A mechanism for acetylcholine receptor clustering distinct from agrin signaling.

W. A. Grow, M. Ferns, H. Gordon

Research output: Contribution to journalArticle

Abstract

Acetylcholine receptors (AChRs) and other postsynaptic molecules cluster spontaneously on cultured C2 myotubes. The frequency of clustering is enhanced by neural agrin, neuraminidase, or calcium through a signaling pathway which includes tyrosine phosphorylation of a muscle-specific kinase (MuSK) and the AChR beta-subunit. Vicia villosa agglutinin (VVA) lectin, previously shown to potentiate agrin-induced clustering on C2 myotubes, is shown here to also potentiate neuraminidase- and calcium-induced clustering of AChRs, while having no effect on the level of tyrosine phosphorylation of MuSK or the AChR beta-subunit. We propose that VVA lectin increases the frequency of AChR clustering through a mechanism that is distinct from agrin signaling, and that may involve alpha-dystroglycan.

Original languageEnglish (US)
Pages (from-to)436-443
Number of pages8
JournalDevelopmental Neuroscience
Volume21
Issue number6
StatePublished - 1999

Fingerprint

Agrin
Cholinergic Receptors
Cluster Analysis
Skeletal Muscle Fibers
Neuraminidase
Tyrosine
Phosphorylation
Dystroglycans
Calcium
Muscles
Vicia lectins

ASJC Scopus subject areas

  • Neuroscience(all)

Cite this

A mechanism for acetylcholine receptor clustering distinct from agrin signaling. / Grow, W. A.; Ferns, M.; Gordon, H.

In: Developmental Neuroscience, Vol. 21, No. 6, 1999, p. 436-443.

Research output: Contribution to journalArticle

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