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DNA聚合酶I参与大肠杆菌K-12中紫外线诱导损伤的复制后修复。

The involvement of DNA polymerase I in the postreplication repair of ultraviolet radiation-induced damage in Escherichia coli K-12.

作者信息

Barfknecht T R, Smith K C

出版信息

Mol Gen Genet. 1978 Nov 16;167(1):37-41. doi: 10.1007/BF00270319.

Abstract

A deficiency in DNA polymerase I increased the ultraviolet (UV) radiation sensitivity of a uvrA strain of Escherichia coli K-12 when plated on minimal growth medium. The slope of the survival curve for the uvrA polA strain was 2.0-times greater than that for the uvrA strain. The fluence-dependent yield of unrepaired deoxyribonucleic acid (DNA) parental-strand breaks following UV irradiation and incubation in minimal growth medium was similar in both strains. However, the fluence-dependent yield of unrepaired DNA daughter-strand gaps observed following UV irradiation was 1.8-fold greater in the uvrA polA strain than in the uvrA strain. These results suggest that DNA polymerase I is involved in the filling of at least some daughter-strand gaps during postreplication repair. Also, the uvrA polA strain was sensitized by a post-UV treatment with chloramphenicol (CAP) to a similar extent as was the uvrA strain, indicating that DNA polymerase I is not involved in the CAP-inhibitable pathway of postreplication repair.

摘要

当接种在基本生长培养基上时,DNA聚合酶I的缺陷增加了大肠杆菌K-12 uvrA菌株对紫外线(UV)辐射的敏感性。uvrA polA菌株存活曲线的斜率比uvrA菌株的斜率大2.0倍。在基本生长培养基中紫外线照射和孵育后,两种菌株中未修复的脱氧核糖核酸(DNA)亲链断裂的通量依赖性产率相似。然而,紫外线照射后观察到的未修复DNA子链缺口的通量依赖性产率在uvrA polA菌株中比uvrA菌株高1.8倍。这些结果表明,DNA聚合酶I参与复制后修复过程中至少一些子链缺口的填补。此外,uvrA polA菌株经紫外线后用氯霉素(CAP)处理后,其敏感性与uvrA菌株相似,这表明DNA聚合酶I不参与复制后修复的CAP抑制途径。

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