首页> 外文期刊>Proceedings of the National Academy of Sciences of the United States of America >MYOCYTE-SPECIFIC ENHANCER FACTOR 2 ACTS COOPERATIVELY WITH A MUSCLE ACTIVATOR REGION TO REGULATE DROSOPHILA TROPOMYOSIN GENE MUSCLE-EXPRESSION
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MYOCYTE-SPECIFIC ENHANCER FACTOR 2 ACTS COOPERATIVELY WITH A MUSCLE ACTIVATOR REGION TO REGULATE DROSOPHILA TROPOMYOSIN GENE MUSCLE-EXPRESSION

机译:肌球蛋白特定增强子因子2与肌激活剂区域协同作用以调节果蝇营养蛋白基因基因的肌肉表达

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MEF2 (myocyte-specific enhancer factor 2) is a MADS box transcription factor that is thought to be a key regulator of myogenesis in vertebrates. Mutations in the Drosophila homologue of the mef2 gene indicate that it plays a key role in regulating myogenesis in Drosophila, We show here that the Drosophila tropomyosin I (TmI) gene is a target gene for mef2 regulation. The TmI gene contains a proximal and a distal muscle enhancer within the first intron of the gene, We show that both enhancers contain a MEF2 binding site and that a mutation in the MEF2 binding site of either enhancer significantly reduces reporter gene expression in embryonic, larval, and adult somatic body wall muscles of transgenic flies. We also show that a high level of proximal enhancer-directed reporter gene expression in somatic muscles requires the cooperative activity of MEF2 and a cis-acting muscle activator region located within the enhancer. Thus, mef2 null mutant embryos show a significant reduction but not an elimination of TmI expression in the body wall myoblasts and muscle fibers that are present. Surprisingly, there is little effect in these mutants on TmI expression in developing visceral muscles and dorsal vessel (heart), despite the fact that MEF2 is expressed in these muscles in wild-type embryos, indicating that TmI expression is regulated differently in these muscles. Taken together, our results show that mef2 is a positive regulator of tropomyosin gene transcription that is necessary but not sufficient for high level expression in somatic muscle of the embryo, larva, and adult. [References: 25]
机译:MEF2(肌细胞特异性增强因子2)是MADS盒转录因子,被认为是脊椎动物肌发生的关键调节因子。 mef2基因的果蝇同源物中的突变表明它在果蝇中调节肌发生中起关键作用。我们在这里表明果蝇原肌球蛋白I(TmI)基因是调节mef2的目标基因。 TmI基因在该基因的第一个内含子中包含一个近端和远端肌肉增强子,我们显示这两个增强子均包含一个MEF2结合位点,并且任一增强子的MEF2结合位点的突变都显着降低了胚胎,幼虫中的报告基因表达。 ,以及成年果蝇的体细胞壁肌肉。我们还显示,在体肌中高水平的近端增强子指导的报告基因表达需要MEF2和位于增强子中的顺式作用肌激活剂区域的协同活性。因此,在存在的体壁成肌细胞和肌纤维中,mef2空突变体胚胎显示出TmI表达的显着降低,但没有消除。出乎意料的是,尽管MEF2在野生型胚胎的这些肌肉中表达,但这些突变体对发育中的内脏肌肉和背血管(心脏)中的TmI表达几乎没有影响,这表明这些肌肉中TmI的表达受到不同的调节。两者合计,我们的结果表明mef2是原肌球蛋白基因转录的正向调节剂,对于在胚胎,幼虫和成年体细胞中高水平表达是必需的,但不足以达到这一目的。 [参考:25]

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