1
Department of Neurobiology, University of Pittsburgh School of Medicine, 3500 Terrace Street, Room E1440 BST, Pittsburgh, Pennsylvania 15261, USA.
2
These authors contributed equally to this work.
Correspondence should be addressed to Zuo-Zhong Wang zzwang@pitt.edu
At the developing neuromuscular junction, motor neuron−derived agrin triggers the differentiation of postsynaptic membrane into a highly specialized structure, where the nicotinic acetylcholine receptors (AChRs) are aggregated into high-density clusters. Agrin acts by activating the muscle-specific kinase MuSK and inducing coaggregation of the 43-kDa protein rapsyn with AChRs on muscle cell membrane1,
2. The signaling mechanism downstream of MuSK is poorly defined. We report here that the mouse tumor suppressor protein adenomatous polyposis coli (APC) has a role in AChR clustering and that the Wnt/-catenin pathway may crosstalk with agrin signaling cascade during synapse formation.
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-catenin pathway may crosstalk with agrin signaling cascade during synapse formation.
