MMEJ repair of double-strand breaks (director's cut): deleted sequences and alternative endings.
MMEJ repair of double-strand breaks (director's cut): deleted sequences and alternative endings.
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DOI：
10.1016/j.tig.2008.08.007
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发表时间：
2008-11
期刊：
影响因子：
--
通讯作者：
Lee SE
中科院分区：
文献类型：
--
作者：
McVey M;Lee SE
DNA双链断裂是细胞分裂和分化的正常结果，必须被精确修复以维持基因组的稳定性。已知有两种机制不同的途径可有效修复双链断裂：同源重组和Ku依赖的非同源末端连接。最近，第三种特征不太明确的修复机制，即微同源介导的末端连接（MMEJ），受到了越来越多的关注。MMEJ通过利用大量微同源性来修复DNA断裂，并且总是导致缺失。此外，它可能有助于人类致癌性染色体重排和遗传变异。在此，我们总结了来自几个模型系统的MMEJ的遗传特性，并讨论了MMEJ与“替代末端连接”之间的关系。我们提出了一个MMEJ的机制模型，并强调了未来研究的重要问题。
DNA double-strand breaks are normal consequences of cell division and differentiation and must be repaired faithfully to maintain genome stability. Two mechanistically distinct pathways are known to efficiently repair double-strand breaks: homologous recombination and Ku-dependent non-homologous end joining. Recently, a third, less characterized repair mechanism, named microhomology-mediated end joining (MMEJ), has received increasing attention. MMEJ repairs DNA breaks via the use of substantial microhomology and always results in deletions. Furthermore, it probably contributes to oncogenic chromosome rearrangements and genetic variation in humans. Here, we summarize the genetic attributes of MMEJ from several model systems and discuss the relationship between MMEJ and ‘alternative end joining’. We propose a mechanistic model for MMEJ and highlight important questions for future research.