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大肠杆菌中缺乏DNA聚合酶I和/或其相关的5'至3'外切核酸酶的突变体中的切除修复。

Excision-repair in mutants of Escherichia coli deficient in DNA polymerase I and/or its associated 5' leads to 3' exonuclease.

作者信息

Cooper P

出版信息

Mol Gen Genet. 1977 Jan 7;150(1):1-12. doi: 10.1007/BF02425319.

Abstract

The ultraviolet (UV) sensitivity of Escherichia coli mutants deficient in the 5' leads to 3' exonuclease activity of DNA polymerase I is intermediate between that of pol+ strains and mutants which are deficient in the polymerizing activity of pol I (polA1). Like polA1 mutants, the 5'-exonclease deficient mutants exhibit increased UV-induced DNA degradation and increased repair synthesis compared to a pol+ strain, although the increase is not as great as in polA1 or in the conditionally lethal mutant BT4113ts deficient in both polymerase I activities. When dimer excision was measured at UV doses low enough to avoid interference from extensive DNA degradation, all three classes of polymerase I deficient mutants were found to remove dimers efficiently from their DNA. We conclude that enzymes alternative to polymerase I can operate in both the excision and resynthesis steps of excision repair and that substitution for either of the polymerase I functions results in longer patches of repair. A model is proposed detailing the possible events in the alternative pathways.

摘要

缺乏DNA聚合酶I 5'至3'核酸外切酶活性的大肠杆菌突变体对紫外线(UV)的敏感性介于野生型菌株和缺乏聚合酶I聚合活性的突变体(polA1)之间。与polA1突变体一样,与野生型菌株相比,缺乏5'核酸外切酶的突变体表现出紫外线诱导的DNA降解增加和修复合成增加,尽管增加的程度不如polA1或同时缺乏两种聚合酶I活性的条件致死突变体BT4113ts。当在足够低的紫外线剂量下测量二聚体切除,以避免广泛DNA降解的干扰时,发现所有三类聚合酶I缺陷突变体都能有效地从其DNA中去除二聚体。我们得出结论,替代聚合酶I的酶可以在切除修复的切除和重新合成步骤中发挥作用,并且替代聚合酶I的任何一种功能都会导致更长的修复片段。提出了一个模型,详细说明了替代途径中可能发生的事件。

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