Homology Requirements and Competition between Gene Conversion and Break-Induced Replication during Double-Strand Break Repair.
Homology Requirements and Competition between Gene Conversion and Break-Induced Replication during Double-Strand Break Repair.
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DOI：
10.1016/j.molcel.2016.12.003
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发表时间：
2017-02-02
期刊：
影响因子：
16
通讯作者：
Haber JE
中科院分区：
文献类型：
--
作者：
Mehta A;Beach A;Haber JE
酿酒酵母交配型转换是由MATA的双链断裂启动的，其一端与hm1α供体完全同源，而第二端在完成基因转化修复(GC)之前必须被处理以去除非同源的尾巴。当匹配端的同源性为≤150bp时，有效的修复依赖于重组增强子，它将HMLα拴在DSB附近。因此，比明显的“最小有效加工片段”短的同源性可以通过拴住断裂处附近的供体来挽救。当第二端的同源性为≤150bp时，第二端捕获变得低效，修复从GC转移到断裂诱导复制(BIR)。但当pol32或pif1突变阻止BIR时，GC增加三倍，表明这些突变阻止的步骤是可逆的。在短的第二端同源性中，RecQ解旋酶Sgs1的缺失促进了合成依赖的链的退火，而FANCM相关的Mph1解旋酶的缺失则促进了BIR。
Saccharomyces cerevisiae mating-type switching is initiated by a double-strand break (DSB) at MATa, leaving one cut end perfectly homologous to the HMLα donor, while the second end must be processed to remove a nonhomologous tail before completing repair by gene conversion (GC). When homology at the matched end is ≤150 bp, efficient repair depends on the Recombination Enhancer, which tethers HMLα near the DSB. Thus homology shorter than an apparent “minimum efficient processing segment” can be rescued by tethering the donor near the break. When homology at the second end is ≤150 bp, second-end capture becomes inefficient and repair shifts from GC to break-induced replication (BIR). But when pol32 or pif1 mutants block BIR, GC increases three-fold, indicating that the steps blocked by these mutations are reversible. With short second-end homology, absence of the RecQ helicase Sgs1 promotes synthesis-dependent strand annealing whereas deletion of the FANCM-related Mph1 helicase promotes BIR.