NEUROMUSCULAR JUNCTION MORPHOLOGY, FIBER-TYPE PROPORTIONS, AND SATELLITE-CELL PROLIFERATION RATES ARE ALTERED IN MyoD-/- MICE
NEUROMUSCULAR JUNCTION MORPHOLOGY, FIBER-TYPE PROPORTIONS, AND SATELLITE-CELL PROLIFERATION RATES ARE ALTERED IN MyoD-/- MICE
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DOI：
10.1002/mus.21637
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发表时间：
2010-07-01
期刊：
影响因子：
3.4
通讯作者：
Patel, Ketan
中科院分区：
文献类型：
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作者：
Macharia, Raymond;Otto, Anthony;Patel, Ketan
生肌调节因子(MRF)家族成员的基因补偿被认为可以解释MyoD(-/-)小鼠明显的正常成年表型。神经和场刺激被用来研究MyoD(-/-)小鼠肌肉的收缩特性，分子方法被用来研究卫星细胞的行为。我们证明MyoD缺失会导致神经肌肉连接的组织发生重大变化，这对骨骼肌的生理收缩特性有很大的影响。其次，我们发现，在没有MyoD的情况下，卫星细胞的谱系进展(特别是最初的增殖)是异常的，并与β-连环蛋白核定位的扰动有关，β-连环蛋白是经典Wnt信号的关键读数。这些结果表明，MyoD在发育中和成年骨骼肌中都具有独特的功能，这是MRF家族的其他成员所没有的。肌肉神经42：38-52,2010
Gene compensation by members of the myogenic regulatory factor (MRF) family has been proposed to explain the apparent normal adult phenotype of MyoD(-/-) mice. Nerve and field stimulation were used to investigate contraction properties of muscle from MyoD(-/-) mice, and molecular approaches were used to investigate satellite-cell behavior. We demonstrate that MyoD deletion results in major alterations in the organization of the neuromuscular junction, which have a dramatic influence on the physiological contractile properties of skeletal muscle. Second, we show that the lineage progression of satellite cells (especially initial proliferation) in the absence of MyoD is abnormal and linked to perturbations in the nuclear localization of beta-catenin, a key readout of canonical Wnt signaling. These results show that MyoD has unique functions in both developing and adult skeletal muscle that are not carried out by other members of the MRF family. Muscle Nerve 42: 38-52, 2010