作者: Raghavan Madhavan , Xiaotao T. Zhao , Albert B. Reynolds , H. Benjamin Peng
DOI: 10.1002/NEU.20320
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摘要: At developing neuromuscular junctions (NMJs), muscles initially contact motor axons by microprocesses, or myopodia, which are induced nerves and nerve-secreted agrin, but it is unclear how myopodia assembled they influence synaptic differentiation at the NMJ. Here, we report that treatment of cultured muscle cells with agrin transiently depleted p120 catenin (p120ctn) from cadherin in situ, increased tyrosine phosphorylation decreased cadherin-association p120ctn cell extracts. Whereas ectopic expression wild-type generated absence a specific dominant-negative mutant form p120ctn, blocks filopodial assembly nonmuscle cells, suppressed nerve- agrin-induction myopodia. Significantly, approaching neurites triggered reduced acetylcholine receptor (AChR) clustering along edges expressing than control although ability to cluster AChRs was itself normal. Our results indicate novel role agrin-induced myopodial suggest increase muscle–nerve contacts muscle's access neural promote NMJ formation. © 2006 Wiley Periodicals, Inc. J Neurobiol,