脱嘌呤/脱嘧啶位点内切核酸酶的缺失增加了N-甲基-N'-硝基-N-亚硝基胍对大肠杆菌的致突变性。
Loss of an apurinic/apyrimidinic site endonuclease increases the mutagenicity of N-methyl-N'-nitro-N-nitrosoguanidine to Escherichia coli.
作者信息
Foster P L, Davis E F
出版信息
Proc Natl Acad Sci U S A. 1987 May;84(9):2891-5. doi: 10.1073/pnas.84.9.2891.
Abstract
xthA- Escherichia coli, which are missing a major cellular apurinic/apyrimidinic (AP) endonuclease, are 5- to 10-fold more sensitive than xthA+ bacteria to mutagenesis by N-methyl-N'-nitro-N-nitrosoguanidine (MNNG) under conditions that induce the "adaptive response." The xthA(-)-dependent mutations are also dependent on SOS mutagenic processing and consist of both transversion and transition base substitutions. When MNNG-adapted xthA- bacteria are challenged with a high dose of MNNG, more xthA(-)-dependent SOS-dependent mutations are induced, and transversions are enhanced relative to transitions. The mutations induced by challenge are eliminated in xthA- alkA- bacteria, which are also deficient for 3-methyladenine glycosylase II activity. These data are consistent with the hypothesis that AP sites, at least some of which are produced by glycosylase activity, are mutagenic intermediates following cellular DNA alkylation.
摘要
缺失主要细胞脱嘌呤/脱嘧啶（AP）内切酶的xthA⁻大肠杆菌，在诱导“适应性反应”的条件下，比xthA⁺细菌对N-甲基-N'-硝基-N-亚硝基胍（MNNG）诱变的敏感性高5至10倍。xthA⁻依赖性突变也依赖于SOS诱变过程，包括颠换和转换碱基替换。当用高剂量MNNG攻击适应MNNG的xthA⁻细菌时，会诱导更多xthA⁻依赖性SOS依赖性突变，并且相对于转换，颠换会增强。攻击诱导的突变在同样缺乏3-甲基腺嘌呤糖基化酶II活性的xthA⁻alkA⁻细菌中被消除。这些数据与以下假设一致：AP位点，其中至少一些是由糖基化酶活性产生的，是细胞DNA烷基化后的诱变中间体。
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