大肠杆菌中DNA连接酶缺陷导致易错修复的诱导。
Induction of error-prone repair as a consequence of DNA ligase deficiency in Escherichia coli.
作者信息
Morse L S, Pauling C
出版信息
Proc Natl Acad Sci U S A. 1975 Nov;72(11):4645-9. doi: 10.1073/pnas.72.11.4645.
Abstract
DNA ligase deficiency is shown to induce generalized mutator activity in E. coli. This mutator activity is unaffected by 3 mug/ml of chloramphenicol but is abolished both in lig-recA double mutants and by incubation with 20 mug/ml of chloramphenicol. Dna ligase deficiency is also shown to reactivate ultraviolet light-irradiated phage lambda and T7 and to increase both spontaneous and ultraviolet light-induced mutagenesis in phage lambda, all of which are abolished in lig-recA strains. Interaction occurs between the molecular events of mutagenesis induced by ultraviolet irradiation and those induced by DNA ligase deficiency. These observations suggest a common pathway, coordinately expressed with the inducible repair mode, that is responsible for mutagenesis.
摘要
已表明DNA连接酶缺陷会在大肠杆菌中诱导普遍的诱变活性。这种诱变活性不受3微克/毫升氯霉素的影响，但在连接酶-recA双突变体中以及与20微克/毫升氯霉素一起孵育时会被消除。还表明DNA连接酶缺陷会重新激活紫外线照射的噬菌体λ和T7，并增加噬菌体λ中的自发诱变和紫外线诱导的诱变，所有这些在连接酶-recA菌株中都会被消除。紫外线照射诱导的诱变分子事件与DNA连接酶缺陷诱导的诱变分子事件之间存在相互作用。这些观察结果表明存在一条与可诱导修复模式协同表达的共同途径，该途径负责诱变。
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