SOS independent survival against mitomycin C induced lethality in a rifampicin-nalidixic acid-resistant mutant of Escherichia coli

Mutation Research/DNA Repair Reports Pub Date : 1988-09-01 DOI:10.1016/0167-8817(88)90013-2

K.R. Kumaresan, R. Jayaraman

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引用次数: 8

Abstract

A combination of specific rifampicin-resistant (rpo B87) and nalidixic acid-resistant (gyrA87) mutations results in a marked increase in the survival of Escherichia coli against mitomycin C-induced lethality in mutants defective for SOS induction and excision repair. Although the response does not seem to be obligatorily dependent upon the RecA protein, the efficiency is markedly increased in its presence, even in a conventionally inactive form. This response is not elicited against lethality due to ultraviolet radiation or N-methyl-N′-nitro-N-nitrosoguanidine exposure. The combination of rpo B87 and gyrA87 mutations also greatly alleviates post-mitomycin C degradation of DNA under SOS non-inducible conditions. It is proposed that the rpo B subunit of RNA polymerase and gyrA subunit of DNA gyrase could participate in the repair of certain types of DNA damage, such as cross-links, in a mode independent of SOS-regulated excision repair and post-replication repair.

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抗丝裂霉素C的SOS独立存活诱导大肠埃希菌抗利福平-萘啶酸突变体致死

特异性耐利福平(rpo B87)和耐萘啶酸(gyrA87)突变的组合导致大肠杆菌在SOS诱导和切除修复缺陷突变体中抗丝裂霉素c诱导的致死率的存活率显著增加。尽管这种反应似乎并不一定依赖于RecA蛋白，但在RecA蛋白的存在下，效率显著提高，即使是在传统的非活性形式下。这种反应不是针对紫外线辐射或n -甲基-n ' -硝基-n -亚硝基胍暴露造成的致死率而引起的。在SOS非诱导条件下，rpo B87和gyrA87突变的组合也极大地缓解了丝裂霉素C后DNA的降解。我们提出RNA聚合酶的rpo B亚基和DNA回转酶的gyrA亚基可以以独立于sos调控的切除修复和复制后修复的模式参与某些类型的DNA损伤的修复，如交联。

本文章由计算机程序翻译，如有差异，请以英文原文为准。

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Mutation Research/DNA Repair Reports

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