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多拷贝质粒上dnaQ-rnh反向转录单元的存在会抑制大肠杆菌中的诱导诱变。

Presence of the dnaQ-rnh divergent transcriptional unit on a multicopy plasmid inhibits induced mutagenesis in Escherichia coli.

作者信息

Foster P L, Sullivan A D, Franklin S B

机构信息

Division of Environmental Health, Boston University School of Public Health, Massachusetts 02118.

出版信息

J Bacteriol. 1989 Jun;171(6):3144-51. doi: 10.1128/jb.171.6.3144-3151.1989.

Abstract

In Escherichia coli the dnaQ+ gene, which encodes epsilon, a fidelity subunit of DNA polymerase III, and the rnh+ gene, which encodes RNase H, share a promoter region but are transcribed in opposite directions. The presence of this divergent transcriptional unit on a multicopy plasmid inhibited by as much as 10-fold mutations induced by the SOS-dependent mutagens methyl methanesulfonate and UV light. Mutations in either gene eliminated the effect, suggesting that both genes contribute either directly or indirectly to the antimutagenic phenotype. Neither survival to mutagen exposure nor induction of the SOS response was comparably affected by the presence of the genes. Although the antimutagenic phenotype was partially suppressed by excess UmuDC proteins, which are required for SOS mutagenesis, the presence of the dnaQ+-rnh+ clone also reduced the induction of mutations by N-methyl-N'-nitro-N-nitrosoguanidine in cells deficient for SOS mutagenic processing. The results suggest that the presence of the dnaQ+-rnh+ divergent transcriptional unit interferes with an underlying mutagenic mechanism that is normally facilitated by the proteins induced as part of the SOS response.

摘要

在大肠杆菌中,编码DNA聚合酶III保真亚基ε的dnaQ⁺基因与编码核糖核酸酶H的rnh⁺基因共享一个启动子区域,但转录方向相反。多拷贝质粒上这种双向转录单元的存在,可将由SOS依赖型诱变剂甲磺酸甲酯和紫外线诱导的突变抑制多达10倍。任一基因发生突变都会消除这种效应,这表明这两个基因直接或间接地导致了抗诱变表型。基因的存在对诱变剂暴露后的存活率或SOS反应的诱导均无类似影响。尽管SOS诱变所需的过量UmuDC蛋白可部分抑制抗诱变表型,但dnaQ⁺-rnh⁺克隆的存在也减少了SOS诱变处理缺陷细胞中N-甲基-N'-硝基-N-亚硝基胍诱导的突变。结果表明,dnaQ⁺-rnh⁺双向转录单元的存在干扰了一种潜在的诱变机制,而这种机制通常由作为SOS反应一部分而诱导产生的蛋白质所促进。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/da8e/210028/6c5615bd1c46/jbacter00172-0247-a.jpg

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