Involvement of DNA mismatch repair in stationary-phase mutagenesis during prolonged starvation of Pseudomonas putida

Saumaa, Signe; Tarassova, Kairi; Tark, Mariliis; Tover, Andres; Tegova, Radi; Kivisaar, Maia

doi:10.1016/j.dnarep.2005.12.003

Cited by 22 publications

(21 citation statements)

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“…Since PolV also belongs to a Y family of DNA polymerases and plays a crucial role in carrying out translesion synthesis past damaged bases in DNA, one may speculate that the effects of RulAB observed in our studies are due to the presence of oxidatively damaged adenine in DNA. Interestingly, the proportion of A-to-G transitions also increased in starved cells of P. putida lacking DNA MMR (66). Notably, Barone et al (5) have suggested that MMR would prevent the accumulation of 2-OH-A in DNA and thereby the accumulation of A-to-G and A-to-T base substitutions.…”

mentioning

confidence: 98%

“…The reporter gene pheA was altered in RSF1010-derived tester plasmids either by ϩ1 frameshift mutation or by introducing a TAG translational stop codon into the pheA gene (75). Conditions for the isolation of phenol-degrading Phe ϩ revertants were the same as those described in our previous study (66). Carbenicillin at a concentration of 1,500 g/ml was used in selective plates to maintain selectin for plasmid.…”

Section: Isolation and Analysis Of Phementioning

confidence: 99%

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Oxidative DNA Damage Defense Systems in Avoidance of Stationary-Phase Mutagenesis in Pseudomonas putida

et al. 2007

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Oxidative damage of DNA is a source of mutation in living cells. Although all organisms have evolved mechanisms of defense against oxidative damage, little is known about these mechanisms in nonenteric bacteria, including pseudomonads. Here we have studied the involvement of oxidized guanine (GO) repair enzymes and DNAprotecting enzyme Dps in the avoidance of mutations in starving Pseudomonas putida. Additionally, we examined possible connections between the oxidative damage of DNA and involvement of the error-prone DNA polymerase (Pol)V homologue RulAB in stationary-phase mutagenesis in P. putida. Our results demonstrated that the GO repair enzymes MutY, MutM, and MutT are involved in the prevention of base substitution mutations in carbonstarved P. putida. Interestingly, the antimutator effect of MutT was dependent on the growth phase of bacteria. Although the lack of MutT caused a strong mutator phenotype under carbon starvation conditions for bacteria, only a twofold increased effect on the frequency of mutations was observed for growing bacteria. This indicates that MutT has a backup system which efficiently complements the absence of this enzyme in actively growing cells. The knockout of MutM affected only the spectrum of mutations but did not change mutation frequency. Dps is known to protect DNA from oxidative damage. We found that dps-defective P. putida cells were more sensitive to sudden exposure to hydrogen peroxide than wild-type cells. At the same time, the absence of Dps did not affect the accumulation of mutations in populations of starved bacteria. Thus, it is possible that the protective role of Dps becomes essential for genome integrity only when bacteria are exposed to exogenous agents that lead to oxidative DNA damage but not under physiological conditions. Introduction of the Y family DNA polymerase PolV homologue rulAB into P. putida increased the proportion of A-to-C and A-to-G base substitutions among mutations, which occurred under starvation conditions. Since PolV is known to perform translesion synthesis past damaged bases in DNA (e.g., some oxidized forms of adenine), our results may imply that adenine oxidation products are also an important source of mutation in starving bacteria.Bacteria spend most of the time under starvation conditions, when their growth is inhibited due to a shortage of energy. Still, populations of stationary-phase bacteria undergo rapid evolution because of mutations. Mutagenesis occurring in resting cells is called adaptive mutation or stationary-phase mutation (22,23). Bacteria have several stress responses (including induction of the error-prone DNA polymerases carrying out translesion synthesis) that provide ways in which mutation rates can be increased in stationary-phase cells (for reviews, see references 24, 47, and 64). Oxidative DNA damage is also an important source of mutagenesis. It is known that the formation of 7,8-dihydro-8-oxo-2Ј-deoxyguanine (8-oxoG or GO) can give rise to stationary-phase mutations in Escherichia coli (13,14). Also, products...

