Cooper P K, Hanawalt P C
Proc Natl Acad Sci U S A. 1972 May;69(5):1156-60. doi: 10.1073/pnas.69.5.1156.
The DNA polymerase I-deficient mutant polA1 is shown to perform an increased amount of UV-stimulated repair synthesis relative to its pol(+) parent. In contrast, a recA recB double mutant is found to perform little detectable repair synthesis. Analysis of the density distribution of sheared DNA of the recA recB mutant reveals that none of the repair synthesis in this strain is in the large repair patches previously demonstrated by us in wild-type strains. These results are interpreted in terms of a model involving both DNA polymerase I and the rec system in the excision-repair process, with polymerase I performing an efficient short patch repair and rec system enzymes producing predominantly large patches of repair synthesis.
与野生型亲本相比，DNA聚合酶I缺陷型突变体polA1表现出更多的紫外线刺激修复合成。相反，recA recB双突变体几乎检测不到修复合成。对recA recB突变体剪切DNA的密度分布分析表明，该菌株中的修复合成均未形成我们之前在野生型菌株中所证明的大的修复片段。这些结果可根据一个涉及DNA聚合酶I和rec系统参与切除修复过程的模型来解释，其中聚合酶I进行高效的短片段修复，而rec系统酶主要产生大的修复合成片段。
