The Journal of Cell Biology, Vol 98, 550-557, Copyright © 1984 by The Rockefeller University Press
Participation of calcium and calmodulin in the formation of acetylcholine receptor clusters
HB Peng
The formation of acetylcholine receptor (AChR) clusters can be
experimentally induced in cultured Xenopus myotomal muscle cells by
positive polypeptide-coated latex beads (Peng, H.B., P.-C. Cheng, and P.W.
Luther, 1981, Nature [Lond.], 292:831-834). This provides a simple
procedure for studying the cellular process of AChR clustering. In this
study, the involvement of calcium and calmodulin in this process was
examined. A deprivation in extracellular calcium by calcium-free medium or
by the addition of calcium antagonists such as divalent cations Co2+ and
Ni2+ (1-5 mM) or organic compounds verapamil and D-600 (0.1-0.5 mM)
suppressed the formation of AChR clusters induced by the latex beads in a
largely reversible manner. Antagonists against calmodulin, including
trifluoperazine (1-5 microM) and the naphthalene sulfonamide W-7 (20
microM), also suppressed AChR clustering. However, the effect of W-7 was
much weaker than that of trifluoperazine (TFP). Although the formation of
AChR clusters is inhibited by these drugs, the stability of the existent
clusters is relatively insensitive to them. These data suggest that the
clustering of AChR involves a Ca2+ and calmodulin- activated process.
Immunofluorescence studies using an antibody against calmodulin indicate
that calmodulin is diffusely distributed in the cytoplasm in addition to
its localization at the I-bands. Thus I propose that a local rise in
intracellular calcium caused by a locally applied stimulus, exemplified
here by the polypeptide-coated latex beads, may trigger the formation of
AChR clusters. Furthermore, the cellular machinery for this process may
involve calmodulin and is diffusely distributed in the muscle cell.
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