RECOMBINATIONAL RESCUE OF THE STALLED DNA-REPLICATION FORK - A MODEL-BASED ON ANALYSIS OF AN ESCHERICHIA-COLI STRAIN WITH A CHROMOSOME REGION DIFFICULT TO REPLICATE
RECOMBINATIONAL RESCUE OF THE STALLED DNA-REPLICATION FORK - A MODEL-BASED ON ANALYSIS OF AN ESCHERICHIA-COLI STRAIN WITH A CHROMOSOME REGION DIFFICULT TO REPLICATE
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DOI：
10.1128/jb.177.3.783-791.1995
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发表时间：
1995-02-01
影响因子：
3.2
通讯作者：
FUJIMURA, Y
中科院分区：
文献类型：
--
作者：
HORIUCHI, T;FUJIMURA, Y
为了研究DNA复制停滞在末端（Ter）的生理效应，我们构建了一个复制阻断的大肠杆菌call菌株，使得两个双向复制叉在两个侧翼Ter位点（一个人工位点和另一个天然位点）受到阻碍，而阻断菌株的生长速度略慢于对照菌株，它具有与关闭菌株相似的异常表型。coli dam突变体，即，hyper-Rec表型、recA（+）-和recB（+）（C+）-依赖性生长以及组成型SOS诱导。这两种明显不相关的突变体引起相似表型的观察使我们设计了一种模型。我们提出，以下顺序事件可能发生在两个菌株。在封闭菌株中，在封闭的复制叉处和在dam突变体中，在进行中的复制叉处发生双链（ds）断裂，RecBCD酶通过该双链断裂进入并降解ds DNA分子，并且降解产物作为SOS诱导的信号分子。当RecBCD酶遇到适当定向的Chi序列时，其DNA酶活性转化为重组酶，该重组酶能够修复ds末端，该模型（i）解释了recA和recB（C）突变体的令人困惑的表型以及限制性条件下polA、lig和dna突变体的SOS诱导表型，（ii）提供了Chi序列的作用的解释，并且（iii）提出了同源重组在DNA复制停滞后细胞存活方面的可能关键作用。
To examine the physiological effects of DNA replication arrest at the terminus (Ter), we constructed a replication-blocked Escherichia call strain so that both bidirectional replication forks would be impeded at two flanking Ter sites, one artificial and the other natural, While the blocked strain grew slightly more slowly than a control strain, it had abnormal phenotypes similar to those off. coli dam mutants, i.e., hyper-Rec phenotype, recA(+)- and recB(+)(C+)-dependent growth, and constitutive SOS induction, The observation that these two apparently unrelated mutants cause similar phenotypes led us to design a model. We propose that the following sequential events may occur in both strains. A double-strand (ds) break occurs at the blocked replication fork in the blocked strain and at the ongoing fork in the dam mutant, through which RecBCD enzyme enters and degrades the ds DNA molecule, and the degradation product serves as the signal molecule for SOS induction, When RecBCD enzyme meets an appropriately oriented Chi sequence, its DNase activity is converted to recombinase enzyme, which is able to repair the ds end, recombinationally, This model (i) explains the puzzling phenotype of recA and recB(C) mutants and the SOS-inducing phenotype of polA, lig, and dna mutants under restrictive conditions, (ii) provides an interpretation for the role of the Chi sequence, and (iii) suggests a possible key role for homologous recombination with regard to cell survival following the arrest of DNA replication.