| First Author | Liu Y | Year | 2012 |
| Journal | Dev Biol | Volume | 366 |
| Issue | 2 | Pages | 255-67 |
| PubMed ID | 22537499 | Mgi Jnum | J:185422 |
| Mgi Id | MGI:5428773 | Doi | 10.1016/j.ydbio.2012.04.003 |
| Citation | Liu Y, et al. (2012) beta-Catenin stabilization in skeletal muscles, but not in motor neurons, leads to aberrant motor innervation of the muscle during neuromuscular development in mice. Dev Biol 366(2):255-67 |
| abstractText | beta-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 beta-catenin gain-of-function mouse model to stabilize beta-catenin selectively in either skeletal muscles or motor neurons. We found that beta-catenin stabilization in skeletal muscles resulted in increased motor axon number and excessive intramuscular nerve defasciculation and branching. In contrast, beta-catenin stabilization in motor neurons had no adverse effect on motor innervation pattern. Furthermore, stabilization of beta-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 beta-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 beta-catenin is mediated by a non-cell autonomous mechanism. |
