作者: Chandan Shee , P. J. Hastings , Susan M. Rosenberg
DOI: 10.1007/978-1-4614-6280-4_2
关键词: Genetics 、 Frameshift mutation 、 Homologous recombination 、 DNA polymerase 、 rpoS 、 DNA 、 Mutation 、 Nucleotide excision repair 、 Biology 、 Mutagenesis
摘要: Evolutionary theory predicted that mutations occur randomly both in time and genomic space. This expectation has been revised by the discoveries of stress-induced mutation mechanisms, which activate mutagenesis pathways under control stress responses. Stress-induced mechanisms produce preferentially when cells or organisms are maladapted to their environment, i.e., they stressed, potentially accelerating evolution. We review stress-induced associated with repair double-strand breaks Escherichia coli. In this mechanism, process DNA break homologous recombination is high-fidelity unstressed cells, but switched a mutagenic mode using error-prone polymerase DinB, other polymerases, RpoS general response. The switch occurs during starvation if upregulated artificially presumably many different stresses Recent work shows mechanism accounts for most spontaneous base-substitution frameshift E. coli, acts not only plasmid also chromosomes plasmid-free illustrates generality circumstances, resolves some old tensions field. studied laboratory likely provide superior models underlying pathogen-host adaptation, antibiotic resistance, cancer progression resistance all problems evolution driven mutations.