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DNA聚合酶III全酶β亚基的过量产生可降低大肠杆菌中的紫外线诱变作用。

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

作者信息

Tadmor Y, Ascarelli-Goell R, Skaliter R, Livneh Z

机构信息

Department of Biochemistry, Weizmann Institute of Science, Rehovot, Israel.

出版信息

J Bacteriol. 1992 Apr;174(8):2517-24. doi: 10.1128/jb.174.8.2517-2524.1992.

DOI:10.1128/jb.174.8.2517-2524.1992
PMID:1556072
原文链接:https://pmc.ncbi.nlm.nih.gov/articles/PMC205890/
Abstract

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.

摘要

DNA聚合酶III全酶β亚基的过量表达导致紫外线诱变率降低5至10倍,同时大肠杆菌对紫外线的敏感性略有增加。在切除缺陷型细胞中也观察到了同样的效果,排除了这些影响是通过切除修复的变化介导的可能性。相比之下,聚合酶α亚基的过量表达既不影响紫外线诱变,也不影响紫外线敏感性。从质粒表达的诱变蛋白MucA和MucB的存在减轻了过量表达的β亚基对紫外线诱变的影响。我们之前曾提出,DNA聚合酶III全酶可以以两种形式存在:富含β亚基的形式无法绕过紫外线损伤,而β亚基含量低的形式能够绕过紫外线损伤(O. Shavitt和Z. Livneh,《生物化学杂志》264:11275-11281,1989)。β亚基含量低的形式可能与DNA聚合酶III的SOS形式有关,该形式旨在在SOS条件下进行跨损伤聚合,从而产生突变。基于此模型,我们提出过量表达的β亚基通过将聚合酶分子隔离到富含β亚基的形式并阻断SOS形式,影响常规复制性富含β亚基的聚合酶和SOS旁路 proficient聚合酶的相对丰度。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d84d/205890/e48893055cec/jbacter00074-0113-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d84d/205890/01f61c0b9ad9/jbacter00074-0111-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d84d/205890/e48893055cec/jbacter00074-0113-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d84d/205890/01f61c0b9ad9/jbacter00074-0111-a.jpg
https://cdn.ncbi.nlm.nih.gov/pmc/blobs/d84d/205890/e48893055cec/jbacter00074-0113-a.jpg

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本文引用的文献

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The SOS regulatory system of Escherichia coli.大肠杆菌的SOS调控系统。
Cell. 1982 May;29(1):11-22. doi: 10.1016/0092-8674(82)90085-x.
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DNA-damaging agents stimulate gene expression at specific loci in Escherichia coli.DNA损伤剂刺激大肠杆菌中特定基因座的基因表达。
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The beta subunit sliding DNA clamp is responsible for unassisted mutagenic translesion replication by DNA polymerase III holoenzyme.β亚基滑动DNA夹负责DNA聚合酶III全酶进行的无辅助易错跨损伤复制。
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Proliferating cell nuclear antigen promotes DNA synthesis past template lesions by mammalian DNA polymerase delta.增殖细胞核抗原通过哺乳动物DNA聚合酶δ促进越过模板损伤的DNA合成。
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Substitution of mucAB or rumAB for umuDC alters the relative frequencies of the two classes of mutations induced by a site-specific T-T cyclobutane dimer and the efficiency of translesion DNA synthesis.用mucAB或rumAB替代umuDC会改变由位点特异性T-T环丁烷二聚体诱导的两类突变的相对频率以及跨损伤DNA合成的效率。
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The dnaN gene codes for the beta subunit of DNA polymerase III holoenzyme of escherichia coli.dnaN基因编码大肠杆菌DNA聚合酶III全酶的β亚基。
Proc Natl Acad Sci U S A. 1981 Sep;78(9):5391-5. doi: 10.1073/pnas.78.9.5391.
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Molecular analysis of the recF gene of Escherichia coli.大肠杆菌recF基因的分子分析
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Mutagenesis and inducible responses to deoxyribonucleic acid damage in Escherichia coli.大肠杆菌中的诱变作用及对脱氧核糖核酸损伤的诱导反应
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Excess beta subunit can bypass the ATP requirement for highly processive synthesis by the Escherichia coli DNA polymerase III holoenzyme.过量的β亚基可以绕过大肠杆菌DNA聚合酶III全酶进行高度连续合成所需的ATP。
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Proteins required for ultraviolet light and chemical mutagenesis. Identification of the products of the umuC locus of Escherichia coli.紫外线和化学诱变所需的蛋白质。大肠杆菌umuC基因座产物的鉴定。
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