Mechanisms of Stationary Phase Mutation: A Decade of Adaptive Mutation

Foster, Patricia L.

doi:10.1146/annurev.genet.33.1.57

Cited by 167 publications

(112 citation statements)

References 159 publications

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“…Changes in recombination may be an incidental by-product of a genome under stress. There is some evidence that mutation rates increase under stress (e.g., Hall 1992;Foster 1999;Goho and Bell 2000). Theory suggests that such a phenomenon is unlikely to be adaptive in sexual organisms (Leigh 1970;Sniegowski et al 2000).…”

Section: Discussionmentioning

confidence: 99%

The Evolution of Plastic Recombination

2005

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Empirical data suggest that recombination rates may change in response to stress. To study the evolution of plastic recombination, we develop a modifier model using the same theoretical framework used to study conventional (nonplastic) modifiers, thus allowing direct comparison. We examine the evolution of plastic recombination in both haploid and diploid systems. In haploids, a plastic modifier spreads by forming associations with selectively favored alleles. Relative to nonplastic effects, selection on the plastic effects of a modifier is both much stronger and less sensitive to the specifics of the selection regime (e.g., epistasis). In contrast, the evolution of plastic recombination in diploids is much more restricted. Selection on plasticity requires the ability to detect DNA damage or cis-trans effects as may occur through maternal effects on fitness.

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Section: Discussionmentioning

confidence: 99%

The Evolution of Plastic Recombination

2005

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“…brano and Kolter 1996), as are pol IV and two other SOSFor providing strains, we thank Mary Berlyn and the E. coli Genetic inducible polymerases (Yeiser et al 2002). Also, apparent 1999) and other bacteria (Ilves et al 2001;Saumaa et al 2002).…”

Section: Rpos and Models For Transient Genetic Instabilitymentioning

confidence: 98%

“…In bacphase mutation mechanisms (Shapiro 1984; Cairns teria and yeast, there are multiple mechanisms of muta et al 1988), three broad classes of model have been tion in growth-limiting environments, some demonstraconsidered to explain apparent increases in adaptive bly different from spontaneous mutation in rapidly mutants under some selective conditions (reviewed by growing cells (Foster 1999b;Rosenberg 2001). Also Foster 1999b;Rosenberg 2001).…”

mentioning

confidence: 99%

General Stress Response Regulator RpoS in Adaptive Mutation and Amplification inEscherichia coli

Lombardo¹,

Aponyi²,

Rosenberg³

2004

Genetics

131

183

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Microbial cells under growth-limiting stress can generate mutations by mechanisms distinct from those in rapidly growing cells. These mechanisms might be specific stress responses that increase mutation rates, potentially altering rates of evolution, or might reflect non-stress-specific processes in rare growing cells.In an Escherichia coli model system, both frameshift reversion mutations and gene amplifications occur as apparent starvation-induced mutations. Whereas frameshift reversion ("point mutation") requires recombination proteins, the SOS response, and error-prone DNA polymerase IV (DinB), amplification requires neither SOS nor pol IV. We report that both point mutation and amplification require the stationaryphase and general stress response transcription factor RpoS ( S ). Growth-dependent mutation does not. Alternative interpretations are excluded. The results imply, first, that point mutation and amplification are stress responses that occur in differentiated stationary-phase (not rare growing) cells and, second, that transient genetic instability, producing both point mutation and genome rearrangement, may be a previously unrecognized component of the RpoS-dependent general stress response.

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“…Such fascinating phenomena of DNA metabolism as instability of repetitive DNA, adaptive mutagenesis, trans-lesion DNA synthesis, and yeast meiotic recombination, which had to be left out because of size limitations, are covered in recent comprehensive or specialized reviews (7,(13)(14)(15)(16). Other papers in this Colloquium issue offer various perspectives.…”

mentioning

confidence: 99%

DNA replication meets genetic exchange: Chromosomal damage and its repair by homologous recombination

Kuzminov

2001

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

198

126

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Proceedings of the National Academy of Sciences Colloquium on the roles of homologous recombination in DNA replication are summarized. Current findings in experimental systems ranging from bacteriophages to mammalian cell lines substantiate the idea that homologous recombination is a system supporting DNA replication when either the template DNA is damaged or the replication machinery malfunctions. There are several lines of supporting evidence: (i) DNA replication aggravates preexisting DNA damage, which then blocks subsequent replication; (ii) replication forks abandoned by malfunctioning replisomes become prone to breakage; (iii) mutants with malfunctioning replisomes or with elevated levels of DNA damage depend on homologous recombination; and (iv) homologous recombination primes DNA replication in vivo and can restore replication fork structures in vitro. The mechanisms of recombinational repair in bacteriophage T4, Escherichia coli, and Saccharomyces cerevisiae are compared. In vitro properties of the eukaryotic recombinases suggest a bigger role for single-strand annealing in the eukaryotic recombinational repair.

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Mechanisms of Stationary Phase Mutation: A Decade of Adaptive Mutation

Cited by 167 publications

References 159 publications

The Evolution of Plastic Recombination

The Evolution of Plastic Recombination

General Stress Response Regulator RpoS in Adaptive Mutation and Amplification inEscherichia coli

DNA replication meets genetic exchange: Chromosomal damage and its repair by homologous recombination

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