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大肠杆菌中的诱变DNA修复。十八。DNA聚合酶IIIα亚基(DnaE蛋白)在紫外线照射后诱变中的作用。

Mutagenic DNA repair in Escherichia coli. XVIII. Involvement of DNA polymerase III alpha-subunit (DnaE protein) in mutagenesis after exposure to UV light.

作者信息

Bridges B A, Bates H

机构信息

MRC Cell Mutation Unit, University of Sussex, Falmer, Brighton, UK.

出版信息

Mutagenesis. 1990 Jan;5(1):35-8. doi: 10.1093/mutage/5.1.35.

DOI:10.1093/mutage/5.1.35
PMID:2184309
Abstract

UV light was unable to induce rifampicin-resistant mutations at 43 degrees C in Escherichia coli ER11 dnaE486. Although DnaE486 gene product is inactive at 43 degrees C, these bacteria contain the pcbA1 mutation which allows DNA replication provided DNA polymerase I is functional. The experiments were carried out under conditions where full expression of rifampicin-resistant mutations could occur so that the lack of induced mutations cannot be ascribed to an effect of incubation at 43 degrees C on mutation expression. UV-mutability at 43 degrees C was restored by the presence of the dnaE+ allele on a plasmid. It is concluded that functional DnaE protein is essential for UV mutagenesis. The dnaE486 mutation also blocked the induction at 43 degrees C of mutations induced by UV plus delayed photoreversal, a procedure that has been postulated to reflect an early misincorporation step in the UV mutagenic process.

摘要

紫外线无法在43摄氏度下诱导大肠杆菌ER11 dnaE486产生利福平抗性突变。尽管DnaE486基因产物在43摄氏度时无活性,但这些细菌含有pcbA1突变,只要DNA聚合酶I有功能,就允许DNA复制。实验是在能够充分表达利福平抗性突变的条件下进行的,因此诱导突变的缺乏不能归因于在43摄氏度下孵育对突变表达的影响。质粒上存在dnaE +等位基因可恢复43摄氏度时的紫外线诱变能力。得出的结论是,功能性DnaE蛋白对于紫外线诱变至关重要。dnaE486突变也阻断了在43摄氏度下由紫外线加延迟光逆转诱导的突变,这一过程被认为反映了紫外线诱变过程中的早期错配步骤。

