Characterization of RAD51-independent break-induced replication that acts preferentially with short homologous sequences
Characterization of RAD51-independent break-induced replication that acts preferentially with short homologous sequences
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DOI：
10.1128/mcb.22.18.6384-6392.2002
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发表时间：
2002-09-01
影响因子：
5.3
通讯作者：
Haber, JE
中科院分区：
文献类型：
--
作者：
Ira, G;Haber, JE
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修复双链断裂需要RAD51。当修复发生在同一质粒的反向重复序列之间时，可以发现rad51依赖性修复和rad51非依赖性修复。完成与rad51无关的质粒修复事件需要RAD52、RAD50、RAD59、TID1 （RDH54）和SRS2，似乎涉及断裂诱导复制和单链退火。令人惊讶的是，与rad51依赖性修复（大约100 bp）相比，非rad51依赖性重组对链入侵的同源性要求更低（30 bp）；事实上，Rad51p的存在损害了短同源性的重组。RAD51-和RAD50/ rad59依赖途径之间的差异解释了两种不同的重组过程在端粒酶缺失的情况下维持酵母端粒的不同方式。
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.