Stress-Induced Mutagenesis in Bacteria

Bjedov, Ivana; Tenaillon, Olivier; Gérard, Bénédicte; Souza, Valeria; Denamur, Erick; Radman, Miroslav; Taddéi, François; Matić, Ivan

doi:10.1126/science.1082240

Cited by 506 publications

(504 citation statements)

References 40 publications

Supporting

Mentioning

485

Contrasting

Unclassified

Order By: Relevance

“…For mutation rate control to have evolved in nature, a first prerequisite is that biological mutation rates can vary and are not simply minimised. There is ample evidence that mutation rates do vary in nature, between distantly (Drake et al, 1998) and closely-related (Matic et al, 1997) organisms, between regions of genomes (Lang and Murray, 2008) and even within an organism in stressful versus benign environments (Bjedov et al, 2003). However, the question of whether there may be an adaptive trait, allowing an individual organism to affect the number of mutations between itself and its offspring, dependent upon environmental cues, remains an open question.…”

Section: Discussionmentioning

confidence: 99%

See 1 more Smart Citation

Theory and Practice of Optimal Mutation Rate Control in Hamming Spaces of DNA Sequences

Belavkin¹,

Channon²,

Aston³

et al. 2011

Ecal 2011

View full text Add to dashboard Cite

We investigate the problem of optimal control of mutation by asexual self-replicating organisms represented by points in a metric space. We introduce the notion of a relatively monotonic fitness landscape and consider a generalisation of Fisher's geometric model of adaptation for such spaces. Using a Hamming space as a prime example, we derive the probability of adaptation as a function of reproduction parameters (e.g. mutation size or rate). Optimal control rules for the parameters are derived explicitly for some relatively monotonic landscapes, and then a general information-based heuristic is introduced. We then evaluate our theoretical control functions against optimal mutation functions evolved from a random population of functions using a meta genetic algorithm. Our experimental results show a close match between theory and experiment. We demonstrate this result both in artificial fitness landscapes, defined by a Hamming distance, and a natural landscape, where fitness is defined by a DNA-protein affinity. We discuss how a control of mutation rate could occur and evolve in natural organisms. We also outline future directions of this work.

show abstract

Section: Discussionmentioning

confidence: 99%

“…Genetic variation also exists in mutation rates within species and in the way mutation rate changes with environment for a single genotype (Bjedov et al, 2003). Therefore, mutation rates and their variation are potentially subject to biological evolution themselves.…”

Section: Introductionmentioning

confidence: 99%

Theory and Practice of Optimal Mutation Rate Control in Hamming Spaces of DNA Sequences

Belavkin¹,

Channon²,

Aston³

et al. 2011

Ecal 2011

View full text Add to dashboard Cite

show abstract

“…Such studies are referred to as MAC. These require plating bacteria on solid media for either 1 or 7 days, followed by determining the frequency of spontaneous rifampicin (Rif)-resistant (Rif R ) mutants in the population after each time period (5)(6)(7). This phenotype is known to at least partially depend on the SOS response.…”

Section: Resultsmentioning

confidence: 99%

An editing-defective aminoacyl-tRNA synthetase is mutagenic in aging bacteria via the SOS response

Bacher

Schimmel

2007

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

View full text Add to dashboard Cite

Mistranslation in bacterial and mammalian cells leads to production of statistical proteins that are, in turn, associated with specific cell or animal pathologies, including death of bacterial cells, apoptosis of mammalian cells in culture, and neurodegeneration in the mouse. A major source of mistranslation comes from heritable defects in the editing activities of aminoacyl-tRNA synthetases. These activities clear errors of aminoacylation by deacylation of mischarged tRNAs. We hypothesized that, in addition to previously reported phenotypes in bacterial and mammalian systems, errors of aminoacylation could be mutagenic and lead to disease. As a first step in testing this hypothesis, the effect of an editing defect in a single tRNA synthetase on the accumulation of mutations in aging bacteria was investigated. A striking, statistically significant, enhancement of the mutation rate in aging bacteria was found. This enhancement comes from an increase in error-prone DNA repair through induction of the bacterial SOS response. Thus, mistranslation, as caused by an editing-defective tRNA synthetase, can lead to heritable genetic changes that could, in principle, be linked to disease.aminoacylation errors ͉ error-prone DNA polymerases ͉ amino acid misincorporation ͉ genetic code ambiguity A s organisms age, mutations accumulate over time owing to direct environmental insults that are incompletely or inaccurately repaired. Recent work directed our attention to the possibility that mistranslation could play a role in producing mutations in aging populations. In particular, mistranslation can arise from editing defects in aminoacyl-tRNA synthetases. These enzymes catalyze the first step of protein synthesis, where each amino acid is linked to its cognate tRNA bearing the anticodon triplet associated with the amino acid. Because of inherent physiochemical limitations of some enzymes to discriminate between structurally similar amino acids, mischarged tRNAs, such as Val-tRNA Ile or Ser-tRNA Ala , are produced. Normally, these mischarged tRNAs are cleared by hydrolytic editing, which occurs at a distinct active site within the synthetase. But even a small defect, caused by a mutation in the editing center, can lead to extreme cell pathologies and disease.For example, mice that carry a mild mutation in the editing domain of alanyl-tRNA synthetase suffer from ataxia (1). The mutant alanyl-tRNA synthetase mischarges tRNA Ala with serine and, as a consequence, mistranslation occurs that leads to induction of the unfolded protein response. That, in turn, leads to the degeneration of Purkinje cells in the cerebellum, beginning within 3 weeks of age. Similarly, in human cell culture, an inducible, editing-defective valyl-tRNA synthetase caused cellular degradation and apoptosis (2).With these recent results in mind, we were motivated to investigate the possibility that mistranslation could also lead to heritable genetic changes. Previously, we generated a knock-in mutant allele of ileS that encodes no functional editing domain (3)....

show abstract

“…60 Hence, it is all the more striking that despite the existence of such potent mechanisms of genetic diversification, self-destruction escape mutants do not rapidly emerge and overtake the whole colony. Death-escaping 'cheater' mutants, biasing differentiation towards spores, have indeed been identified in some myxobacteria species, 61 but their persistence depends on the 'presence of ready-to-die neighbors, implying the existence of constraints limiting the spread of such escape mutants.…”

Section: Walking Along the Evolutionary Tree Upwards From The C Elegmentioning

confidence: 99%

Looking for death at the core of life in the light of evolution

Ameisen

2003

Cell Death Differ

View full text Add to dashboard Cite

Stress-Induced Mutagenesis in Bacteria

Cited by 506 publications

References 40 publications

Theory and Practice of Optimal Mutation Rate Control in Hamming Spaces of DNA Sequences

Theory and Practice of Optimal Mutation Rate Control in Hamming Spaces of DNA Sequences

An editing-defective aminoacyl-tRNA synthetase is mutagenic in aging bacteria via the SOS response

Looking for death at the core of life in the light of evolution

Contact Info

Product

Resources

About