, Oregon Health and Science University, Portland, OR 97239
3 Division of Neuroscience, Oregon National Primate Research Center, Beaverton, OR 97006
4 National Institute for Neuroscience, Center for Neurology and Psychiatry, Tokyo 187-8502, Japan
5 Renal Division, Washington University School of Medicine, St. Louis, MO 63110

Correspondence to Bruce L. Patton: pattonb{at}ohsu.edu

Schwann cells form basal laminae (BLs) containing laminin-2 (Ln-2; heterotrimer {alpha}2ß1{gamma}1) and Ln-8 ({alpha}4ß1{gamma}1). Loss of Ln-2 in humans and mice carrying {alpha}2-chain mutations prevents developing Schwann cells from fully defasciculating axons, resulting in partial amyelination. The principal pathogenic mechanism is thought to derive from structural defects in Schwann cell BLs, which Ln-2 scaffolds. However, we found loss of Ln-8 caused partial amyelination in mice without affecting BL structure or Ln-2 levels. Combined Ln-2/Ln-8 deficiency caused nearly complete amyelination, revealing Ln-2 and -8 together have a dominant role in defasciculation, and that Ln-8 promotes myelination without BLs. Transgenic Ln-10 ({alpha}5ß1{gamma}1) expression also promoted myelination without BL formation. Rather than BL structure, we found Ln-2 and -8 were specifically required for the increased perinatal Schwann cell proliferation that attends myelination. Purified Ln-2 and -8 directly enhanced in vitro Schwann cell proliferation in collaboration with autocrine factors, suggesting Lns control the onset of myelination by modulating responses to mitogens in vivo.

Abbreviations used in this paper: BL, basal lamina; CNS, central nervous system; Ln, laminin.


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