Defects in the Error Prevention Oxidized Guanine System Potentiate Stationary-Phase Mutagenesis in
            <i>Bacillus subtilis</i>

Vidales, Luz E.; Cárdenas, Lluvia C.; Robleto, Eduardo A.; Yasbin, Ronald E.; Pedraza-Reyes, Mario

doi:10.1128/jb.01210-08

Cited by 39 publications

(66 citation statements)

References 47 publications

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“…Cells deficient for mutT, yvcI, or yjhB showed virtually no change in mutation frequency relative to a wild-type strain; a similar result occurred when all three genes were disrupted (355,356). There is evidence suggesting that the ytkD gene may encode an activity that is similar to that of E. coli MutT (55,324,428). It was shown that YtkD can specifically hydrolyze 8-oxo-(d)GTP, as well as complement a mutT deficiency in E. coli.…”

Section: The "Go" Systemmentioning

confidence: 59%

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DNA Repair and Genome Maintenance in Bacillus subtilis

Lenhart

Schroeder

Walsh

et al. 2012

Microbiol Mol Biol Rev

151

155

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SUMMARY From microbes to multicellular eukaryotic organisms, all cells contain pathways responsible for genome maintenance. DNA replication allows for the faithful duplication of the genome, whereas DNA repair pathways preserve DNA integrity in response to damage originating from endogenous and exogenous sources. The basic pathways important for DNA replication and repair are often conserved throughout biology. In bacteria, high-fidelity repair is balanced with low-fidelity repair and mutagenesis. Such a balance is important for maintaining viability while providing an opportunity for the advantageous selection of mutations when faced with a changing environment. Over the last decade, studies of DNA repair pathways in bacteria have demonstrated considerable differences between Gram-positive and Gram-negative organisms. Here we review and discuss the DNA repair, genome maintenance, and DNA damage checkpoint pathways of the Gram-positive bacterium Bacillus subtilis. We present their molecular mechanisms and compare the functions and regulation of several pathways with known information on other organisms. We also discuss DNA repair during different growth phases and the developmental program of sporulation. In summary, we present a review of the function, regulation, and molecular mechanisms of DNA repair and mutagenesis in Gram-positive bacteria, with a strong emphasis on B. subtilis.

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Section: The "Go" Systemmentioning

confidence: 59%

“…It was shown that YtkD can specifically hydrolyze 8-oxo-(d)GTP, as well as complement a mutT deficiency in E. coli. It was also shown that cells deficient for ytkD are more susceptible to oxidative DNA damage (55,324,428). However, others have presented evidence that YtkD fails to hydrolyze 8-oxo-dGTP selectively over dGTP (458).…”

Section: The "Go" Systemmentioning

confidence: 99%

DNA Repair and Genome Maintenance in Bacillus subtilis

Lenhart

Schroeder

Walsh

et al. 2012

Microbiol Mol Biol Rev

151

155

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“…In agreement with this idea, it has been shown that the genetic inactivation of the mismatch (MMR) and guanine-oxidized (GO) systems potentiates the mutagenic events that occur in nongrowing B. subtilis cells (6,7). Thus, it appears that the accumulation of mismatched and oxidized DNA bases in nongrowing B. subtilis cells is a key factor that promotes mutations under conditions of nutritional or metabolic stress (6,7).…”

mentioning

confidence: 52%

Error-Prone Processing of Apurinic/Apyrimidinic (AP) Sites by PolX Underlies a Novel Mechanism That Promotes Adaptive Mutagenesis in Bacillus subtilis

et al. 2014

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cIn growing cells, apurinic/apyrimidinic (AP) sites generated spontaneously or resulting from the enzymatic elimination of oxidized bases must be processed by AP endonucleases before they compromise cell integrity. Here, we investigated how AP sites and the processing of these noncoding lesions by the AP endonucleases Nfo, ExoA, and Nth contribute to the production of mutations (hisC952, metB5, and leuC427) in starved cells of the Bacillus subtilis YB955 strain. Interestingly, cells from this strain that were deficient for Nfo, ExoA, and Nth accumulated a greater amount of AP sites in the stationary phase than during exponential growth. Moreover, under growth-limiting conditions, the triple nfo exoA nth knockout strain significantly increased the amounts of adaptive his, met, and leu revertants produced by the B. subtilis YB955 parental strain. Of note, the number of stationary-phase-associated reversions in the his, met, and leu alleles produced by the nfo exoA nth strain was significantly decreased following disruption of polX. In contrast, during growth, the reversion rates in the three alleles tested were significantly increased in cells of the nfo exoA nth knockout strain deficient for polymerase X (PolX). Therefore, we postulate that adaptive mutations in B. subtilis can be generated through a novel mechanism mediated by error-prone processing of AP sites accumulated in the stationary phase by the PolX DNA polymerase.

