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RNA聚合酶II起始速率的降低可抑制THO突变体的过度重组和转录延伸损伤。

A reduction in RNA polymerase II initiation rate suppresses hyper-recombination and transcription-elongation impairment of THO mutants.

作者信息

Jimeno Sonia, García-Rubio Maria, Luna Rosa, Aguilera Andrés

机构信息

Centro Andaluz de Biologia Molecular y Medicina Regenerativa CABIMER, Universidad de Sevilla-CSIC, Av. Américo Vespucio s/n, 41092 Sevilla, Spain.

出版信息

Mol Genet Genomics. 2008 Oct;280(4):327-36. doi: 10.1007/s00438-008-0368-8. Epub 2008 Aug 6.

DOI:10.1007/s00438-008-0368-8
PMID:18682986
Abstract

Hrs1/Med3, a component of the Mediator involved in transcription initiation, was previously isolated as a suppressor of hpr1Delta hyper-recombination linked to transcription elongation. Here we show that hrs1Delta-mediated suppression is specific of transcription-associated hyper-recombination (TAR). The decrease in recombination associated with hrs1Delta, either in wild-type or hpr1Delta cells is only observed in DNA repeats constructs in which transcription is Hrs1-dependent. We propose that the suppression of THO mutants by hrs1Delta is due to the specific effect of hrs1Delta on transcription initiation of the recombination system. In parallel we show that the higher the transcription of a gene the more important becomes the THO complex for its expression, implying that the in vivo relevance of this complex is dependent on the frequency of RNAPII transcription initiation. This study furthers the understanding of the importance of THO in transcription and the maintenance of genome stability.

摘要

Hrs1/Med3是中介体的一个组成部分,参与转录起始,此前被分离为与转录延伸相关的hpr1Delta高重组的抑制因子。在此我们表明,hrs1Delta介导的抑制是转录相关高重组(TAR)所特有的。与hrs1Delta相关的重组减少,无论是在野生型还是hpr1Delta细胞中,仅在转录依赖于Hrs1的DNA重复构建体中观察到。我们提出,hrs1Delta对THO突变体的抑制是由于hrs1Delta对重组系统转录起始的特定作用。同时我们表明,一个基因的转录越高,THO复合物对其表达就越重要,这意味着该复合物在体内的相关性取决于RNA聚合酶II转录起始的频率。这项研究进一步加深了对THO在转录和基因组稳定性维持中的重要性的理解。

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