• 主题
高级搜索  >
历史搜索 清空历史
首页> 外文期刊>Molecular and Cellular Biology >A synthetic silencer mediates SIR-dependent functions in Saccharomyces cerevisiae.
【24h】

A synthetic silencer mediates SIR-dependent functions in Saccharomyces cerevisiae.

机译：合成的消音剂可在酿酒酵母中介导SIR依赖性功能。

获取原文
           
页面导航
  • 摘要
  • 著录项
  • 相似文献
  • 相关主题

摘要

Copies of the mating-type genes are present at three loci on chromosome III of the yeast Saccharomyces cerevisiae. The genes at the MAT locus are transcribed, whereas the identical genes at the silent loci, HML and HMR, are not transcribed. Several genes, including the four SIR genes, and two sites, HMR-E and HMR-I, are required for repression of transcription at the HMR locus. Three elements have been implicated in the function of the HMR-E silencer: a binding site for the RAP1 protein, a binding site for the ABF1 protein, and an 11-bp consensus sequence common to nearly all autonomously replicating sequence (ARS) elements (putative origins of DNA replication). RAP1 and ABF1 binding sites of different sequence than those found at HMR-E were joined with an 11-bp ARS consensus sequence to form a synthetic silencer. The synthetic silencer was able to repress transcription of the HMRa1 gene, confirming that binding sites for RAP1 and ABF1 and the 11-bp ARS consensus sequence were the functional components of the silencer in vivo. Mutations in the ABF1 binding site or in the ARS consensus sequence of the synthetic silencer caused nearly complete derepression of transcription at HMR. The ARS consensus sequence mutation also eliminated the ARS activity of the synthetic silencer. These data suggested that replication initiation at the HMR-E silencer was required for establishment of the repressed state at the HMR locus.
机译：交配型基因的拷贝存在于酿酒酵母Saccharomyces cerevisiae的染色体III的三个基因座上。 MAT基因座上的基因被转录，而沉默位点HML和HMR上的相同基因没有被转录。抑制HMR基因座上的转录需要几个基因，包括四个SIR基因和两个位点HMR-E和HMR-1。 HMR-E沉默子的功能涉及三个要素：RAP1蛋白的结合位点，ABF1蛋白的结合位点和几乎所有自主复制序列（ARS）元素共有的11 bp共有序列（ DNA复制的推定来源）。与在HMR-E处发现的序列不同的RAP1和ABF1结合位点与11 bp的ARS共有序列连接在一起，形成合成的沉默子。合成的沉默子能够抑制HMRa1基因的转录，从而证实RAP1和ABF1的结合位点以及11 bp的ARS共有序列是沉默子在体内的功能组件。合成沉默子的ABF1结合位点或ARS共有序列中的突变几乎导致HMR转录的完全抑制。 ARS共有序列突变也消除了合成消音器的ARS活性。这些数据表明，在HMR位点建立抑制状态需要在HMR-E沉默子处启动复制。

著录项

相似文献

  • 外文文献
  • 中文文献
  • 专利
获取原文

客服邮箱：kefu@zhangqiaokeyan.com

京公网安备：11010802029741号 ICP备案号：京ICP备15016152号-6 六维联合信息科技 (北京) 有限公司©版权所有

  • 客服微信

  • 服务号