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首页> 外文期刊>Journal of bacteriology >Induction of transversion mutations in Escherichia coli by N-methyl-N'-nitro-N-nitrosoguanidine is SOS dependent.
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Induction of transversion mutations in Escherichia coli by N-methyl-N'-nitro-N-nitrosoguanidine is SOS dependent.

机译：N-甲基-N'-硝基-N-亚硝基胍在大肠杆菌中诱导转化突变是SOS依赖性的。

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摘要

Escherichia coli alkA mutants, which are deficient for an inducible DNA glycosylase, 3-methyladenine-DNA glycosylase II, are sensitive to mutagenesis by low doses of the alkylating agent N-methyl-N'-nitro-N-nitrosoguanidine (MNNG). As many as 90% of the alkA-dependent mutations induced by MNNG are also umuC+ dependent and thus are due to DNA lesions that are substrates for the mutagenic functions of the SOS response. A great number of these mutations are base substitutions at A . T sites, particularly A . T transversions. We discuss which DNA lesions may be responsible for these mutations. Our results show that the induction of 3-methyladenine-DNA glycosylase II, which occurs as part of the adaptive response to alkylating agents such as MNNG, significantly reduces the mutagenicity as well as the lethality of alkylation damage.
机译：缺乏可诱导的DNA糖基化酶3-甲基腺嘌呤-DNA糖基化酶II的大肠杆菌alkA突变体对低剂量的烷基化剂N-甲基-N'-硝基-N-亚硝基胍（MNNG）诱变敏感。由MNNG诱导的多达90％的alkA依赖性突变也是umuC +依赖性的，因此归因于DNA损伤，这些损伤是SOS响应的诱变功能的底物。这些突变中有很多是A处的碱基取代。 T网站，尤其是A网站。 T颠换。我们讨论哪些DNA损伤可能是这些突变的原因。我们的结果表明，3-甲基腺嘌呤-DNA糖基化酶II的诱导（这是对烷基化剂（例如MNNG）的适应性反应的一部分）显着降低了烷基化损伤的诱变性和致死性。

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