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首页> 外文期刊>Journal of bacteriology >Polynucleotide Phosphorylase Plays an Important Role in the Generation of Spontaneous Mutations in Escherichia coli
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Polynucleotide Phosphorylase Plays an Important Role in the Generation of Spontaneous Mutations in Escherichia coli

机译：多核苷酸磷酸化酶在大肠杆菌中自发突变的产生中起重要作用

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Polynucleotide phosphorylase (PNP) plays a central role in RNA degradation, generating a pool of ribonucleoside diphosphates (rNDPs) that can be converted to deoxyribonucleoside diphosphates (dNDPs) by ribonucleotide reductase. We report here that spontaneous mutations resulting from replication errors, which are normally repaired by the mismatch repair (MMR) system, are sharply reduced in a PNP-deficient Escherichia coli strain. This is true for base substitution mutations that occur in the rpoB gene leading to Rifr and the gyrB gene leading to Nalr and for base substitution and frameshift mutations that occur in the lacZ gene. These results suggest that the increase in the rNDP pools generated by polynucleotide phosphorylase (PNP) degradation of RNA is responsible for the spontaneous mutations observed in an MMR-deficient background. The PNP-derived pool also appears responsible for the observed mutations in the mutT mutator background and those that occur after treatment with 5-bromodeoxyuridine, as these mutations are also drastically reduced in a PNP-deficient strain. However, mutation frequencies are not reduced in a mutY mutator background or after treatment with 2-aminopurine. These results highlight the central role in mutagenesis played by the rNDP pools (and the subsequent dNTP pools) derived from RNA degradation.
机译：多核苷酸磷酸化酶（PNP）在RNA降解中起着重要作用，产生了核糖核苷二磷酸（rNDP）集合，可通过核糖核苷酸还原酶转化为脱氧核糖核苷二磷酸（dNDP）。我们在这里报告说，在PNP缺陷的大肠杆菌菌株中，通常由错配修复（MMR）系统修复的复制错误导致的自发突变急剧减少。对于 rpoB 基因导致Rif r 和 gyrB 基因导致Nal r < / sup>以及 lacZ 基因中发生的碱基替换和移码突变。这些结果表明，由RNA的多核苷酸磷酸化酶（PNP）降解产生的rNDP库增加是造成MMR缺陷背景下自发突变的原因。 PNP衍生的库似乎也负责在 mutT 突变体背景中观察到的突变以及在用5-溴脱氧尿苷处理后发生的突变，因为在PNP缺陷菌株中这些突变也被大大降低。但是，在 mutY 突变体背景下或用2-氨基嘌呤处理后，突变频率不会降低。这些结果突出了在rNDP池（和随后的dNTP池）中从RNA降解产生的诱变中的核心作用。

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