Seeberg E, Strike P
J Bacteriol. 1976 Mar;125(3):787-95. doi: 10.1128/jb.125.3.787-795.1976.
A system of cells made permeable by treatment with high concentrations of surcrose (plasmolysis) has been exploited to study the excision repair of ultraviolet-irradiated deoxyribonucleic acid in Escherichia coli. It is demonstrated that adenosine 5'-triphosphate is required for incision breaks to be made in the bacterial chromosome as well as in covalently closed bacteriophage lambda deoxyribonucleic acid. After plasmolysis, uvrC mutant strains appear as defective in the incision step as the uvrA-mutated strains. This is in contrast to the situation in intact cells where uvrC mutants accumulate single-strand breaks during postirradiation incubation. These observations have led to the proposal of a model for excision repair, in which the ultraviolet-specific endonuclease, coded for by the uvrA and uvrB genes, exists in a complex with the uvrC gene product. The complex is responsible for the incision and possibly also the excision steps of repair. The dark-repair inhibitors acriflavine and caffeine are both shown to interfere with the action of the adenosine 5'-triphosphate-dependent enzyme.
一种通过用高浓度蔗糖处理（质壁分离）而使其具有通透性的细胞系统，已被用于研究大肠杆菌中紫外线照射的脱氧核糖核酸的切除修复。结果表明，在细菌染色体以及共价闭合的噬菌体λ脱氧核糖核酸中产生切口断裂都需要腺苷5'-三磷酸。质壁分离后，uvrC突变菌株在切口步骤中表现出与uvrA突变菌株一样的缺陷。这与完整细胞中的情况形成对比，在完整细胞中，uvrC突变体在照射后孵育期间会积累单链断裂。这些观察结果导致提出了一种切除修复模型，其中由uvrA和uvrB基因编码的紫外线特异性内切核酸酶与uvrC基因产物形成复合物存在。该复合物负责修复的切口步骤，也可能负责切除步骤。暗修复抑制剂吖啶黄素和咖啡因均显示会干扰依赖腺苷5'-三磷酸的酶的作用。
