Mutation as a stress response and the regulation of evolvability

被引:436
作者
Galhardo, Rodrigo S.
Hastings, P. J.
Rosenberg, Susan M.
机构
[1] Baylor Coll Med, Dept Mol & Human Genet, Houston, TX 77030 USA
[2] Baylor Coll Med, Dan L Duncan Canc Ctr, Dept Biochem & Mol Biol, Houston, TX 77030 USA
[3] Baylor Coll Med, Dan L Duncan Canc Ctr, Dept Mol Virol, Houston, TX 77030 USA
[4] Baylor Coll Med, Dan L Duncan Canc Ctr, Dept Microbiol, Houston, TX 77030 USA
关键词
adaptive mutation; evolution; mutation rates; error-prone DNA polymerases; stress responses; recombination; DNA repair; SOS response; sigma(s); RpoS; cancer; genome instability; microbial pathogenesis; antibiotic resistance;
D O I
10.1080/10409230701648502
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Our concept of a stable genome is evolving to one in which genomes are plastic and responsive to environmental changes. Growing evidence shows that a variety of environmental stresses induce genomic instability in bacteria, yeast, and human cancer cells, generating occasional fitter mutants and potentially accelerating adaptive evolution. The emerging molecular mechanisms of stress-induced mutagenesis vary but share telling common components that underscore two common themes. The first is the regulation of mutagenesis in time by cellular stress responses, which promote random mutations specifically when cells are poorly adapted to their environments, i.e., when they are stressed. A second theme is the possible restriction of random mutagenesis in genomic space, achieved via coupling of mutation-generating machinery to local events such as DNA-break repair or transcription. Such localization may minimize accumulation of deleterious mutations in the genomes of rare fitter mutants, and promote local concerted evolution. Although mutagenesis induced by stresses other than direct damage to DNA was previously controversial, evidence for the existence of various stress-induced mutagenesis programs is now overwhelming and widespread. Such mechanisms probably fuel evolution of microbial pathogenesis and antibiotic-resistance, and tumor progression and chemotherapy resistance, all of which occur under stress, driven by mutations. The emerging commonalities in stress-induced-mutation mechanisms provide hope for new therapeutic interventions for all of these processes.
引用
收藏
页码:399 / 435
页数:37
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