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酿酒酵母中DNA甲基化损伤的碱基切除修复需要DNA聚合酶δ。

DNA polymerase delta is required for base excision repair of DNA methylation damage in Saccharomyces cerevisiae.

作者信息

Blank A, Kim B, Loeb L A

机构信息

Joseph Gottstein Memorial Cancer Research Laboratory, Department of Pathology, University of Washington, Seattle 98195.

出版信息

Proc Natl Acad Sci U S A. 1994 Sep 13;91(19):9047-51. doi: 10.1073/pnas.91.19.9047.

Abstract

We present evidence that DNA polymerase delta of Saccharomyces cerevisiae, an enzyme that is essential for viability and chromosomal replication, is also required for base excision repair of exogenous DNA methylation damage. The large catalytic subunit of DNA polymerase delta is encoded by the CDC2(POL3) gene. We find that the mutant allele cdc2-2 confers sensitivity to killing by methyl methanesulfonate (MMS) but allows wild-type levels of UV survival. MMS survival of haploid cdc2-2 strains is lower than wild type at the permissive growth temperature of 20 degrees C. Survival is further decreased relative to wild type by treatment with MMS at 36 degrees C, a nonpermissive temperature for growth of mutant cells. A second DNA polymerase delta allele, cdc2-1, also confers a temperature-sensitive defect in MMS survival while allowing nearly wild-type levels of UV survival. These observations provide an in vivo genetic demonstration that a specific eukaryotic DNA polymerase is required for survival of exogenous methylation damage. MMS sensitivity of a cdc2-2 mutant at 20 degrees C is complemented by expression of mammalian DNA polymerase beta, an enzyme that fills single-strand gaps in duplex DNA in vitro and whose only known catalytic activity is polymerization of deoxyribonucleotides. We conclude, therefore, that the MMS survival deficit in cdc2-2 cells is caused by failure of mutant DNA polymerase delta to fill single-strand gaps arising in base excision repair of methylation damage. We discuss our results in light of current concepts of the physiologic roles of DNA polymerases delta and epsilon in DNA replication and repair.

摘要

我们提供的证据表明,酿酒酵母的DNA聚合酶δ是一种对细胞活力和染色体复制至关重要的酶,在外源DNA甲基化损伤的碱基切除修复中也不可或缺。DNA聚合酶δ的大型催化亚基由CDC2(POL3)基因编码。我们发现,突变等位基因cdc2 - 2使细胞对甲磺酸甲酯(MMS)杀伤敏感,但能维持野生型水平的紫外线抗性。在20℃的允许生长温度下,单倍体cdc2 - 2菌株对MMS的抗性低于野生型。在36℃(突变细胞生长的非允许温度)用MMS处理后,相对于野生型,其抗性进一步降低。另一个DNA聚合酶δ等位基因cdc2 - 1在MMS抗性方面也表现出温度敏感缺陷,同时能维持接近野生型水平的紫外线抗性。这些观察结果提供了体内遗传学证据,表明特定的真核DNA聚合酶是外源甲基化损伤存活所必需的。在20℃时,cdc2 - 2突变体对MMS的敏感性可通过哺乳动物DNA聚合酶β的表达得到互补,该酶在体外可填补双链DNA中的单链缺口,其唯一已知的催化活性是脱氧核糖核苷酸的聚合。因此,我们得出结论,cdc2 - 2细胞中MMS抗性缺陷是由于突变的DNA聚合酶δ无法填补甲基化损伤碱基切除修复中产生的单链缺口所致。我们根据目前关于DNA聚合酶δ和ε在DNA复制和修复中的生理作用的概念来讨论我们的结果。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/eff9/44744/efbc82814815/pnas01141-0331-a.jpg

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