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大肠杆菌K-12 uvrB菌株中复制后修复多条途径的遗传控制

Genetic control of multiple pathways of post-replicational repair in uvrB strains of Escherichia coli K-12.

作者信息

Youngs D A, Smith K C

出版信息

J Bacteriol. 1976 Jan;125(1):102-10. doi: 10.1128/jb.125.1.102-110.1976.

Abstract

The effect of the recA, uvrD, exrA, and recB mutations and of post-irradiation treatment with chloramphenicol on the survival and post-replication repair after ultraviolet irradiation of uvrB strains of Escherichia coli K-12 was examined. Each of these mutations or treatments was found to decrease survival and the extent of repair. The interactions of the inhibitory effects of the uvrD, exaA, and recB mutations and chloramphenicol treatment were determined by examining the survival and repair characteristics of the several multiple mutants. The survival results suggest that the post-replication repair process in uvrB strains may be subdivided into at least five different branches. These include three branches that are blocked by the exrA, recB, or uvrD mutation, a fourth branch that is blocked by any of these mutations and is also sensitive to chloramphenicol treatment, and at least one additional branch that is not sensitive to either of these mutations or to chloramphenicol treatment. The extent of post-replicational repair observed with each of the strains is in general agreement with the pathways postulated on the basis of the survival data, although there are several apparent exceptions to this correlation.

摘要

研究了recA、uvrD、exrA和recB突变以及用氯霉素进行辐照后处理对大肠杆菌K - 12的uvrB菌株紫外线照射后的存活及复制后修复的影响。发现这些突变或处理中的每一种都会降低存活率和修复程度。通过检测几种多重突变体的存活和修复特征,确定了uvrD、exaA和recB突变以及氯霉素处理的抑制作用之间的相互作用。存活结果表明,uvrB菌株中的复制后修复过程可能至少可细分为五个不同的分支。其中包括三个被exrA、recB或uvrD突变阻断的分支,第四个分支被这些突变中的任何一个阻断且对氯霉素处理敏感,以及至少一个对这些突变或氯霉素处理均不敏感的额外分支。尽管这种相关性存在几个明显的例外情况,但每个菌株观察到的复制后修复程度总体上与根据存活数据推测的途径一致。

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本文引用的文献

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Absorption effects in volume irradiation of microorganisms.微生物体照射中的吸收效应。
Science. 1950 Mar 3;111(2879):229. doi: 10.1126/science.111.2879.229-a.
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DNA repair.DNA修复
Annu Rev Biochem. 1968;37:175-200. doi: 10.1146/annurev.bi.37.070168.001135.

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