Mistranslation induced by streptomycin provokes a RecABC/RuvABC-dependent mutator phenotype in Escherichia coli cells 1 1Edited by M. Gottesman

Balashov, Sergey; Humayun, M. Zafri

doi:10.1006/jmbi.2001.5273

Cited by 49 publications

(47 citation statements)

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“…The growth defects observed in rpsD14 mutants are ameliorated in rpsD14 rpsL1408 double mutants in the absence of streptomycin, a finding that is consistent with the increased translational accuracy conferred by the rpsL1408 allele. The addition of streptomycin to the growth medium reverses the ameliorating effects of the rpsL1408 allele in rpsD14 cells, as indicated by an increase in doubling time and a reacquisition of temperature sensitivity, both of which are consistent with increased mistranslation in rpsL1408 cells in the presence of streptomycin (6).…”

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“…Subsequent to this finding, other work revealed that mutations in many other genes that specify tRNAs (10,26) or tRNA-modifying enzymes (32) lead to a similar phenotype presumably mediated by mistranslation. Moreover, exposure to streptomycin, an antibiotic known to promote mistranslation, induces a very similar phenotype in cells bearing certain mutations in rpsL, the gene specifying the 30S ribosomal protein S12 (6). Thus, mistranslation appears to be causally required for provoking the mutator phenotype, termed TSM for translational stress-induced mutagenesis (12).…”

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“…Whereas ribosomal ambiguity mutations (such as certain rpsD mutations) increase mistranslation, ribosomal restrictive mutations (such as those in rpsL, which encodes the 30S ribosomal protein S12) increase translational accuracy and are streptomycin resistant (Str r ). We have previously isolated and characterized rpsL1408, which bears a K87E mutation in S12, with very interesting dual properties: in the absence of streptomycin, rpsL1408 cells show hyperaccurate translation (high restrictivity relative to rpsL ϩ wild-type cells), whereas in the presence of 100 g of streptomycin/ml, rpsL1408 cells display significantly elevated mistranslation levels (6).…”

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“…The TSM mutator phenotype can be conveniently detected by colony papillation based on a lacZ3 lacZ ϩ reversion on P-Gal (phenyl-␤-D-galactoside) minimal plates containing X-Gal (5-bromo-4-chloro-3-indolyl-␤-D-galactopyranoside) (6). The lacZ allele used in the present investigation reverts only by AT3TA transversions at a specific base pair (8).…”

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Escherichia coli Cells Bearing a Ribosomal Ambiguity Mutation in rpsD Have a Mutator Phenotype That Correlates with Increased Mistranslation

Balashov

Humayun

2003

J Bacteriol

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Escherichia coli cells bearing certain mutations in rpsD (coding for the 30S ribosomal protein S4) show a ribosomal ambiguity (Ram) phenotype characterized by increased translational error rates. Here we show that spontaneous mutagenesis increases in Ram cells bearing the rpsD14 allele, suggesting that the recently described translational stress-induced mutagenesis pathway is activated in Ram cells.

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Escherichia coli Cells Bearing a Ribosomal Ambiguity Mutation in rpsD Have a Mutator Phenotype That Correlates with Increased Mistranslation

Balashov

Humayun

2003

J Bacteriol

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“…For example, amino acid starvation can lead to a 10-to 100-fold increase in mistranslation (70). As first proposed in 1991 by Ninio (52) and later confirmed by others (3,4,5,30), mistranslation of DNA repair and replication proteins can create a transient mutator phenotype. Hence, taking these results together, we suppose that, in addition to oxidative DNA lesions, mistranslation and oxidative damage of proteins may also affect DNA replication fidelity and thereby increase the mutation frequency in rpoS-deficient bacteria under the conditions studied.…”

