scholarly journals The evolution of bacterial mutation rates under simultaneous selection by interspecific and social parasitism

2013 ◽  
Vol 280 (1773) ◽  
pp. 20131913 ◽  
Author(s):  
Siobhán O'Brien ◽  
Antonio M. M. Rodrigues ◽  
Angus Buckling
Keyword(s):  
Mutation Rate ◽  
Social Parasitism ◽  
Mutation Rates ◽  
Bacterial Populations ◽  
Simultaneous Selection ◽  
Bacterial Mutation ◽  
Selection For ◽  
Intraspecific Parasitism ◽  
Theory And Experiments ◽  
Mutation Rate Evolution

Many bacterial populations harbour substantial numbers of hypermutable bacteria, in spite of hypermutation being associated with deleterious mutations. One reason for the persistence of hypermutators is the provision of novel mutations, enabling rapid adaptation to continually changing environments, for example coevolving virulent parasites. However, hypermutation also increases the rate at which intraspecific parasites (social cheats) are generated. Interspecific and intraspecific parasitism are therefore likely to impose conflicting selection pressure on mutation rate. Here, we combine theory and experiments to investigate how simultaneous selection from inter- and intraspecific parasitism affects the evolution of bacterial mutation rates in the plant-colonizing bacterium Pseudomonas fluorescens. Both our theoretical and experimental results suggest that phage presence increases and selection for public goods cooperation (the production of iron-scavenging siderophores) decreases selection for mutator bacteria. Moreover, phages imposed a much greater growth cost than social cheating, and when both selection pressures were imposed simultaneously, selection for cooperation did not affect mutation rate evolution. Given the ubiquity of infectious phages in the natural environment and clinical infections, our results suggest that phages are likely to be more important than social interactions in determining mutation rate evolution.

scholarly journals Death and population dynamics affect mutation rate estimates and evolvability under stress in bacteria

2017 ◽  
Author(s):  
Antoine Frénoy ◽  
Sebastian Bonhoeffer
Keyword(s):  
Population Dynamics ◽  
Mutation Rate ◽  
Death Rate ◽  
Mutation Rates ◽  
Resistance Mutations ◽  
Bacterial Populations ◽  
Plasmid Segregation ◽  
Genome Wide ◽  
Response To Stress ◽  
Induced Mutagenesis

AbstractThe stress-induced mutagenesis paradigm postulates that in response to stress, bacteria increase their genome-wide mutation rate, in turn increasing the chances that a descendant is able to withstand the stress. This has implications for antibiotic treatment: exposure to sub-inhibitory doses of antibiotics has been reported to increase bacterial mutation rates, and thus probably the rate at which resistance mutations appear and lead to treatment failure.Measuring mutation rates under stress, however, is problematic, because existing methods assume there is no death. Yet sub-inhibitory stress levels may induce a substantial death rate. Death events need to be compensated by extra replication to reach a given population size, thus giving more opportunities to acquire mutations. We show that ignoring death leads to a systematic overestimation of mutation rates under stress.We developed a system using plasmid segregation to measure death and growth rates simultaneously in bacterial populations. We use it to replicate classical experiments reporting antibiotic-induced mutagenesis. We found that a substantial death rate occurs at the tested sub-inhibitory concentrations, and taking this death into account lowers and sometimes removes the signal for stress-induced mutagenesis. Moreover even when antibiotics increase mutation rate, sub-inhibitory treatments do not increase genetic diversity and evolvability, again because of effects of the antibiotics on population dynamics.Beside showing that population dynamic is a crucial but neglected parameter affecting evolvability, we provide better experimental and computational tools to study evolvability under stress, leading to a re-assessment of the magnitude and significance of the stress-induced mutagenesis paradigm.

