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首页> 外文期刊>Mutation Research. Reviews in Mutation Research >Kinetic models reveal the in vivo mechanisms of mutagenesis in microbes and man
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Kinetic models reveal the in vivo mechanisms of mutagenesis in microbes and man

机译：动力学模型揭示了微生物和人体内诱变的体内机制

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This review summarizes the evidence indicating that mutagenic mechanisms in vivo are essentially the same in all living cells. Unique metabolic reactions to a particular environmental stress apparently target specific genes for increased rates of transcription and mutation, resulting in higher mutation rates for those genes most likely to solve the problem. Kinetic models which have demonstrated predictive value are described and are shown to simulate mutagenesis in vivo in Escherichia coli, the p53 tumor suppressor gene, and somatic hypermutation. In all three models, direct correlations are seen between mutation frequencies and transcription rates. G and C nucleosides in single-stranded DNA (ssDNA) are intrinsically mutable, and G and C silent mutations in p53 and in VH framework regions provide compelling evidence for intrinsic mechanisms of mutability, since mutation outcomes are neutral and are not selected. During transcription, the availability of unpaired bases in the ssDNA of secondary structures is rate-limiting for, and determines the frequency of mutations in vivo. In vitro analyses also verify the conclusion that intrinsically mutable bases are in fact located in ssDNA loops of predicted stem-loop structures (SLSs).
机译：这篇综述总结了表明体内诱变机制在所有活细胞中基本相同的证据。对特定环境压力的独特代谢反应显然是针对特定基因，以提高转录和突变率，从而导致那些最有可能解决该问题的基因具有更高的突变率。描述了具有预测价值的动力学模型，并显示了其在大肠杆菌，p53抑癌基因和体细胞高突变中模拟体内诱变的动力学模型。在所有三个模型中，可以看到突变频率和转录速率之间的直接相关性。单链DNA（ssDNA）中的G和C核苷本质上是可变的，p53和VH框架区的G和C沉默突变为突变的内在机制提供了令人信服的证据，因为突变结果是中性的且未被选择。在转录过程中，二级结构的ssDNA中不成对碱基的可用性限制了速率，并决定了体内突变的频率。体外分析也证实了结论，即固​​有可变碱基实际上位于预测的茎环结构（SLSs）的ssDNA环中。

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