Β-Catenin stabilization in skeletal muscles, but not in motor neurons, leads to aberrant motor innervation of the muscle during neuromuscular development in mice

Yun Liu, Yoshie Sugiura, Fenfen Wu, Wentao Mi, Makoto M. Taketo, Steve Cannon, Thomas Carroll, Weichun Lin

Research output: Contribution to journalArticle

25 Scopus citations

Abstract

Β-Catenin, a key component of the Wnt signaling pathway, has been implicated in the development of the neuromuscular junction (NMJ) in mice, but its precise role in this process remains unclear. Here we use a Β-catenin gain-of-function mouse model to stabilize Β-catenin selectively in either skeletal muscles or motor neurons. We found that Β-catenin stabilization in skeletal muscles resulted in increased motor axon number and excessive intramuscular nerve defasciculation and branching. In contrast, Β-catenin stabilization in motor neurons had no adverse effect on motor innervation pattern. Furthermore, stabilization of Β-catenin, either in skeletal muscles or in motor neurons, had no adverse effect on the formation and function of the NMJ. Our findings demonstrate that Β-catenin levels in developing muscles in mice are crucial for proper muscle innervation, rather than specifically affecting synapse formation at the NMJ, and that the regulation of muscle innervation by Β-catenin is mediated by a non-cell autonomous mechanism.

Original languageEnglish (US)
Pages (from-to)255-267
Number of pages13
JournalDevelopmental Biology
Volume366
Issue number2
DOIs
StatePublished - Jun 15 2012

Keywords

  • Acetylcholine receptor
  • Mouse genetics
  • Nerve defasciculation
  • Neuromuscular junction
  • Synaptic transmission

ASJC Scopus subject areas

  • Molecular Biology
  • Developmental Biology
  • Cell Biology

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