相似文献

1
Mutagenic DNA repair in Escherichia coli. XVIII. Involvement of DNA polymerase III alpha-subunit (DnaE protein) in mutagenesis after exposure to UV light.大肠杆菌中的诱变DNA修复。十八。DNA聚合酶IIIα亚基(DnaE蛋白)在紫外线照射后诱变中的作用。
Mutagenesis. 1990 Jan;5(1):35-8. doi: 10.1093/mutage/5.1.35.
2
Mutagenic DNA repair in Escherichia coli. XVII. Effect of temperature-sensitive DnaE proteins on the induction of streptomycin-resistant mutations by UV light.大肠杆菌中的诱变DNA修复。十七。温度敏感型DnaE蛋白对紫外线诱导链霉素抗性突变的影响。
Mutagenesis. 1990 Jan;5(1):31-4. doi: 10.1093/mutage/5.1.31.
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Mutagenic DNA repair in Escherichia coli. XIV. Influence of two DNA polymerase III mutator alleles on spontaneous and UV mutagenesis.大肠杆菌中的诱变DNA修复。十四。两种DNA聚合酶III突变等位基因对自发诱变和紫外线诱变的影响。
Mol Gen Genet. 1987 Jul;208(3):542-8. doi: 10.1007/BF00328153.
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Current understanding of UV-induced base pair substitution mutation in E. coli with particular reference to the DNA polymerase III complex.当前对大肠杆菌中紫外线诱导的碱基对替换突变的理解,特别涉及DNA聚合酶III复合物。
Mutat Res. 1987 Dec;181(2):219-26. doi: 10.1016/0027-5107(87)90099-6.
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Suppression of dnaE nonsense mutations by pcbA1.通过pcbA1抑制dnaE无义突变
J Bacteriol. 1989 Jun;171(6):3139-43. doi: 10.1128/jb.171.6.3139-3143.1989.
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Mutagenic DNA repair in Escherichia coli. XIII. Proofreading exonuclease of DNA polymerase III holoenzyme is not operational during UV mutagenesis.大肠杆菌中的诱变DNA修复。十三。DNA聚合酶III全酶的校对核酸外切酶在紫外线诱变过程中不起作用。
Mutat Res. 1987 Jan;183(1):31-7. doi: 10.1016/0167-8817(87)90042-3.
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[Effect of plasmid R6K on expression of the temperature-sensitive mutation in gene dnaE of Escherichia coli K-12].[质粒R6K对大肠杆菌K-12 dnaE基因温度敏感突变表达的影响]
Genetika. 1980;16(10):1775-85.
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Mutagenic DNA repair in Escherichia coli. XII. Ultraviolet mutagenesis in excision-proficient umuC and lexA (ind-) bacteria as revealed by delayed photoreversal.大肠杆菌中的诱变DNA修复。十二。通过延迟光逆转揭示的切除能力正常的umuC和lexA(ind-)细菌中的紫外线诱变。
Mutagenesis. 1986 Mar;1(2):111-7. doi: 10.1093/mutage/1.2.111.
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Overproduction of the epsilon subunit of DNA polymerase III counteracts the SOS mutagenic response of Escherichia coli.DNA聚合酶III的ε亚基过量产生可抵消大肠杆菌的SOS诱变反应。
Proc Natl Acad Sci U S A. 1988 Dec;85(23):9124-7. doi: 10.1073/pnas.85.23.9124.
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DNA polymerase III of Escherichia coli is required for UV and ethyl methanesulfonate mutagenesis.大肠杆菌的DNA聚合酶III是紫外线和甲磺酸乙酯诱变所必需的。
Proc Natl Acad Sci U S A. 1987 Jun;84(12):4195-9. doi: 10.1073/pnas.84.12.4195.

引用本文的文献

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An SOS-regulated operon involved in damage-inducible mutagenesis in Caulobacter crescentus.一个参与新月柄杆菌损伤诱导诱变的SOS调节操纵子。
Nucleic Acids Res. 2005 May 10;33(8):2603-14. doi: 10.1093/nar/gki551. Print 2005.
2
Intrinsic polymerase activities of UmuD'(2)C and MucA'(2)B are responsible for their different mutagenic properties during bypass of a T-T cis-syn cyclobutane dimer.UmuD'(2)C和MucA'(2)B的内在聚合酶活性决定了它们在绕过T-T顺式-环丁烷二聚体时具有不同的诱变特性。
J Bacteriol. 2000 Apr;182(8):2285-91. doi: 10.1128/JB.182.8.2285-2291.2000.
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Efficient translesion replication in the absence of Escherichia coli Umu proteins and 3'-5' exonuclease proofreading function.
在缺乏大肠杆菌Umu蛋白和3'-5'核酸外切酶校对功能的情况下进行高效跨损伤复制。
Proc Natl Acad Sci U S A. 1998 Dec 22;95(26):15519-24. doi: 10.1073/pnas.95.26.15519.
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Genetic requirements and mutational specificity of the Escherichia coli SOS mutator activity.大肠杆菌SOS诱变活性的遗传要求和突变特异性。
J Bacteriol. 1997 Dec;179(23):7435-45. doi: 10.1128/jb.179.23.7435-7445.1997.
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Mutagenesis after exposure of bacteria to ultraviolet light and delayed photoreversal.细菌暴露于紫外线后发生的诱变作用及延迟光逆转。
Mol Gen Genet. 1992 Jun;233(3):331-6. doi: 10.1007/BF00265428.
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Overproduction of the beta subunit of DNA polymerase III holoenzyme reduces UV mutagenesis in Escherichia coli.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。
J Bacteriol. 1992 Apr;174(8):2517-24. doi: 10.1128/jb.174.8.2517-2524.1992.