SbcCD causes a double-strand break at a DNA palindrome in the Escherichia coli chromosome
SbcCD causes a double-strand break at a DNA palindrome in the Escherichia coli chromosome
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DOI：
10.1016/j.molcel.2007.12.020
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发表时间：
2008-03-14
期刊：
影响因子：
16
通讯作者：
Leach, David R. F.
中科院分区：
文献类型：
--
作者：
Eykelenboom, John K.;Blackwood, John K.;Leach, David R. F.
长DNA回文是原核和真核细胞中基因组不稳定性（缺失、扩增和易位）的位点。在大肠杆菌中，遗传证据表明它们是SbcCD复合物切割DNA的位点，可以通过同源重组修复。在这里，我们获得在体内的物理证据SbcCD诱导的DNA双链断裂（DSB）在大肠杆菌染色体中的回文序列，并表明，两端的休息刺激重组。切割依赖于DNA的复制，但观察到断裂处的两端表明切割并不发生在复制叉处。遗传分析表明，该断裂的修复需要RecBCD重组途径和PriA，这表明细菌DNA DSB修复机制涉及复制叉的建立。
Long DNA palindromes are sites of genome instability (deletions, amplification, and translocations) in both prokaryotic and eukaryotic cells. In Escherichia coli, genetic evidence has suggested that they are sites of DNA cleavage by the SbcCD complex that can be repaired by homologous recombination. Here we obtain in vivo physical evidence of an SbcCD-induced DNA double-strand break (DSB) at a palindromic sequence in the E coli chromosome and show that both ends of the break stimulate recombination. Cleavage is dependent on DNA replication, but the observation of two ends at the break argues that cleavage does not occur at the replication fork. Genetic analysis shows repair of the break requires the RecBCD recombination pathway and PriA, suggesting a mechanism of bacterial DNA DSB repair involving the establishment of replication forks.