|
|
|
|
|
|
|
||
* National Institute of Mental Health, National Institutes of Health, Bethesda, Maryland 20892; and 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 Regeneron
Pharmaceuticals, Inc., Tarrytown, New York 10591
/ 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.
CiteULike 
Complore 
Connotea 
Del.icio.us 
Digg 
Reddit 
Technorati What's this?
This article has been cited by other articles:
|
|
