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Msh1p在线粒体碱基切除修复中发挥多种作用的证据。

Evidence that msh1p plays multiple roles in mitochondrial base excision repair.

作者信息

Pogorzala Leah, Mookerjee Shona, Sia Elaine A

机构信息

Department of Biology, University of Rochester, Rochester, New York 14627, USA.

出版信息

Genetics. 2009 Jul;182(3):699-709. doi: 10.1534/genetics.109.103796. Epub 2009 Apr 27.

Abstract

Mitochondrial DNA is thought to be especially prone to oxidative damage by reactive oxygen species generated through electron transport during cellular respiration. This damage is mitigated primarily by the base excision repair (BER) pathway, one of the few DNA repair pathways with confirmed activity on mitochondrial DNA. Through genetic epistasis analysis of the yeast Saccharomyces cerevisiae, we examined the genetic interaction between each of the BER proteins previously shown to localize to the mitochondria. In addition, we describe a series of genetic interactions between BER components and the MutS homolog MSH1, a respiration-essential gene. We show that, in addition to their variable effects on mitochondrial function, mutant msh1 alleles conferring partial function interact genetically at different points in mitochondrial BER. In addition to this separation of function, we also found that the role of Msh1p in BER is unlikely to be involved in the avoidance of large-scale deletions and rearrangements.

摘要

线粒体DNA被认为特别容易受到细胞呼吸过程中通过电子传递产生的活性氧物种的氧化损伤。这种损伤主要通过碱基切除修复(BER)途径来减轻,BER是少数几个已证实对线粒体DNA有活性的DNA修复途径之一。通过对酿酒酵母的遗传上位性分析,我们研究了先前显示定位于线粒体的每种BER蛋白之间的遗传相互作用。此外,我们描述了BER组分与MutS同源物MSH1(一个呼吸必需基因)之间的一系列遗传相互作用。我们表明,除了它们对线粒体功能的可变影响外,赋予部分功能的突变msh1等位基因在线粒体BER的不同点上发生遗传相互作用。除了这种功能分离外,我们还发现Msh1p在BER中的作用不太可能涉及避免大规模缺失和重排。

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