Modulation of Saccharomyces cerevisiae DNA double-strand break repair by SRS2 and RAD51.
Modulation of Saccharomyces cerevisiae DNA double-strand break repair by SRS2 and RAD51.
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发表时间：
1995-03
期刊：
影响因子：
3.3
通讯作者：
G. T. Milne;T. Ho;D. Weaver
中科院分区：
文献类型：
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作者：
G. T. Milne;T. Ho;D. Weaver
酿酒酵母中几乎所有 DNA 双链断裂修复和重组事件都需要 RAD52 功能。为了更深入地了解 RAD52 介导的修复机制，我们筛选了在突变或过度表达时抑制 RAD52 部分活性等位基因的基因。这里描述的是 SRS2 表型无效等位基因的分离，其抑制 RAD52 (rad52B、rad52D、rad52-1 和 KlRAD52) 和 RAD51 (KlRAD51) 的多个等位基因，但未能抑制 rad52 delta 或 rad51 delta。这些结果表明SRS2在重组修复中拮抗RAD51和RAD52功能。 srs2 抑制 RAD52 等位基因的机制与之前描述的 RAD51 过表达的机制不同，因为这两种条件都显示出对 rad52B 等位基因的叠加作用。此外，RAD52 或 RAD51 的过表达增强了 srs2 delta RAD52 菌株的重组依赖性敏感性，表明 RAD52 和 RAD51 对重组修复机制有积极影响。因此，RAD52依赖性重组修复受到正向和负向控制。
RAD52 function is required for virtually all DNA double-strand break repair and recombination events in Saccharomyces cerevisiae. To gain greater insight into the mechanism of RAD52-mediated repair, we screened for genes that suppress partially active alleles of RAD52 when mutant or overexpressed. Described here is the isolation of a phenotypic null allele of SRS2 that suppressed multiple alleles of RAD52 (rad52B, rad52D, rad52-1 and KlRAD52) and RAD51 (KlRAD51) but failed to suppress either a rad52 delta or a rad51 delta. These results indicate that SRS2 antagonizes RAD51 and RAD52 function in recombinational repair. The mechanism of suppression of RAD52 alleles by srs2 is distinct from that which has been previously described for RAD51 overexpression, as both conditions were shown to act additively with respect to the rad52B allele. Furthermore, overexpression of either RAD52 or RAD51 enhanced the recombination-dependent sensitivity of an srs2 delta RAD52 strain, suggesting that RAD52 and RAD51 positively influence recombinational repair mechanisms. Thus, RAD52-dependent recombinational repair is controlled both negatively and positively.