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重组对于大肠杆菌dam(DNA腺嘌呤甲基转移酶)突变体的生存能力至关重要。

Recombination is essential for viability of an Escherichia coli dam (DNA adenine methyltransferase) mutant.

作者信息

Marinus M G

机构信息

Department of Pharmacology, University of Massachusetts Medical School, Worcester, Massachusetts 01655, USA.

出版信息

J Bacteriol. 2000 Jan;182(2):463-8. doi: 10.1128/JB.182.2.463-468.2000.

Abstract

Double mutants of Escherichia coli dam (DNA adenine methyltransferase) strains with ruvA, ruvB, or ruvC could not be constructed, whereas dam derivatives with recD, recF, recJ, and recR were viable. The ruv gene products are required for Holliday junction translocation and resolution of recombination intermediates. A dam recG (Holliday junction translocation) mutant strain was isolated but at a very much lower frequency than expected. The inviability of a dam lexA (Ind(-)) host was abrogated by the simultaneous presence of plasmids encoding both recA and ruvAB. This result indicates that of more than 20 SOS genes, only recA and ruvAB need to be derepressed to allow for dam mutant survival. The presence of mutS or mutL mutations allowed the construction of dam lexA (Ind(-)) derivatives. The requirement for recA, recB, recC, ruvA, ruvB, ruvC, and possibly recG gene expression indicates that recombination is essential for viability of dam bacteria probably to repair DNA double-strand breaks. The effect of mutS and mutL mutations indicates that DNA mismatch repair is the ultimate source of most of these DNA breaks. The requirement for recombination also suggests an explanation for the sensitivity of dam cells to certain DNA-damaging agents.

摘要

无法构建大肠杆菌dam(DNA腺嘌呤甲基转移酶)菌株与ruvA、ruvB或ruvC的双突变体,而带有recD、recF、recJ和recR的dam衍生物是可行的。Ruv基因产物是霍利迪连接体易位和重组中间体解离所必需的。分离出了dam recG(霍利迪连接体易位)突变株,但频率比预期低得多。同时存在编码recA和ruvAB的质粒可消除dam lexA(Ind(-))宿主的不可存活性。这一结果表明,在20多个SOS基因中,只有recA和ruvAB需要去阻遏才能使dam突变体存活。mutS或mutL突变的存在使得dam lexA(Ind(-))衍生物得以构建。对recA、recB、recC、ruvA、ruvB、ruvC以及可能的recG基因表达的需求表明,重组对于dam细菌的存活至关重要,可能是为了修复DNA双链断裂。mutS和mutL突变的影响表明,DNA错配修复是这些DNA断裂中大多数的最终来源。对重组的需求也为dam细胞对某些DNA损伤剂的敏感性提供了一种解释。

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