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用烷化剂进行亚致死处理对特定大肠杆菌基因的诱导作用。

Induction of specific Escherichia coli genes by sublethal treatments with alkylating agents.

作者信息

Volkert M R, Nguyen D C

出版信息

Proc Natl Acad Sci U S A. 1984 Jul;81(13):4110-4. doi: 10.1073/pnas.81.13.4110.

Abstract

Fusions of the lac operon to genes induced by treatment with sublethal levels of alkylating agents have been selected from random insertions of the Mu-dl(ApRlac) phage by screening for induction of beta-galactosidase activity in the presence of methyl methanesulfonate. Genetic analysis reveals that these fusions resulted from insertion of Mu-dl(ApRlac) into two regions of the chromosome. One region (aidA) is near his and, based on phenotypic effects, appears to represent insertion into the alkA gene. The other region (aidB) is in the 92.3- to 98-min region, which harbors no previously identified genes involved in repair of alkylation damage. The aidB fusions caused increased resistance to alkylating agents and caused little or no change in the biological effects of adaptation to alkylating agents. Unlike the aidA fusions, aidB fusions showed increased beta-galactosidase activity in untreated cells in a growth phase-dependent fashion. The ada-5 mutation, which blocks expression of the adaptive response, decreased induction of beta-galactosidase activity in both aidA and aidB fusions after alkylation treatments. Thus, both aidA and aidB share with adaptive response a common regulatory mechanism involving the ada gene. The growth phase-dependent control of the aidB fusions, however, is unaffected by ada, suggesting that a second regulatory mechanism exists that controls only aidB.

摘要

通过在甲磺酸甲酯存在下筛选β-半乳糖苷酶活性的诱导,从Mu-dl(ApRlac)噬菌体的随机插入中选择了与用亚致死水平的烷基化剂处理诱导的基因融合的乳糖操纵子。遗传分析表明,这些融合是由于Mu-dl(ApRlac)插入染色体的两个区域所致。一个区域(aidA)靠近his,基于表型效应,似乎代表插入alkA基因。另一个区域(aidB)在92.3至98分钟区域,该区域没有先前鉴定的参与烷基化损伤修复的基因。aidB融合导致对烷基化剂的抗性增加,并且在适应烷基化剂的生物学效应方面几乎没有变化或没有变化。与aidA融合不同,aidB融合在未处理的细胞中以生长阶段依赖性方式显示出增加的β-半乳糖苷酶活性。阻断适应性反应表达的ada-5突变,在烷基化处理后降低了aidA和aidB融合中β-半乳糖苷酶活性的诱导。因此,aidA和aidB都与适应性反应共享一种涉及ada基因的共同调节机制。然而aidB融合的生长阶段依赖性控制不受ada影响,这表明存在仅控制aidB的第二种调节机制。

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