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首页> 外文期刊>Molecular and Cellular Biology >Accelerated Response of the myogenin Gene to Denervation in Mutant Mice Lacking Phosphorylation of Myogenin at Threonine 87
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Accelerated Response of the myogenin Gene to Denervation in Mutant Mice Lacking Phosphorylation of Myogenin at Threonine 87

机译：在苏氨酸87缺乏肌生成素磷酸化的突变小鼠中，肌生成素基因对神经支配的加速反应。

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Gene expression in skeletal muscle is regulated by a family of myogenic basic helix-loop-helix (bHLH) proteins. The binding of these bHLH proteins, notably MyoD and myogenin, to E-boxes in their own regulatory regions is blocked by protein kinase C (PKC)-mediated phosphorylation of a single threonine residue in their basic region. Because electrical stimulation increases PKC activity in skeletal muscle, these data have led to an attractive model suggesting that electrical activity suppresses gene expression by stimulating phosphorylation of this critical threonine residue in myogenic bHLH proteins. We show that electrical activity stimulates phosphorylation of myogenin at threonine 87 (T87) in vivo and that calmodulin-dependent kinase II (CaMKII), as well as PKC, catalyzes this reaction in vitro. We find that phosphorylation of myogenin at T87 is dispensable for skeletal muscle development. We show, however, that the decrease in myogenin (myg) expression following innervation is delayed and that the increase in expression following denervation is accelerated in mutant mice lacking phosphorylation of myogenin at T87. These data indicate that two distinct innervation-dependent mechanisms restrain myogenin activity: an inactivation mechanism mediated by phosphorylation of myogenin at T87, and a second, novel regulatory mechanism that regulates myg gene activity independently of T87 phosphorylation.
机译：骨骼肌中的基因表达受成肌碱性螺旋-环-螺旋（bHLH）蛋白家族的调节。这些bHLH蛋白（特别是MyoD和肌生成素）与它们自身调控区域中的E-box的结合被其基本区域中单个苏氨酸残基的蛋白激酶C（PKC）介导的磷酸化所阻断。因为电刺激增加了骨骼肌中PKC的活性，所以这些数据导致了一个有吸引力的模型，表明电活性通过刺激成肌bHLH蛋白中该关键苏氨酸残基的磷酸化来抑制基因表达。我们表明电活动刺激苏氨酸87（T87）在体内的肌生成素的磷酸化和钙调蛋白依赖性激酶II（CaMKII），以及PKC，在体外催化该反应。我们发现，T87时肌生成素的磷酸化对于骨骼肌发育是必不可少的。然而，我们表明，神经支配后 myogenin （ myg ）的表达延迟被延迟，去神经支配后表达的增加在缺乏肌原蛋白磷酸化的突变小鼠中被加速。 T87。这些数据表明，两种不同的神经支配依赖性机制抑制肌生成素的活性：一种由T87上的肌生成素的磷酸化介导的失活机制，以及第二种新颖的调节机制，其独立于T87的磷酸化来调节 myg 基因的活性。

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