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首页> 外文期刊>Molecular and Cellular Biology >Transcription of the dominant-negative helix-loop-helix protein Id1 is regulated by a protein complex containing the immediate-early response gene Egr-1.
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Transcription of the dominant-negative helix-loop-helix protein Id1 is regulated by a protein complex containing the immediate-early response gene Egr-1.

机译：显性负螺旋-环-螺旋蛋白Id1的转录受包含立即反应基因Egr-1的蛋白复合物调控。

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The expression of Id1, a helix-loop-helix protein which inhibits the activity of basic helix-loop-helix transcription factors, is down-regulated during cellular differentiation and cell cycle withdrawal both in tissue culture models and in mouse embryos. In order to study the mechanism of control of Idl expression, we have isolated a 210-bp enhancer element in the upstream region of the Id1 gene whose activity recapitulates Id1 expression in C2C12 muscle cells and C3H10T1/2 fibroblasts: i.e., this element is active in proliferating cells in the presence of serum and completely inactivated upon mitogen depletion, cell cycle withdrawal, and (in the case of C2C12) induced myoblast differentiation. Using linker-scanning mutations and site-directed mutagenesis in transient transfection experiments, we have identified two functional elements within the 210-bp enhancer which are required for proper serum responsiveness. One element (A) contains a consensus Egr-1 binding site and additional flanking sequences required for optimal activity, and the other element (B) fits no known consensus. Gel shift experiments demonstrate that the protein complex binding to the A site contains Egr-1 and other proteins. This complex as well as a protein complex that binds to the B site is lost within 24 h of serum depletion, correlating with the down-regulation of Id1 expression. On the basis of these findings, we propose that the regulation of the Id1 response to serum is mediated in part by the early response gene Egr-1 and as such provides a signaling link between the early-growth-response transcription factors and dominant-negative helix-loop-helix proteins.
机译：在组织培养模型和小鼠胚胎中，在细胞分化和细胞周期退出过程中，Id1的表达下调，Id1是一种抑制基本螺旋-环-螺旋转录因子活性的螺旋-环-螺旋蛋白。为了研究控制Idl表达的机制，我们在Id1基因的上游区域分离了一个210 bp的增强子元件，该元件的活性概括了C2C12肌肉细胞和C3H10T1 / 2成纤维细胞中Id1的表达：即，该元件具有活性在血清存在下增殖细胞中，并在有丝分裂原耗竭，细胞周期停滞和（在C2C12的情况下）诱导成肌细胞分化时完全失活。在瞬时转染实验中使用接头扫描突变和定点诱变，我们确定了210 bp增强子中的两个功能元件，这些元件是适当的血清反应性所必需的。一个元素（A）包含一个共有的Egr-1结合位点和最佳活性所需的其他侧翼序列，另一个元素（B）不符合已知的共识。凝胶位移实验表明与A位点结合的蛋白质复合物包含Egr-1和其他蛋白质。该复合物以及与B位点结合的蛋白质复合物在血清耗尽后24小时内消失，这与Id1表达的下调相关。基于这些发现，我们建议对Id1血清的应答的调节部分由早期应答基因Egr-1介导，因此提供了早期应答转录因子与显性负应答之间的信号传导联系。螺旋-环-螺旋蛋白。

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