Schendel P F, Defais M, Jeggo P, Samson L, Cairns J
J Bacteriol. 1978 Aug;135(2):466-75. doi: 10.1128/jb.135.2.466-475.1978.
Mutagenesis by simple alkylating agents is thought to occur by either a lexA+-dependent process called error-prone repair or a lex-independent process often attributed to mispairing during replication. We show here that error-prone repair is responsible for the majority of mutants formed after a large dose of alkylating agent, but it is unlikely that it contributes significantly to mutagenesis during exposure to low concentrations of these chemicals. The mutagenicity of these low doses of alkylating agent is reduced by a repair system constitutively present in lexA+ cells but absent in lexA mutants. This system reduces mutagenesis until a second error-free system, called the adaptive responses, can be induced [P. Jeggo, M. Defais, L. Samson, and P. Schendel, Mol. Gen. Genet, 157:1-9, 1977; L. Samson and J. Cairns, Nature (London) 267:281-283, 1977]. The adaptive response is capable of dealing with a much larger amount of alkylation damage than the constitutive system and, when induced, appears to be able to reduce mutagenesis by both decreasing the number of sites available for mutagenesis and delaying the induction of error-prone repair enzymes. Finally, we discuss a model of chemically induced mutagenesis based on these findings which maintains that the observed mutation frequency is dependent on a "race" between these two error-free systems and the two mutagenic pathways.
简单烷基化剂诱导的诱变作用被认为是通过一种名为易错修复的依赖lexA+的过程，或者是一种通常归因于复制过程中错配的不依赖lexA的过程发生的。我们在此表明，易错修复是大剂量烷基化剂处理后形成的大多数突变体的原因，但在暴露于低浓度这些化学物质期间，它不太可能对诱变作用有显著贡献。这些低剂量烷基化剂的诱变性被lexA+细胞中组成性存在但lexA突变体中不存在的修复系统降低。该系统会降低诱变作用，直到可以诱导出另一种无差错系统，即适应性反应[P. Jeggo、M. Defais、L. Samson和P. Schendel，《分子与普通遗传学》，157:1 - 9，1977；L. Samson和J. Cairns，《自然》（伦敦）267:281 - 283，1977]。适应性反应能够处理比组成性系统多得多的烷基化损伤，并且在被诱导时，似乎能够通过减少可用于诱变的位点数量和延迟易错修复酶的诱导来降低诱变作用。最后，我们基于这些发现讨论了一种化学诱导诱变的模型，该模型认为观察到的突变频率取决于这两种无差错系统和两种诱变途径之间的“竞争”。
