大肠杆菌中耐药性质粒pKM101的自发突变特异性
Spontaneous mutational specificity of drug resistance plasmid pKM101 in Escherichia coli.
作者信息
Fowler R G, McGinty L, Mortelmans K E
出版信息
J Bacteriol. 1979 Dec;140(3):929-37. doi: 10.1128/jb.140.3.929-937.1979.
Abstract
Plasmid pKM101 enhances the frequency of spontaneous and ultraviolet light-induced mutations in Escherichia coli and protects the cells against the lethal effects of ultraviolet irradiation. By analyzing reversion patterns of defined trpA alleles, we showed that pKM101 caused all types of spontaneous base-pair substitution mutations with the possible exception of guanine . cytosine leads to adenine. thymine transitions. Neither insertion nor deletion frameshift mutations were enhanced. Transversions were more strongly enhanced than transitions, and adenine . thymine base pairs appeared more susceptible to pKM101 mutator activity than guanine . cytosine base pairs. In addition, there were effects from neighboring base pairs and genetic background that influenced the mutator activity of pKM101.
摘要
质粒pKM101可提高大肠杆菌自发突变和紫外线诱导突变的频率，并保护细胞免受紫外线照射的致死效应。通过分析特定trpA等位基因的回复模式，我们发现pKM101会引发除鸟嘌呤·胞嘧啶到腺嘌呤·胸腺嘧啶转换外的所有类型的自发碱基对替换突变。插入或缺失移码突变均未增强。颠换比转换增强得更强烈，并且腺嘌呤·胸腺嘧啶碱基对比鸟嘌呤·胞嘧啶碱基对似乎更易受pKM101诱变活性的影响。此外，相邻碱基对和遗传背景也会对pKM101的诱变活性产生影响。
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