在单个双链断裂附近的大反向重复序列强烈影响缺乏Rad51的酵母二倍体中的修复。
Large inverted repeats in the vicinity of a single double-strand break strongly affect repair in yeast diploids lacking Rad51.
作者信息
Downing Brandon, Morgan Rachel, VanHulle Kelly, Deem Angela, Malkova Anna
机构信息
Department of Biology, School of Science, IUPUI, Indianapolis, IN 46202-5132, USA.
出版信息
Mutat Res. 2008 Oct 14;645(1-2):9-18. doi: 10.1016/j.mrfmmm.2008.07.013. Epub 2008 Aug 5.
Abstract
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 rad51Delta yeast diploids that was stimulated by a DNA region termed "facilitator of break-induced replication" (FBI) located approximately 30kb 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 rad54Delta 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.
摘要
DNA双链断裂（DSBs）是关键的损伤，可导致细胞死亡或染色体重排。尽管存在许多不依赖RAD51的途径，但Rad51对于大多数有丝分裂和减数分裂DSB修复事件是必需的。此前，我们描述了rad51Delta酵母二倍体中的DSB修复，该修复受到一个称为“断裂诱导复制促进因子”（FBI）的DNA区域的刺激，该区域位于HO诱导的DSB位点约30kb处。在这里，我们证明FBI是一个大的反向DNA重复序列，它将DSB的修复引导到单链退火-大规模染色体重排（SSA-GCR）途径。此外，对rad54Delta细胞中DSB修复的分析使我们提出，在Rad51p存在的情况下，SSA-GCR修复途径受到抑制。因此，Rad51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免于不稳定。
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