首页> 外文OA文献 >Global regulation of mitochondrial biogenesis in Saccharomyces cerevisiae: ABF1 and CPF1 play opposite roles in regulating expression of the QCR8 gene, which encodes subunit VIII of the mitochondrial ubiquinol-cytochrome c oxidoreductase.
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Global regulation of mitochondrial biogenesis in Saccharomyces cerevisiae: ABF1 and CPF1 play opposite roles in regulating expression of the QCR8 gene, which encodes subunit VIII of the mitochondrial ubiquinol-cytochrome c oxidoreductase.

机译:酿酒酵母中线粒体生物发生的整体调节:ABF1和CPF1在调节QCR8基因的表达中起相反的作用,该基因编码线粒体泛醌-细胞色素c氧化还原酶的VIII亚基。

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摘要

The multifunctional DNA-binding proteins ABF1 and CPF1 bind in a mutually exclusive manner to the promoter region of the QCR8 gene, which encodes 11-kDa subunit VIII of the Saccharomyces cerevisiae mitochondrial ubiquinol-cytochrome c oxidoreductase (QCR). We investigated the roles that the two factors play in transcriptional regulation of this gene. To this end, the overlapping binding sites for ABF1 and CPF1 were mutated and placed in the chromosomal context of the QCR8 promoter. The effects on transcription of the QCR8 gene were analyzed both under steady-state conditions and during nutritional shifts. We found that ABF1 is required for repressed and derepressed transcription levels and for efficient induction of transcription upon escape from catabolite repression, independently of DNA replication. CPF1 acts as a negative regulator, modulating the overall induction response. Alleviation of repression through CPF1 requires passage through the S phase. Implications of these findings for the roles played by ABF1 and CPF1 in global regulation of mitochondrial biogenesis are discussed.
机译:多功能DNA结合蛋白ABF1和CPF1以互斥的方式结合到QCR8基因的启动子区域,该基因编码酿酒酵母线粒体泛醌-细胞色素c氧化还原酶(QCR)的11-kDa VIII亚基。我们调查了两个因素在该基因的转录调控中的作用。为此,ABF1和CPF1的重叠结合位点被突变并置于QCR8启动子的染色体背景中。在稳态条件下和营养转移期间均分析了对QCR8基因转录的影响。我们发现,ABF1是抑制和降低抑制转录水平以及逃离分解代谢物抑制后有效诱导转录所必需的,而与DNA复制无关。 CPF1充当负调节器,调节整体感应响应。通过CPF1缓解压力需要经过S期。讨论了这些发现对ABF1和CPF1在线粒体生物发生的整体调控中所起的作用的含义。

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  • 作者

    de Winde, J H; Grivell, L A;

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  • 年度 1992
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  • 原文格式 PDF
  • 正文语种 en
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