scholarly journals Statistical concepts in the theory of bacterial mutation

1953 ◽  
Vol 51 (2) ◽  
pp. 162-184 ◽  
Author(s):  
P. Armitage
Keyword(s):  
Mutation Rate ◽  
Phenotypic Expression ◽  
Theoretical Distribution ◽  
Mutation Rates ◽  
Safe Procedure ◽  
Short Term ◽  
Mutant Type ◽  
Bacterial Populations ◽  
Long Term Experiment

This paper is a short exposition of the mathematical and statistical theory of the growth of bacterial populations subject to mutation.A mathematical model for the long-term development of a mixed population with two types of organism is proposed. The proportion of organisms which are of the mutant type eventually approaches an asymptotic value, which is independent of the initial composition of the population. A procedure is outlined for estimating the forward and backward mutation rates from a long-term experiment.The exact interpretation of the constants representing mutation rates requires some assumption about the point of time, during an individual life cycle, at which mutations occur. The usual assumption is that mutations can occur with equal frequency at all instants during the cycle.In short-term experiments, in which the proportion of mutants is at all times negligible, it is important to consider the variation between the numbers of mutants developing in replicate cultures. The theoretical distribution of Lea & Coulson may be disturbed by the failure of any one of a number of assumptions; the effects of such disturbances are considered in some detail.Various methods of estimating the mutation rate from an observed series of replicate cultures are examined. Two of the main sources of disturbance of the theoretical distribution may be delay of phenotypic expression, and the existence of multinucleate cells with dominant mutation. These factors affect particularly the lower tail of the distribution, and it is suggested that a fairly safe procedure may be to estimate the mutation rate from the upper quartile of the observed distribution. Tables 3 and 4 enable the estimate of the mutation rate, together with 95% confidence limits, to be readily calculated.

scholarly journals A speed-fidelity trade-off determines the mutation rate and virulence of an RNA virus

2018 ◽  
Author(s):  
William Fitzsimmons ◽  
Robert J. Woods ◽  
John T. McCrone ◽  
Andrew Woodman ◽  
Jamie J. Arnold ◽  
...  
Keyword(s):  
Mutation Rate ◽  
Experimental Evolution ◽  
Rna Viruses ◽  
Fundamental Problem ◽  
Rna Virus ◽  
Mutation Rates ◽  
Direct Selection ◽  
Growth Defect ◽  
Infection Model ◽  
Selection For

AbstractMutation rates can evolve through genetic drift, indirect selection due to genetic hitchhiking, or direct selection on the physicochemical cost of high fidelity. However, for many systems, it has been difficult to disentangle the relative impact of these forces empirically. In RNA viruses, an observed correlation between mutation rate and virulence has led many to argue that their extremely high mutation rates are advantageous, because they may allow for increased adaptability. This argument has profound implications, as it suggests that pathogenesis in many viral infections depends on rare orde novomutations. Here we present data for an alternative model whereby RNA viruses evolve high mutation rates as a byproduct of selection for increased replicative speed. We find that a poliovirus antimutator, 3DG64S, has a significant replication defect and that wild type and 3DG64Spopulations have similar adaptability in two distinct cellular environments. Experimental evolution of 3DG64Sunder r-selection led to reversion and compensation of the fidelity phenotype. Mice infected with 3DG64Sexhibited delayed morbidity at doses well above the LD50, consistent with attenuation by slower growth as opposed to reduced mutational supply. Furthermore, compensation of the 3DG64Sgrowth defect restored virulence, while compensation of the fidelity phenotype did not. Our data are consistent with the kinetic proofreading model for biosynthetic reactions and suggest that speed is more important than accuracy. In contrast to what has been suggested for many RNA viruses, we find that within host spread is associated with viral replicative speed and not standing genetic diversity.Author SummaryMutation rate evolution has long been a fundamental problem in evolutionary biology. The polymerases of RNA viruses generally lack proofreading activity and exhibit extremely high mutation rates. Since most mutations are deleterious and mutation rates are tuned by natural selection, we asked why hasn’t the virus evolved to have a lower mutation rate? We used experimental evolution and a murine infection model to show that RNA virus mutation rates may actually be too high and are not necessarily adaptive. Rather, our data indicate that viral mutation rates are driven higher as a result of selection for viruses with faster replication kinetics. We suggest that viruses have high mutation rates, not because they facilitate adaption, but because it is hard to be both fast and accurate.

