Cooper P K
Mol Gen Genet. 1982;185(2):189-97. doi: 10.1007/BF00330785.
Excision repair in ultraviolet-irradiated wild-type Escherichia coli produces a bimodal distribution of repair patch sizes in the DNA. Approximately 99% of the repair events result in short patches of 20-30 nucleotides produced by a constitutive repair system. The remaining 1% result in patches which are at least 1,500 nucleotides in length. This long patch repair is shown to be a damage-inducible process under control of the rec-lex regulatory circuit. The kinetics of the two processes differ; short patch synthesis begins immediately after irradiation and is virtually completed prior to synthesis of the majority of the long patches. Long patch repair synthesis is a linear function of UV dose up to a plateau at 60 J/m2, and hence each long patch event is the consequence of a single UV-induced lesion. Long patch repair does not appear to be necessarily error-prone, since no alteration in repair synthesis occurs as a result of a mutation umuC- which renders cells nonmutable by UV. Evidence is presented suggesting that DNA polymerase I is responsible for both long and short patch synthesis in wild type cells under inducing conditions. In the absence of polymerase I the constitutive patch size averages 80-90 nucleotides, and this distribution is unchanged by induction.
紫外线照射的野生型大肠杆菌中的切除修复会在DNA中产生双峰分布的修复补丁大小。大约99%的修复事件会产生由组成型修复系统产生的20 - 30个核苷酸的短补丁。其余1%会产生长度至少为1500个核苷酸的补丁。这种长补丁修复被证明是在rec-lex调节回路控制下的损伤诱导过程。这两个过程的动力学不同;短补丁合成在照射后立即开始,并且在大多数长补丁合成之前几乎完成。长补丁修复合成是紫外线剂量的线性函数,直到在60 J/m²达到平稳期,因此每个长补丁事件都是单个紫外线诱导损伤的结果。长补丁修复似乎不一定容易出错,因为umuC-突变(使细胞对紫外线不可诱变)不会导致修复合成发生改变。有证据表明,在诱导条件下,DNA聚合酶I负责野生型细胞中的长补丁和短补丁合成。在没有聚合酶I的情况下,组成型补丁大小平均为80 - 90个核苷酸,并且这种分布不会因诱导而改变。