Dechesne C A, Wei Q, Eldridge J, Gannoun-Zaki L, Millasseau P, Bougueleret L, Caterina D, Paterson B M
Laboratory of Biochemistry, National Cancer Institute, National Institutes of Health, Bethesda, Maryland 20892.
Mol Cell Biol. 1994 Aug;14(8):5474-86. doi: 10.1128/mcb.14.8.5474-5486.1994.
Members of the MyoD family of gene-regulatory proteins (MyoD, myogenin, myf5, and MRF4) have all been shown not only to regulate the transcription of numerous muscle-specific genes but also to positively autoregulate and cross activate each other's transcription. In the case of muscle-specific genes, this transcriptional regulation can often be correlated with the presence of a DNA consensus in the regulatory region CANNTG, known as an E box. Little is known about the regulatory interactions of the myogenic factors themselves; however, these interactions are thought to be important for the activation and maintenance of the muscle phenotype. We have identified the minimal region in the chicken MyoD (CMD1) promoter necessary for muscle-specific transcription in primary cultures of embryonic chicken skeletal muscle. The CMD1 promoter is silent in primary chick fibroblast cultures and in muscle cell cultures treated with the thymidine analog bromodeoxyuridine. However, CMD1 and chicken myogenin, as well as, to a lesser degree, chicken Myf5 and MRF4, expressed in trans can activate transcription from the minimal CMD1 promoter in these primary fibroblast cultures. Here we show that the CMD1 promoter contains numerous E-box binding sites for CMD1 and the other myogenic factors, as well as a MEF-2 binding site. Surprisingly, neither muscle-specific and the other myogenic factors, as well as a MEF-2 binding site. Surprisingly, neither muscle-specific expression, autoregulation, or cross activation depends upon the presence of of these E-box or MEF-2 binding sites in the CMD1 promoter. These results demonstrate that the autoregulation and cross activation of the chicken MyoD promoter through the putative direct binding of the myogenic basic helix-loop-helix regulatory factors is mediated through an indirect pathway that involves unidentified regulatory elements and/or ancillary factors.
基因调控蛋白MyoD家族的成员(MyoD、肌细胞生成素、Myf5和MRF4)不仅已被证明可调节众多肌肉特异性基因的转录,还能正向自我调节并相互交叉激活转录。就肌肉特异性基因而言,这种转录调控通常与调控区域中称为E盒的DNA共有序列CANNTG的存在相关。关于生肌因子本身的调控相互作用知之甚少;然而,这些相互作用被认为对肌肉表型的激活和维持很重要。我们已经确定了鸡MyoD(CMD1)启动子中对于胚胎鸡骨骼肌原代培养物中肌肉特异性转录所必需的最小区域。CMD1启动子在原代鸡成纤维细胞培养物以及用胸苷类似物溴脱氧尿苷处理的肌肉细胞培养物中是沉默的。然而,反式表达的CMD1和鸡肌细胞生成素,以及程度稍低的鸡Myf5和MRF4,可激活这些原代成纤维细胞培养物中最小CMD1启动子的转录。在这里我们表明,CMD1启动子包含许多用于CMD1和其他生肌因子的E盒结合位点,以及一个MEF-2结合位点。令人惊讶的是,肌肉特异性表达、自我调节或交叉激活均不依赖于CMD1启动子中这些E盒或MEF-2结合位点的存在。这些结果表明,鸡MyoD启动子通过生肌碱性螺旋-环-螺旋调控因子的假定直接结合进行的自我调节和交叉激活是通过一条间接途径介导的,该途径涉及未鉴定的调控元件和/或辅助因子。