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“…General and specific DNA repair systems, mismatch repair, and oxidative damage repair (GO system) have been shown to be repressed or inefficient in cells under conditions of stress in eukaryotic and bacterial systems (19,25,28,45) while errorprone polymerases are active in stationary-phase cells (11,12,19,42,43). Thus, one can speculate that the combination of transcriptional derepression and DNA repair inadequacies under conditions of nongrowth biases mutations to transcribed regions.…”

Section: Resultsmentioning

confidence: 99%

“…Spontaneous cellular processes such as deamination, oxidation, and base loss generate uracil, 8-oxo-7,8-dihydroguanine (8-oxoG), and apurinic/apyrimidinic (AP) sites in DNA, respectively (reviewed in reference 37). Of these DNA-insulting processes, those causing oxidative damage have been shown to be significant in B. subtilis cells under conditions of starvation (45). The ability of RNA polymerase to bypass these and perhaps other types of lesions may result in base misinsertion in the transcript, generating mutant proteins resulting in the appearance of pseudo-prototrophs in nondividing cells (4,22,37).…”

Section: Vol 192 2010 Stress-induced Mutagenesis In B Subtilis Celmentioning

confidence: 99%

Transcription-Associated Mutation in Bacillus subtilis Cells under Stress

et al. 2010

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Adaptive (stationary phase) mutagenesis is a phenomenon by which nondividing cells acquire beneficial mutations as a response to stress. Although the generation of adaptive mutations is essentially stochastic, genetic factors are involved in this phenomenon. We examined how defects in a transcriptional factor, previously reported to alter the acquisition of adaptive mutations, affected mutation levels in a gene under selection. The acquisition of mutations was directly correlated to the level of transcription of a defective leuC allele placed under selection. To further examine the correlation between transcription and adaptive mutation, we placed a point-mutated allele, leuC427, under the control of an inducible promoter and assayed the level of reversion to leucine prototrophy under conditions of leucine starvation. Our results demonstrate that the level of Leu ؉ reversions increased significantly in parallel with the induced increase in transcription levels. This mutagenic response was not observed under conditions of exponential growth. Since transcription is a ubiquitous biological process, transcription-associated mutagenesis may influence evolutionary processes in all organisms.The generation of mutations has been traditionally ascribed to spontaneous processes affecting actively growing, dividing cells. Nevertheless, by the mid-1950s, several reports describing mutagenesis in nondividing cells of bacteria, plants, flies, and fungi appeared in the scientific literature (reference 36 and references therein). Much of the initial characterization of this process in bacteria took place in the laboratory of Francis Ryan, who observed Escherichia coli mutants capable of synthesizing histidine arising from his mutant (auxotrophic) cells undergoing prolonged starvation (36) while cell turnover remained undetectable, and DNA replication slowed with increasing time (26). Renewed interest in adaptive mutation was generated when Cairns and coworkers published their work on the generation of Lac ϩ reversions in E. coli cells unable to use the lactose provided as the sole carbon source in a minimal medium (6). This work demonstrated that adaptive mutations can arise as a result of stress rather than from selection of preexisting mutations. The generation of stress-induced Lac ϩ reversions, assayed via a plasmid-borne system, has been studied intensively by several laboratories (reviewed in references 13, 15, and 34; 32) and is dependent on activation of the SOS and/or stress responses. Further studies have also suggested that a subpopulation within the Lac Ϫ stressed cells engage in an exquisitely regulated transient state of hypermutation limited in time and to DNA sites near double-stranded DNA breaks (reviewed in reference 15). Collectively, the results from studies on this system have provided interesting insights into the acquisition of beneficial mutations and demonstrated the role of several genetic factors in the adaptive mutation phenomenon.

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Defects in the Error Prevention Oxidized Guanine System Potentiate Stationary-Phase Mutagenesis in Bacillus subtilis

Cited by 39 publications

References 47 publications

DNA Repair and Genome Maintenance in Bacillus subtilis

DNA Repair and Genome Maintenance in Bacillus subtilis

Error-Prone Processing of Apurinic/Apyrimidinic (AP) Sites by PolX Underlies a Novel Mechanism That Promotes Adaptive Mutagenesis in Bacillus subtilis

Transcription-Associated Mutation in Bacillus subtilis Cells under Stress

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