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.
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