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The CUP1 upstream repeated element renders CUP1 promoter activation insensitive to mutations in the RNA polymerase II transcription complex

机译:CUP1上游重复元件使CUP1启动子激活对RNA聚合酶II转录复合物中的突变不敏感

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摘要

Activation of transcription in eukaryotes requires the concerted action of numerous components of the RNA polymerase II transcriptional apparatus. The degree of dependence on many of these components varies from gene to gene and it is still largely unknown how the requirement for any particular component is determined at any given gene. We show that removal of Gal11 from the yeast transcription complex can affect activation from the CUP1 UAS in a manner dependent on its genomic context. Our results indicate a novel function for the CUP1 upstream repeated element (CURE) located upstream of the CUP1 UAS at the naturally multimerized CUP1 locus. The presence of CURE endowed the CUP1 UAS with a reduced susceptibility to the effects of deleting Gal11. Similar results were obtained with the Srb/mediator subunit Srb5. Restoration of activation from the CUP1 promoter to wild-type levels by he CURE correlated with changes in the accessibility of local chromatin to nucleases. The CURE sequence may serve to protect the stress-inducible CUP1 UAS-promoter elements against reduced activation that may result from crippled transcription complexes under stress conditions.
机译:真核生物中转录的激活需要RNA聚合酶II转录装置的许多成分的协同作用。依赖于这些成分中的许多成分的程度因基因而异,并且在很大程度上仍然未知如何在任何给定的基因上确定对任何特定成分的需求。我们显示,从酵母转录复合物中去除Gal11可以影响CUP1 UAS的活化,具体取决于其基因组背景。我们的结果表明,CUP1上游重复元件(CURE)在天然多聚CUP1基因座上位于CUP1 UAS上游的一种新功能。 CURE的存在使CUP1 UAS对删除Gal11的影响的敏感性降低。用Srb /介体亚基Srb5获得了相似的结果。 CURE将CUP1启动子的激活恢复到野生型水平与局部染色质对核酸酶可及性的改变有关。 CURE序列可用于保护应激诱导的CUP1 UAS启动子元件免受在应激条件下由残废的转录复合物引起的降低的活化。

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