β-Catenin stabilization in skeletal muscles, but not in motor neurons, leads to aberrant motor innervation of the muscle during neuromuscular development in mice
Autor: | Yun Liu, Wentao Mi, Thomas L. Carroll, Yoshie Sugiura, Weichun Lin, Fenfen Wu, Steve C. Cannon, Makoto Mark Taketo |
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Rok vydání: | 2012 |
Předmět: |
medicine.medical_specialty
Beta-catenin Neuromuscular Junction Mouse genetics Neurotransmission Biology Article Neuromuscular junction Mice 03 medical and health sciences 0302 clinical medicine Internal medicine medicine Animals Synaptic transmission Acetylcholine receptor Axon Muscle Skeletal Molecular Biology Process (anatomy) beta Catenin 030304 developmental biology Motor Neurons 0303 health sciences Wnt signaling pathway Cell Biology medicine.anatomical_structure Endocrinology nervous system Nerve defasciculation Organ Specificity Catenin Synapses biology.protein Neuroscience 030217 neurology & neurosurgery Developmental Biology |
Zdroj: | Developmental Biology. 366:255-267 |
ISSN: | 0012-1606 |
DOI: | 10.1016/j.ydbio.2012.04.003 |
Popis: | 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. |
Databáze: | OpenAIRE |
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