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首页> 外文期刊>Genetics: A Periodical Record of Investigations Bearing on Heredity and Variation >The N-Terminal DNA-Binding Domain of Rad52 Promotes RAD51-Independent Recombination in Saccharomyces cerevisiae
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The N-Terminal DNA-Binding Domain of Rad52 Promotes RAD51-Independent Recombination in Saccharomyces cerevisiae

机译:Rad52的N末端DNA结合域促进酿酒酵母中RAD51独立的重组。

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In Saccharomyces cerevisiae , the Rad52 protein plays a role in both RAD51 -dependent and RAD51 -independent recombination pathways. We characterized a rad52 mutant, rad52-329 , which lacks the C-terminal Rad51-interacting domain, and studied its role in RAD51 -independent recombination. The rad52-329 mutant is completely defective in mating-type switching, but partially proficient in recombination between inverted repeats. We also analyzed the effect of the rad52-329 mutant on telomere recombination. Yeast cells lacking telomerase maintain telomere length by recombination. The rad52-329 mutant is deficient in RAD51 -dependent telomere recombination, but is proficient in RAD51 -independent telomere recombination. In addition, we examined the roles of other recombination genes in the telomere recombination. The RAD51 -independent recombination in the rad52-329 mutant is promoted by a paralogue of Rad52, Rad59. All components of the Rad50-Mre11-Xrs2 complex are also important, but not essential, for RAD51 -independent telomere recombination. Interestingly, RAD51 inhibits the RAD51 -independent, RAD52 -dependent telomere recombination. These findings indicate that Rad52 itself, and more precisely its N-terminal DNA-binding domain, promote an essential reaction in recombination in the absence of RAD51 .
机译:在酿酒酵母中,Rad52蛋白在依赖RAD51和不依赖RAD51的重组途径中均起作用。我们表征了一个rad52突变体rad52-329,它缺乏C末端Rad51相互作用域,并研究了其在RAD51独立重组中的作用。 rad52-329突变体在交配型转换中完全有缺陷,但在反向重复之间的重组方面有部分优势。我们还分析了rad52-329突变体对端粒重组的影响。缺乏端粒酶的酵母细胞通过重组保持端粒长度。 rad52-329突变体缺乏RAD51依赖的端粒重组,但擅长RAD51依赖的端粒重组。此外,我们检查了端粒重组中其他重组基因的作用。 Rad52-Rad59的旁系同源基因促进rad52-329突变体中不依赖RAD51的重组。 Rad50-Mre11-Xrs2复合体的所有组件对于不依赖RAD51的端粒重组也很重要,但不是必需的。有趣的是,RAD51抑制了RAD51依赖性,RAD52依赖性端粒重组。这些发现表明,Rad52本身,更确切地说是其N端DNA结合结构域,在不存在RAD51的情况下,促进了重组中的重要反应。

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