scholarly journals The effect of bacterial mutation rate on the evolution of CRISPR-Cas adaptive immunity

2019 ◽  
Vol 374 (1772) ◽  
pp. 20180094 ◽  
Author(s):  
Anne Chevallereau ◽  
Sean Meaden ◽  
Stineke van Houte ◽  
Edze R. Westra ◽  
Clare Rollie
Keyword(s):  
Mutation Rate ◽  
Mutation Rates ◽  
Repair System ◽  
Immune Systems ◽  
Adaptive Immune ◽  
Dominant Phenotype ◽  
Mismatch Repair System ◽  
Bacterial Mutation ◽  
Negative Epistasis ◽  
Adaptive Immune Systems

CRISPR-Cas immune systems are present in around half of bacterial genomes. Given the specificity and adaptability of this immune mechanism, it is perhaps surprising that they are not more widespread. Recent insights into the requirement for specific host factors for the function of some CRISPR-Cas subtypes, as well as the negative epistasis between CRISPR-Cas and other host genes, have shed light on potential reasons for the partial distribution of this immune strategy in bacteria. In this study, we examined how mutations in the bacterial mismatch repair system, which are frequently observed in natural and clinical isolates and cause elevated host mutation rates, influence the evolution of CRISPR-Cas–mediated immunity. We found that hosts with a high mutation rate very rarely evolved CRISPR-based immunity to phage compared to wild-type hosts. We explored the reason for this effect and found that the higher frequency at which surface mutants pre-exist in the mutator host background causes them to rapidly become the dominant phenotype under phage infection. These findings suggest that natural variation in bacterial mutation rates may, therefore, influence the distribution of CRISPR-Cas adaptive immune systems. This article is part of a discussion meeting issue ‘The ecology and evolution of prokaryotic CRISPR-Cas adaptive immune systems’.

scholarly journals Evolution of local mutation rate and its determinants

2016 ◽  
Author(s):  
Nadezhda V. Terekhanova ◽  
Vladimir B. Seplyarskiy ◽  
Ruslan A. Soldatov ◽  
Georgii A. Bazykin
Keyword(s):  
Human Genome ◽  
Mutation Rate ◽  
Recombination Rate ◽  
Mutation Rates ◽  
Genomic Features ◽  
Dna Molecule ◽  
Local Properties ◽  
Genomic Regions ◽  
Shed Light ◽  
Mutation Rate Evolution

Mutation rate varies along the human genome, and part of this variation is explainable by measurable local properties of the DNA molecule. Moreover, mutation rates differ between orthologous genomic regions of different species, but the drivers of this change are unclear. Here, we compare the local mutation rates of several species. We show that these rates are very similar between human and apes, implying that their variation has a strong underlying cryptic component not explainable by the known genomic features. Mutation rates become progressively less similar in more distant species, and these changes are partially explainable by changes in the local genomic features of orthologous regions, most importantly, in the recombination rate. However, they are much more rapid, implying that the cryptic component underlying the mutation rate is more ephemeral than the known genomic features. These findings shed light on the determinants of mutation rate evolution.

scholarly journals Molecular mechanisms involved in the regulation of mutation rates in bacteria

2017 ◽  
Vol 118 (4) ◽  
Author(s):  
Ivan Matic
Keyword(s):  
Mutation Rate ◽  
Molecular Mechanisms ◽  
Point Of View ◽  
Mutation Rates ◽  
Beneficial Mutations ◽  
Bacterial Populations ◽  
Multiple Strategies ◽  
Induced Mutagenesis ◽  
The Cost ◽  
Evolutionary Point

