大肠杆菌中缺乏DNA聚合酶I、II和/或III的突变体中的DNA修复
DNA repair in Escherichia coli mutants deficient in DNA polymerases I, II and-or 3.
作者信息
Tait R C, Harris A L, Smith D W
出版信息
Proc Natl Acad Sci U S A. 1974 Mar;71(3):675-9. doi: 10.1073/pnas.71.3.675.
E. coli mutants deficient in DNA polymerase I, in DNA polymerases I and II, or in DNA polymerase III, can efficiently and completely execute excision repair and post-replication repair of UV-damaged DNA at 43 degrees when assayed by alkaline sucrose gradients. Repair by cells deficient in polymerase I and in polymerases I and II is inhibited by 1-beta-D-arabinofuranosylcytosine at 43 degrees , whereas that by cells deficient in polymerase III is insensitive to the inhibitor. When both DNA polymerases I and III are deficient, both excision repair and post-replication repair are greatly reduced at 43 degrees , and the residual repair capability is inhibited by 1-beta-D-arabinofuranosylcytosine. Very little dark repair is observed in cells deficient in DNA polymerases I, II, and III, and the DNA is extensively degraded. These results suggest that either DNA polymerase I or DNA polymerase III is required for complete and efficient repair, and that when both DNA polymerases I and III are deficient, DNA polymerase II mediates a limited, incomplete dark repair of UV-damaged DNA. DNA polymerases I and III thus appear to be important enzymes in both DNA replication and DNA dark repair.
当通过碱性蔗糖梯度分析时，缺乏DNA聚合酶I、缺乏DNA聚合酶I和II或缺乏DNA聚合酶III的大肠杆菌突变体，在43摄氏度时能够高效且完全地进行紫外线损伤DNA的切除修复和复制后修复。缺乏聚合酶I以及缺乏聚合酶I和II的细胞在43摄氏度时的修复会受到1-β-D-阿拉伯呋喃糖基胞嘧啶的抑制，而缺乏聚合酶III的细胞的修复对该抑制剂不敏感。当DNA聚合酶I和III都缺乏时，在43摄氏度时切除修复和复制后修复都会大大减少，并且残余的修复能力会受到1-β-D-阿拉伯呋喃糖基胞嘧啶的抑制。在缺乏DNA聚合酶I、II和III的细胞中观察到极少的暗修复，并且DNA会被广泛降解。这些结果表明，完全且高效的修复需要DNA聚合酶I或DNA聚合酶III，并且当DNA聚合酶I和III都缺乏时，DNA聚合酶II介导对紫外线损伤DNA的有限、不完全的暗修复。因此，DNA聚合酶I和III似乎在DNA复制和DNA暗修复中都是重要的酶。
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