首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >Activation of the myogenin promoter during mouse embryogenesis in the absence of positive autoregulation.
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Activation of the myogenin promoter during mouse embryogenesis in the absence of positive autoregulation.

机译:在没有正向自动调节的情况下,小鼠胚胎发生过程中肌生成素启动子的激活。

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摘要

Myogenin, a member of the MyoD family of helix-loop-helix proteins, can induce myogenesis in a wide range of cell types. In addition to activating muscle structural genes, members of the MyoD family can autoactivate their own and cross-activate one another's expression in transfected cells. This has led to the hypothesis that autoregulatory loops among these factors provide a mechanism for amplifying and maintaining the muscle-specific gene expression program in vivo. Here, we make use of myogenin-null mice to directly test this hypothesis. To investigate whether the myogenin protein autoregulates the myogenin gene during embryogenesis, we introduced a myogenin-lacZ transgene into mice harboring a null mutation at the myogenin locus. Despite a severe deficiency of skeletal muscle in myogenin-null neonates, the myogenin-lacZ transgene was expressed normally in myogenic cells throughout embryogenesis. These results show that myogenin is not required for regulation of the myogenin gene and argue against the existence of a myogenin autoregulatory loop in the embryo.
机译:肌生成素是螺旋-环-螺旋蛋白MyoD家族的成员,可以在多种细胞类型中诱导肌发生。除了激活肌肉结构基因之外,MyoD家族的成员还可以自身激活自身并交叉激活彼此在转染细胞中的表达。这导致了这样一个假设,即这些因素之间的自动调节环提供了一种在体内扩增和维持肌肉特异性基因表达程序的机制。在这里,我们利用无肌生成素的小鼠直接检验这一假设。为了研究肌生成素蛋白是否在胚胎发生过程中自动调节肌生成素基因,我们将肌生成素-lacZ转基因引入了在肌生成素基因位点具有空突变的小鼠中。尽管无肌生成素的新生儿骨骼肌严重缺乏,但在整个胚胎发生过程中,肌生成素-lacZ转基因在肌生成细胞中正常表达。这些结果表明,肌生成素不是调控肌生成素基因所必需的,并且反对胚胎中肌生成素自调节环的存在。

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