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© The Rockefeller University Press, 0021-9525/1997//181 $5.00
The Journal of Cell Biology, Volume 139, Number 1, , 1997 181-191

Article

Laminin-induced Acetylcholine Receptor Clustering: An Alternative Pathway



J.E. Sugiyama*, D.J. Glass{ddagger}, G.D. Yancopoulos{ddagger}, and Z.W. Hall*

* National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892; and {ddagger} Regeneron Pharmaceuticals, Inc., Tarrytown, New York 10591

The induction of acetylcholine receptor (AChR) clustering by neurally released agrin is a critical, early step in the formation of the neuromuscular junction. Laminin, a component of the muscle fiber basal lamina, also induces AChR clustering. We find that induction of AChR clustering in C2 myotubes is specific for laminin-1; neither laminin-2 (merosin) nor laminin-11 (a synapse-specific isoform) are active. Moreover, laminin-1 induces AChR clustering by a pathway that is independent of that used by neural agrin. The effects of laminin-1 and agrin are strictly additive and occur with different time courses. Most importantly, laminin- 1–induced clustering does not require MuSK, a receptor tyrosine kinase that is part of the receptor complex for agrin. Laminin-1 does not cause tyrosine phosphorylation of MuSK in C2 myotubes and induces AChR clustering in myotubes from MuSK–/– mice that do not respond to agrin. In contrast to agrin, laminin-1 also does not induce tyrosine phosphorylation of the AChR, demonstrating that AChR tyrosine phosphorylation is not required for clustering in myotubes. Laminin-1 thus acts by a mechanism that is independent of that used by agrin and may provide a supplemental pathway for AChR clustering during synaptogenesis.

Address all correspondence to Dr. Zach Hall, Office of the Director, National Institute of Neurological Disorders and Stroke, National Institutes of Health, Bethesda, MD 20892. Tel.: (301) 496-9746; Fax: (301) 496-0296.

1. Abbreviation used in this paper: AChR, acetylcholine receptor.


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