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Overproduction of the beta subunit of DNA polymerase III holoenzyme reduces UV mutagenesis in Escherichia coli.

机译:DNA聚合酶III全酶的β亚基的过量产生减少了大肠杆菌中的UV诱变。

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摘要

Overproduction of the beta subunit of DNA polymerase III holoenzyme caused a 5- to 10-fold reduction of UV mutagenesis along with a slight increase in sensitivity to UV light in Escherichia coli. The same effects were observed in excision-deficient cells, excluding the possibility that they were mediated via changes in excision repair. In contrast, overproduction of the alpha subunit of the polymerase did not influence either UV mutagenesis or UV sensitivity. The presence of the mutagenesis proteins MucA and MucB expressed from a plasmid alleviated the effect of overproduced beta on UV mutagenesis. We have previously suggested that DNA polymerase III holoenzyme can exist in two forms: beta-rich form unable to bypass UV lesions and a beta-poor form capable of bypassing UV lesions (O. Shavitt and Z. Livneh, J. Biol. Chem. 264:11275-11281, 1989). The beta-poor form may be related to an SOS form of DNA polymerase III designed to perform translesion polymerization under SOS conditions and thereby generate mutations. On the basis of this model, we propose that the overproduced beta subunit affects the relative abundance of the regular replicative beta-rich polymerase and the SOS bypass-proficient polymerase by sequestering the polymerase molecules to the beta-rich form and blocking the SOS form.
机译:DNA聚合酶III全酶的β亚基的过量生产导致紫外线诱变减少5到10倍,同时对大肠杆菌中对紫外线的敏感性略有增加。在切除缺陷的细胞中观察到了相同的效果,但排除了它们是通过切除修复的改变来介导的。相反,聚合酶α亚基的过量生产不影响UV诱变或UV敏感性。由质粒表达的诱变蛋白MucA和MucB的存在减轻了过度产生的β对UV诱变的影响。我们以前曾提出过DNA聚合酶III全酶可以以两种形式存在:富含β的形式不能绕过UV损伤和缺乏β的形式可以绕过UV损伤(O.Shavitt和Z.Livneh,J.Biol。 264:11275-11281,1989)。 β-贫乏形式可能与DNA聚合酶III的SOS形式有关,该DNA聚合酶III设计为在SOS条件下进行跨病变聚合,从而产生突变。在此模型的基础上,我们提出,过量生产的β亚基通过将聚合酶分子螯合为富含β的形式并阻断SOS形式,从而影响常规复制性富含β的聚合酶和SOS旁路高效聚合酶的相对丰度。

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