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羟基脲在大肠杆菌K12中诱导SOS反应。

Induction of the SOS response by hydroxyurea in Escherichia coli K12.

作者信息

Barbé J, Villaverde A, Guerrero R

机构信息

Department of Microbiology, Faculty of Sciences, Autonomous University of Barcelona, Spain.

出版信息

Mutat Res. 1987 Oct;192(2):105-8. doi: 10.1016/0165-7992(87)90105-9.

DOI:10.1016/0165-7992(87)90105-9
PMID:3309645
Abstract

Hydroxyurea at concentrations higher than 10(-2) M induced the recA and sfiA genes of E. coli as well as the lambda prophage by a pathway independent of the recBC genes. In addition, the hydroxyurea-mediated induction of the SOS response is accompanied by a recA-dependent decrease on the cellular ATP pool. The presence of the multicopy plasmid pPS2, harboring the nrdAB genes (encoding the ribonucleoside reductase enzyme), abolished the hydroxyurea-induced expression of the recA gene. These data lead us to suggest that induction of the SOS response by hydroxyurea is due to the blocking of DNA replication by the inhibition of the ribonucleoside reductase complex activity.

摘要

浓度高于10⁻² M的羟基脲通过一条独立于recBC基因的途径诱导大肠杆菌的recA和sfiA基因以及λ原噬菌体。此外,羟基脲介导的SOS应答诱导伴随着细胞ATP池的recA依赖性减少。携带nrdAB基因(编码核糖核苷还原酶)的多拷贝质粒pPS2的存在消除了羟基脲诱导的recA基因表达。这些数据使我们认为,羟基脲诱导SOS应答是由于核糖核苷还原酶复合体活性受到抑制从而阻断了DNA复制。

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