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优先作用于短同源序列的不依赖RAD51的断裂诱导复制的特征分析。

Characterization of RAD51-independent break-induced replication that acts preferentially with short homologous sequences.

作者信息

Ira Grzegorz, Haber James E

机构信息

Rosenstiel Center and Department of Biology, Brandeis University, Waltham, Massachussetts 02454-9110, USA.

出版信息

Mol Cell Biol. 2002 Sep;22(18):6384-92. doi: 10.1128/MCB.22.18.6384-6392.2002.

Abstract

Repair of double-strand breaks by gene conversions between homologous sequences located on different Saccharomyces cerevisiae chromosomes or plasmids requires RAD51. When repair occurs between inverted repeats of the same plasmid, both RAD51-dependent and RAD51-independent repairs are found. Completion of RAD51-independent plasmid repair events requires RAD52, RAD50, RAD59, TID1 (RDH54), and SRS2 and appears to involve break-induced replication coupled to single-strand annealing. Surprisingly, RAD51-independent recombination requires much less homology (30 bp) for strand invasion than does RAD51-dependent repair (approximately 100 bp); in fact, the presence of Rad51p impairs recombination with short homology. The differences between the RAD51- and RAD50/RAD59-dependent pathways account for the distinct ways that two different recombination processes maintain yeast telomeres in the absence of telomerase.

摘要

通过位于不同酿酒酵母染色体或质粒上的同源序列之间的基因转换来修复双链断裂需要RAD51。当在同一质粒的反向重复序列之间发生修复时,会发现既有依赖RAD51的修复,也有不依赖RAD51的修复。不依赖RAD51的质粒修复事件的完成需要RAD52、RAD50、RAD59、TID1(RDH54)和SRS2,并且似乎涉及与单链退火偶联的断裂诱导复制。令人惊讶的是,与依赖RAD51的修复(约100 bp)相比,不依赖RAD51的重组在链侵入时所需的同源性要少得多(30 bp);事实上,Rad51p的存在会损害与短同源性的重组。依赖RAD51和依赖RAD50/RAD59的途径之间的差异解释了在没有端粒酶的情况下,两种不同的重组过程维持酵母端粒的不同方式。

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