Stress responses and genetic variation in bacteria

Foster, Patricia L.

doi:10.1016/j.mrfmmm.2004.07.017

Cited by 176 publications

(119 citation statements)

References 75 publications

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“…LexA levels fluctuate with pH variation as well as in ageing colonies. LexA inactivation during starvation or under oxidative stress induces polymerase Pol IV, which is expected to increase the error rate of DNA synthesis (Foster, 2005) and to result in multiple mutations during the transient hypermutation state (Tompkins et al, 2003) (Fig. 2).…”

Section: Role Of the Sos System?mentioning

confidence: 99%

Bacterial hypermutation: clinical implications

Jolivet‐Gougeon

Kovács

Gall‐David

et al. 2011

Journal of Medical Microbiology

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Heritable hypermutation in bacteria is mainly due to alterations in the methyl-directed mismatch repair (MMR) system. MMR-deficient strains have been described from several bacterial species, and all of the strains exhibit increased mutation frequency and recombination, which are important mechanisms for acquired drug resistance in bacteria. Antibiotics select for drug-resistant strains and refine resistance determinants on plasmids, thus stimulating DNA recombination via the MMR system. Antibiotics can also act as indirect promoters of antibiotic resistance by inducing the SOS system and certain error-prone DNA polymerases. These alterations have clinical consequences in that efficacious treatment of bacterial infections requires high doses of antibiotics and/or a combination of different classes of antimicrobial agents. There are currently few new drugs with low endogenous resistance potential, and the development of such drugs merits further research. IntroductionEradication of infectious diseases is constantly challenged by micro-organisms that develop new survival strategies. Previous studies suggest that mutational events play a predominant role in bacterial adaptation and confer a selective advantage (Chou et al., 2009;Cooper, 2007). Early experiments aimed at detecting mutators used mutagenized laboratory strains of bacteria, sometimes coupled with different selection strategies. LeClerc et al. (1996) reported high mutation frequency among Escherichia coli and Salmonella pathogens, challenging the theory that mutators were rare among bacterial populations. Taken together, these findings demonstrated that natural populations could respond to environmental selection in two ways, i.e. by enhanced mutation frequencies and by recombination. Transient mutator status, which involves reversion or recombination within the mutator alleles or depletion of the methyl-directed mismatch repair (MMR) system proteins, allows the organism to temporarily benefit from the elevated mutation frequency for adaptation while reducing the risk of accumulating deleterious mutations. Using a mathematical model, Rosche & Foster (1999) showed that transient hypermutators play a role in adaptive mutation in E. coli. Molecular mechanisms of hypermutationProteins involved in the DNA mismatch repair pathway help replace nucleotides introduced erroneously into the replicated DNA and also hinder recombination between non-identical DNA sequences. Deficiencies in any of the DNA mismatch repair pathway mechanisms can lead to a hypermutator phenotype. DNA repairSiegel & Bryson (1967) discovered the mutS gene in an azaserine-resistant derivative of E. coli that had a mutator phenotype and carried a deletion in the mutS gene. The majority of naturally occurring strong mutators have defects in the MMR system; the mutations are mainly in mutS (Oliver et al., 2002), but deletions in genes encoding beta-clamp proteins and in mutH, mutL and mutU (uvrD) have also been described (Fig. 1). Inactivation of basal excision repair genes, e.g. mutY, mutM, ...

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Section: Role Of the Sos System?mentioning

confidence: 99%

Bacterial hypermutation: clinical implications

Jolivet‐Gougeon

Kovács

Gall‐David

et al. 2011

Journal of Medical Microbiology

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“…In reality, the frequency of sex generally depends on the condition of an individual, a pattern found broadly across both facultatively sexual prokaryotes and eukaryotes (Bell 1982). Individuals that are starved undergo sex at higher rates in a wide variety of organisms, including bacteria (Dubnau 1991;Redfield 1993;Jarmer et al 2002;Foster 2005), yeast (Kassir et al 1988;Mai and Breeden 2000), Chlamydomonas reinhardtii (Harris 1989), and daphnia (in combination with photoperiod and density cues; Kleiven et al 1992). Cells with DNA damage have also been shown to undergo sex at higher rates in viruses (Bernstein 1987), bacteria (Wojciechowski et al 1989), and yeast (Bernstein and Johns 1989).…”

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The Evolution of Condition-Dependent Sex in the Face of High Costs

Hadany

Otto

2007

Genetics

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Facultatively sexual organisms often engage in sex more often when in poor condition. We show that such condition-dependent sex carries evolutionary advantages and can explain the evolution of sexual reproduction even when sex entails high costs. Specifically, we show that alleles promoting individuals of low fitness to have sex more often than individuals of high fitness spread through a population. Such alleles are more likely to segregate out of bad genetic backgrounds and onto good genetic backgrounds, where they tend to remain. This ''abandon-ship'' mechanism provides a plausible model for the evolution and maintenance of facultative sex.

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“…Under selection, 100 colonies appear from 10 8 plated cells over 6 days. This behavior suggested that selective stress might activate a mechanism to increase the general mutation rate (3)(4)(5). However, modeling indicated that such a mechanism would reduce long-term fitness (6,7).…”

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Multiple pathways of selected gene amplification during adaptive mutation

Kugelberg

Kofoid

Reams

et al. 2006

Proc. Natl. Acad. Sci. U.S.A.

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In a phenomenon referred to as ''adaptive mutation,'' a population of bacterial cells with a mutation in the lac operon (lac ؊ ) accumulates Lac ؉ revertants during prolonged exposure to selective growth conditions (lactose). Evidence was provided that selective conditions do not increase the mutation rate but instead favor the growth of rare cells with a duplication of the leaky lac allele. A further increase in copy number (amplification) improves growth and increases the likelihood of a sequence change by adding more mutational targets to the clone (cells and lac copies per cell). These duplications and amplifications are described here. Before selection, cells with large (134-kb) lac duplications and long junction sequences (>1 kb) were common (0.2%). The same large repeats were found after selection in cells with a low-copy-number lac amplification. Surprisingly, smaller repeats (average, 34 kb) were found in high-copy-number amplifications. The small-repeat duplications form when deletions modify a preexisting large-repeat duplication. The shorter repeat size allowed higher lac amplification and better growth on lactose. Thus, selection favors a succession of gene-amplification types that make sequence changes more probable by adding targets. These findings are relevant to genetic adaptation in any biological systems in which fitness can be increased by adding gene copies (e.g., cancer and bacterial drug resistance).gene duplication ͉ genetic adaptation ͉ natural selection ͉ genome instability ͉ mutation under selection

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Stress responses and genetic variation in bacteria

Cited by 176 publications

References 75 publications

Bacterial hypermutation: clinical implications

Bacterial hypermutation: clinical implications

The Evolution of Condition-Dependent Sex in the Face of High Costs

Multiple pathways of selected gene amplification during adaptive mutation

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