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

Citation data:

The Journal of cell biology, ISSN: 0021-9525, Vol: 168, Issue: 4, Page: 655-66

Publication Year:
2005
Usage 75
Abstract Views 56
Downloads 19
Citations 105
Citation Indexes 105
Repository URL:
https://digitalcommons.wustl.edu/open_access_pubs/580; https://ohsu.pure.elsevier.com/en/publications/28b32eae-2458-4c7e-b61d-a0b9ddb25b6d
PMID:
15699217
DOI:
10.1083/jcb.200411158
PMCID:
PMC2171752
Author(s):
Yang, Dongren; Bierman, Jesse; Tarumi, Yukie S.; Zhong, Yong-Ping; Rangwala, Reshma; Proctor, Thomas M.; Miyagoe-Suzuki, Yuko; Takeda, Shin'ichi; Miner, Jeffrey H.; Sherman, Larry S.; Gold, Bruce G.; Patton, Bruce L. Show More Hide
Publisher(s):
Rockefeller University Press
Tags:
Biochemistry, Genetics and Molecular Biology; Cell Biology
article description
Schwann cells form basal laminae (BLs) containing laminin-2 (Ln-2; heterotrimer alpha2beta1gamma1) and Ln-8 (alpha4beta1gamma1). Loss of Ln-2 in humans and mice carrying alpha2-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 (alpha5beta1gamma1) 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.