Large inverted repeats in the vicinity of a single double-strand break strongly affect repair in yeast diploids lacking Rad51
Large inverted repeats in the vicinity of a single double-strand break strongly affect repair in yeast diploids lacking Rad51
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DOI：
10.1016/j.mrfmmm.2008.07.013
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发表时间：
2008-10-14
影响因子：
2.3
通讯作者：
Malkova, Anna
中科院分区：
文献类型：
--
作者：
Downing, Brandon;Morgan, Rachel;Malkova, Anna
DNA双链断裂（DSB）是可导致细胞死亡或染色体重排的关键病变。Rad 51对于大多数有丝分裂和减数分裂DSB修复事件是必需的，尽管存在许多不依赖于Rad 51的途径。以前，我们描述了DSB修复在rad 51三角洲酵母二倍体，被称为“促进剂的断裂诱导的复制”（FBI）位于约30 kb的HO诱导的DSB的网站的DNA区域刺激。在这里，我们证明了FBI是一个大的反向DNA重复，通道的单链退火-总染色体重排（SSA-GCR）途径的DSB的修复。此外，在rad 54 δ细胞中DSB修复的分析使我们能够提出SSA-GCR修复途径在Rad 51 p存在下被抑制。因此，Rad 51的另一个作用可能是通过防止染色体重排来保护真核基因组不稳定。(C)2008 Elsevier B. V.保留所有权利。
DNA double-strand breaks (DSBs) are critical lesions that can lead to cell death or chromosomal rearrangements. Rad51 is necessary for most mitotic and meiotic DSB repair events, although a number of RAD51-independent pathways exist. Previously, we described DSB repair in rad51 Delta yeast diploids that was stimulated by a DNA region termed "facilitator of break-induced replication" (FBI) located approximately 30 kb from the site of an HO-induced DSB. Here, we demonstrate that FBI is a large inverted DNA repeat that channels the repair of DSBs into the single-strand annealing-gross chromosomal rearrangements (SSA-GCR) pathway. Further, analysis of DSB repair in rad54 Delta cells allowed us to propose that the SSA-GCR repair pathway is suppressed in the presence of Rad51p. Therefore, an additional role of Rad51 might be to protect eukaryotic genomes from instabilities by preventing chromosomal rearrangements. (C) 2008 Elsevier B.V. All rights reserved.