摘要： 基于大肠杆菌FC40菌株的研究结果表明，适应性突变依赖RecBCD重组途径的酶，要求SOS反应的部分基因功能，lac+回复突变序列都是在单核苷酸短重复序列处的一个碱基缺失。有证据表明有的适应性突变来自一个或多个暂时性的超突变的细胞亚群，它们的基因组发生大量的突变，转座子高频丢失。产生这种暂时性的超突变的增变子可能是因为细胞的MMR活性暂时不足，或是因错误翻译产生丧失了校读活性的DNA聚合酶III。其他一些研究系统虽然得到了一些同FC40菌株不一致的结论，但所有实验证据都表明，在饥饿等环境胁迫因子作用下，非生长或缓慢生长的细胞可以产生突变，这种突变具有生长依赖的自发突变所不同的一些遗传学特征。
Abstract:The research based on the Escherichia coli FC40 showed that adaptive mutations required the enzymes of RecBCD recombination pathway and some unknown proteins of SOS response,and the mutation spectrum of lac+ revertants is single-base deletions in the small mononucleotide repeats.Some evidence showed that the revertants with adaptive mutations partly come from one (or some) subset of transient hypermutable subpopulation of cells,in which high frequently losing of transposons and genome-wide mutations were observed.It was suggested that this kind of transient hypermutability may be due to the transient deficient activity of mismatch repair (MMR) system,or a defective epsilon unit of DNA polymerase III generated by mistranslation.Although other systems demonstrated some different mechanisms from FC40,all research works suggested that,adaptive mutations occurred in nondividing or nongrowing cells under environmental stresses,for example,starvation,displayed different genetic features from growth-dependent spontaneous mutation.