适应性大肠杆菌中O6-甲基鸟嘌呤的修复
Repair of O6-methylguanine in adapted Escherichia coli.
作者信息
Schendel P F, Robins P E
出版信息
Proc Natl Acad Sci U S A. 1978 Dec;75(12):6017-20. doi: 10.1073/pnas.75.12.6017.
Abstract
Cells exposed to sublethal concentrations of simple alkylating agents develop resistance to their mutagenic effects. This results from the induction of a system that we have called the adaptive response. During exposure to N-methyl-N'-nitro-N-nitrosoguanidine (MNNG), Escherichia coli cells induced for the adaptive response accumulate substantially less O6-methylguanine in their DNA than control cells. If O6-methylguanine does form, adapted cells possess a repair system for removing it from their DNA. The capacity of this system is limited and the system ceases to function when too much alkylation has occurred. From this point onwards O6-methylguanine starts to accumulate, and the cells begin to develop mutations at a rate directly proportional to their rate of O6-methylguanine accumulation. Our data support the idea that the O6 methylation of guanine accounts for most MNNG-induced mutagenesis.
摘要
暴露于亚致死浓度简单烷化剂的细胞会对其诱变效应产生抗性。这是由一种我们称为适应性反应的系统的诱导所导致的。在暴露于N-甲基-N'-硝基-N-亚硝基胍（MNNG）期间，被诱导产生适应性反应的大肠杆菌细胞在其DNA中积累的O6-甲基鸟嘌呤比对照细胞少得多。如果O6-甲基鸟嘌呤确实形成，适应的细胞拥有一个将其从DNA中去除的修复系统。该系统的能力是有限的，当发生过多烷基化时该系统就会停止运作。从这一点开始，O6-甲基鸟嘌呤开始积累，并且细胞开始以与其O6-甲基鸟嘌呤积累速率成正比的速率发生突变。我们的数据支持这样一种观点，即鸟嘌呤的O6甲基化是大多数MNNG诱导诱变的原因。
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