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Elevated Mutation Frequency in Surviving Populations of Carbon-Starved rpoS -Deficient Pseudomonas putida Is Caused by Reduced Expression of Superoxide Dismutase and Catalase

et al. 2009

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RpoS is a bacterial sigma factor of RNA polymerase which is involved in the expression of a large number of genes to facilitate survival under starvation conditions and other stresses. The results of our study demonstrate that the frequency of emergence of base substitution mutants is significantly increased in long-term-starved populations of rpoS-deficient Pseudomonas putida cells. The increasing effect of the lack of RpoS on the mutation frequency became apparent in both a plasmid-based test system measuring Phe ؉ reversion and a chromosomal rpoB system detecting rifampin-resistant mutants. The elevated mutation frequency coincided with the death of about 95% of the cells in a population of rpoS-deficient P. putida. Artificial overexpression of superoxide dismutase or catalase in the rpoS-deficient strain restored the survival of cells and resulted in a decline in the mutation frequency. This indicated that, compared to wild-type bacteria, rpoS-deficient cells are less protected against damage caused by reactive oxygen species. 7,8-Dihydro-8-oxoguanine (GO) is known to be one of the most stable and frequent base modifications caused by oxygen radical attack on DNA. However, the spectrum of base substitution mutations characterized in rpoS-deficient P. putida was different from that in bacteria lacking the GO repair system: it was broader and more similar to that identified in the wild-type strain. Interestingly, the formation of large deletions was also accompanied by a lack of RpoS. Thus, the accumulation of DNA damage other than GO elevates the frequency of mutation in these bacteria. It is known that oxidative damage of proteins and membrane components, but not that of DNA, is a major reason for the death of cells. Since the increased mutation frequency was associated with a decline in the viability of bacteria, we suppose that the elevation of the mutation frequency in the surviving population of carbon-starved rpoS-deficient P. putida may be caused both by oxidative damage of DNA and enzymes involved in DNA replication and repair fidelity.Accumulation of reactive oxygen species (ROS) such as superoxide anion, hydrogen peroxide, and hydroxyl radicals leads to nucleic acid, protein, and cell membrane damage. ROS have been implicated in cancer, aging, and various diseases in humans but also in the death of microorganisms (53). Many microorganisms are continuously faced with ROS derived from different sources. For example, during infection, pathogenic bacteria are exposed to the exogenous oxidative stress that phagocytes use as a host defense mechanism (25, 47). Additionally, ROS are constantly generated as by-products of aerobic metabolism. To counteract oxidative stress, both prokaryotic and eukaryotic cells maintain inducible defense systems to detoxify oxidants and repair damage (14, 32). Gram-negative bacteria commonly synthesize both cytoplasmic and periplasmic isozymes of superoxide dismutases (SOD) to eliminate superoxide anions (40). Hydrogen peroxide is scavenged in most organisms by peroxidases an...

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Low pesticide rates may hasten the evolution of resistance by increasing mutation frequencies

Gressel

2010

Pest Management Science

161

126

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At very low pesticide rates, a certain low proportion of pests may receive a sublethal dose, are highly stressed by the pesticide and yet survive. Stress is a general enhancer of mutation rates. Thus, the survivors are likely to have more than normal mutations, which might include mutations leading to pesticide resistance, both for multifactorial (polygenic, gene amplification, sequential allelic mutations) and for major gene resistance. Management strategies should consider how to eliminate the subpopulation of pests with the high mutation rates, but the best strategy is probably to avoid too low application rates of pesticides from the outset.

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Mistranslation induced by streptomycin provokes a RecABC/RuvABC-dependent mutator phenotype in Escherichia coli cells 1 1Edited by M. Gottesman

Cited by 49 publications

References 69 publications

Escherichia coli Cells Bearing a Ribosomal Ambiguity Mutation in rpsD Have a Mutator Phenotype That Correlates with Increased Mistranslation

Escherichia coli Cells Bearing a Ribosomal Ambiguity Mutation in rpsD Have a Mutator Phenotype That Correlates with Increased Mistranslation

Elevated Mutation Frequency in Surviving Populations of Carbon-Starved rpoS -Deficient Pseudomonas putida Is Caused by Reduced Expression of Superoxide Dismutase and Catalase

Low pesticide rates may hasten the evolution of resistance by increasing mutation frequencies

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