Organisms live in constantly changing environments in which, the nature, severity and frequency of the environmental stresses are very variable. Organisms possess multiple strategies for coping with the environmental fluctuations. One such strategy is modulation of mutation rates as a function of the degree of adaptation to the environment. When adaptation is limited by the available genetic variability, natural selection favors cells having high mutation rates in bacterial populations. High mutation rates can be advantageous because they increase the probability of generation of beneficial mutations. Constitutive mutator alleles are carried to high frequency through hitchhiking with beneficial mutations they generate. However, once the adaptation is achieved, the cost of deleterious mutations generated by constitutive mutator alleles reduces cellular fitness. For this reason, the possibility of adapting the mutation rate to environmental conditions is interesting from an evolutionary point of view. Stress-induced mutagenesis allows rapid adaptation to complex environmental challenges without compromising the population fitness because it reduces the overall cost of a high mutation rate. Here we review the molecular mechanisms involved in the control of modulation of mutation rates in bacteria.

Mapping a gene conferring resistance to Pseudocercosporella herpotrichoides on chromosome 4V of Dasypyrum villosum in a wheat background

Genome ◽  
1998 ◽  
Vol 41 (1) ◽  
pp. 1-6 ◽  
Author(s):  
Ahmet Yildirim ◽  
Stephen S Jones ◽  
Timothy D Murray
Keyword(s):  
Distal Part ◽  
Dominant Gene ◽  
Rflp Markers ◽  
Addition Line ◽  
Dasypyrum Villosum ◽  
Pseudocercosporella Herpotrichoides ◽  
Eyespot Resistance ◽  
Double Recombination ◽  
Simultaneous Selection ◽  
Selection For

The objectives of this study were to map and tag the previously undescribed eyespot resistance gene PchDv on chromosome 4V of Dasypyrum villosum in a wheat background. The 82 F2 plants used for mapping were produced from a cross between a susceptible\i wheat 'Yangmai-5' (4V(4D)) substitution line and a resistant wheat 'Chinese Spring' disomic addition line of chromosome 4V of D. villosum. Segregation for resistance and susceptibility among F2 plants was 3:1, indicating that resistance was controlled by a single dominant gene. PchDv mapped to the distal part of chromosome 4V and was bracketed by two RFLP markers, Xcdo949 and Xbcd588, in a 33-cM interval. This distance could not be reduced, owing to a lack of polymorphic loci in this region. Theoretically, double recombination in this region occurs in 3.3% of the individuals; therefore, 96.7% of the selected genotypes would have PchDv, with simultaneous selection for both flanking markers. Double recombination between the flanking markers was observed in 2 out of 82 (2.4%) F2 individuals.

scholarly journals Mutation rate analysis via parent–progeny sequencing of the perennial peach. II. No evidence for recombination-associated mutation

2016 ◽  
Vol 283 (1841) ◽  
pp. 20161785 ◽  
Author(s):  
Long Wang ◽  
Yanchun Zhang ◽  
Chao Qin ◽  
Dacheng Tian ◽  
Sihai Yang ◽  
...  
Keyword(s):  
Mutation Rate ◽  
Recombination Rate ◽  
Mutation Rates ◽  
Recombination Rates ◽  
Rate Analysis ◽  
A Genome ◽  
Break Points ◽  
New Mutations

Mutation rates and recombination rates vary between species and between regions within a genome. What are the determinants of these forms of variation? Prior evidence has suggested that the recombination might be mutagenic with an excess of new mutations in the vicinity of recombination break points. As it is conjectured that domesticated taxa have higher recombination rates than wild ones, we expect domesticated taxa to have raised mutation rates. Here, we use parent–offspring sequencing in domesticated and wild peach to ask (i) whether recombination is mutagenic, and (ii) whether domesticated peach has a higher recombination rate than wild peach. We find no evidence that domesticated peach has an increased recombination rate, nor an increased mutation rate near recombination events. If recombination is mutagenic in this taxa, the effect is too weak to be detected by our analysis. While an absence of recombination-associated mutation might explain an absence of a recombination–heterozygozity correlation in peach, we caution against such an interpretation.

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