HOMOLOGOUS RECOMBINATION-DEPENDENT INITIATION OF DNA-REPLICATION FROM DNA DAMAGE-INDUCIBLE ORIGINS IN ESCHERICHIA-COLI
HOMOLOGOUS RECOMBINATION-DEPENDENT INITIATION OF DNA-REPLICATION FROM DNA DAMAGE-INDUCIBLE ORIGINS IN ESCHERICHIA-COLI
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DOI：
10.1002/j.1460-2075.1993.tb05998.x
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发表时间：
1993-08-01
期刊：
影响因子：
11.4
通讯作者：
KOGOMA, T
中科院分区：
文献类型：
--
作者：
ASAI, T;SOMMER, S;KOGOMA, T
诱导SOS反应的大肠杆菌细胞表达诱导型稳定DNA复制（iSDR）作为SOS功能。iSDR的启动不依赖于转录、翻译和DnaA蛋白，这对于从oriC启动DNA复制是必需的。我们发现重组缺陷但精通SOS诱导的recA突变体不能引起iSDR。相比之下，iSDR被recD和recJ突变增强，所述recD和recJ突变分别抑制RecBCD酶的核酸外切酶V活性和RecJ核酸外切酶活性。ruvC基因中阻断重组中间体（即Holliday结构）分解的突变也增强了iSDR。此外，recG或ruvAB突变对分支迁移的抑制显著增加了iSDR活性。recBC突变体在iSDR诱导中是有缺陷的，但该缺陷被sbcA基因中的突变抑制。iSDR复制的微型染色体的主要产物是共价闭合的环状单体。我们认为RecA重组酶和RecBC（D）解旋酶作用产生的重组中间体（即D环结构）在iSDR的起始中起着核心作用。
Escherichia coli cells induced for the SOS response express inducible stable DNA replication (iSDR) as an SOS function. Initiation of iSDR is independent of transcription, translation and DnaA protein, which are essential for initiation of DNA replication from oriC. We found that a recA mutant that is defective in recombination but proficient in SOS induction could not elicit iSDR. In contrast, iSDR was enhanced by recD and recJ mutations that inactivate the exonuclease V activity of the RecBCD enzyme and the RecJ exonuclease activity, respectively. A mutation in the ruvC gene that blocks the resolution of recombination intermediates (i.e. Holliday structures) also enhanced iSDR. Furthermore, inhibition of branch migration by recG or ruvAB mutations dramatically increased the iSDR activity. recBC mutants are defective in iSDR induction but the defect was suppressed by a mutation in the sbcA gene. The major product of minichromosomes replicated by iSDR was covalently closed circular monomers. We propose that recombination intermediates (i.e. D-loop structures) created by the action of RecA recombinase and RecBC(D) helicase play a central role in initiation of iSDR.