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confidence: 98%

Section: Isolation and Analysis Of Phementioning

confidence: 99%

Oxidative DNA Damage Defense Systems in Avoidance of Stationary-Phase Mutagenesis in Pseudomonas putida

et al. 2007

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“…In addition to direct epigenetic silencing of DNA repair pathways, their inactivation may follow persistent suppression of genes involved in cell cycle control (like APC gene and p53), because these genes mediate DNA repair in mammalian cells. A loss or a decrease of the efficiency of DNA repair and a related increase in the rate of adaptive mutations in the bacterial stationary phase is also well documented [70,[98][99][100][101]. A recent study of adaptive mutagenesis in E. coli showed that the bacterial generalstress-response sigma factor RpoS may control a switch between a high-fidelity DNA repair and an error-prone repair in the case of double-strand breaks [102].…”

Section: Decreased Efficiency Of Dna Repairmentioning

confidence: 99%

“…Accumulation of ppGpp in response to stress changes the competition between two sigma factors (RpoS and 70 ) in the structure of RNA polymerase in favour of the equipment of this enzyme with RpoS instead of 70 factor. RpoS, an E. coli general stress response sigma factor, is nearly absent in rapidly growing cells, but it is strongly induced during entry into stationary phase and causes rapid changes in the pattern of gene expression.…”

Section: Stress-induced Proliferative and Sur-vival Signalling Drivesmentioning

confidence: 99%

“…In Pseudomonas putida, increased death of bacterial cells takes place under the conditions of prolonged starvation; and this phenomenon might be important for the generation of stationary phase mutations in the bacteria [70]. Programmed cell death may be considered as a survival strategy, because it allows bacteria to eliminate defective cells in the population, and thus to release deficient nutrients and signalling molecules to support survivors.…”

Section: Programmed Cell Deathmentioning

confidence: 99%

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Bacterial Stationary-State Mutagenesis and Mammalian Tumorigenesis as Stress-Induced Cellular Adaptations and the Role of Epigenetics

Karpinets

Greenwood²,

Pogribny³

et al. 2006

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Mechanisms of cellular adaptation may have some commonalities across different organisms. Revealing these common mechanisms may provide insight in the organismal level of adaptation and suggest solutions to important problems related to the adaptation. An increased rate of mutations, referred as the mutator phenotype, and beneficial nature of these mutations are common features of the bacterial stationary-state mutagenesis and of the tumorigenic transformations in mammalian cells. We argue that these commonalities of mammalian and bacterial cells result from their stressinduced adaptation that may be described in terms of a common model. Specifically, in both organisms the mutator phenotype is activated in a subpopulation of proliferating stressed cells as a strategy to survival. This strategy is an alternative to other survival strategies, such as senescence and programmed cell death, which are also activated in the stressed cells by different subpopulations. Sustained stress-related proliferative signalling and epigenetic mechanisms play a decisive role in the choice of the mutator phenotype survival strategy in the cells. They reprogram cellular functions by epigenetic silencing of cell-cycle inhibitors, DNA repair, programmed cell death, and by activation of repetitive DNA elements. This reprogramming leads to the mutator phenotype that is implemented by error-prone cell divisions with the involvement of Y family polymerases. Studies supporting the proposed model of stress-induced cellular adaptation are discussed. Cellular mechanisms involved in the bacterial stress-induced adaptation are considered in more detail.

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Stress‐induced Mutagenesis in Bacteria

Foster

2011

Encyclopedia of Life Sciences

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Bacteria spend their lives experiencing repeated rounds of feast and famine. In addition, they are buffeted by a variety of environmental insults such as fluctuations in temperature, pH, osmotic pressure, as well as exposure to DNA damaging agents and antibiotics. To cope with these changing conditions, bacteria have a variety of stress‐responses that result in profound but temporary cell‐wide changes in gene expression and protein activities. Keyed into these responses are a variety of ways in which the potential for genetic change is enhanced. Research has provided a number of examples of stress‐induced mutagenesis. Such transient mutator states may be important for adaptive evolution. Key Concepts: Bacteria respond to stress by inducing temporary cell‐wide changes in gene expression and protein activities. Some of these changes can increase the cell's potential for genetic change. Adaptive evolution can be accelerated when mutation rates are high, but persistent high mutation rates are also deleterious. Thus, transient increases in mutation rates are potentially of greater evolutionary advantage than permanent increases. Stress‐induced mutagenesis appears to be widespread among bacteria. There are many mechanisms that contribute to stress‐induced mutagenesis.

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Involvement of DNA mismatch repair in stationary-phase mutagenesis during prolonged starvation of Pseudomonas putida

Cited by 22 publications

References 46 publications

Oxidative DNA Damage Defense Systems in Avoidance of Stationary-Phase Mutagenesis in Pseudomonas putida

Oxidative DNA Damage Defense Systems in Avoidance of Stationary-Phase Mutagenesis in Pseudomonas putida

Bacterial Stationary-State Mutagenesis and Mammalian Tumorigenesis as Stress-Induced Cellular Adaptations and the Role of Epigenetics

Stress‐induced Mutagenesis in Bacteria

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