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Inhibition of MuSK Expression by CREB Interacting with a CRE-Like Element and MyoD

机译：CREB与CRE样元素和MyoD相互作用抑制MuSK表达

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The type I receptor-like protein tyrosine kinase MuSK is essential for the neuromuscular junction formation. MuSK expression is tightly regulated during development, but the underlying mechanisms were unclear. Here we identified a novel mechanism by which MuSK expression may be regulated. A cyclic AMP response element (CRE)-like element in the 5′-flanking region of the MuSK gene binds to CREB1 (CRE-binding protein 1). Mutation of this element increases the MuSK promoter activity, suggesting a role for CREB1 in attenuation of MuSK expression. Interestingly, CREB mutants unable to bind to DNA also inhibit MuSK promoter activity, suggesting a CRE-independent inhibitory mechanism. In agreement, CREB1 could inhibit a mutant MuSK transgene reporter whose CRE site was mutated. We provide evidence that CREB interacts directly with MyoD, a myogenic factor essential for MuSK expression in muscle cells. Suppression of CREB expression by small interfering RNA increases MuSK promoter activity. These results demonstrate an important role for CREB1 in the regulation of MuSK expression.
机译：I型受体样蛋白酪氨酸激酶MuSK对于神经肌肉接头的形成至关重要。在开发过程中，MuSK的表达受到严格的调控，但其潜在机制尚不清楚。在这里，我们确定了一种新的机制，通过它可以调节MuSK表达。 MuSK基因5'侧翼区域的环状AMP反应元件（CRE）样元件与CREB1（CRE结合蛋白1）结合。该元素的突变增加了MuSK启动子的活性，提示CREB1在MuSK表达的减弱中起作用。有趣的是，无法结合DNA的CREB突变体也抑制MuSK启动子活性，提示了CRE依赖性抑制机制。一致地，CREB1可以抑制突变的MuSK转基因报告基因，其CRE位点被突变。我们提供的证据表明CREB与MyoD直接相互作用，MyoD是肌肉细胞中MuSK表达所必需的成肌因子。小干扰RNA抑制CREB表达可增加MuSK启动子活性。这些结果证明了CREB1在MuSK表达的调节中的重要作用。

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