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1
Trindade, Sandra, Lilia Perfeito, and Isabel Gordo. "Rate and effects of spontaneous mutations that affect fitness in mutator Escherichia coli." Philosophical Transactions of the Royal Society B: Biological Sciences 365, no. 1544 (2010): 1177–86. http://dx.doi.org/10.1098/rstb.2009.0287.
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Knowledge of the mutational parameters that affect the evolution of organisms is of key importance in understanding the evolution of several characteristics of many natural populations, including recombination and mutation rates. In this study, we estimated the rate and mean effect of spontaneous mutations that affect fitness in a mutator strain of Escherichia coli and review some of the estimation methods associated with mutation accumulation (MA) experiments. We performed an MA experiment where we followed the evolution of 50 independent mutator lines that were subjected to repeated bottlenecks of a single individual for approximately 1150 generations. From the decline in mean fitness and the increase in variance between lines, we estimated a minimum mutation rate to deleterious mutations of 0.005 (±0.001 with 95% confidence) and a maximum mean fitness effect per deleterious mutation of 0.03 (±0.01 with 95% confidence). We also show that any beneficial mutations that occur during the MA experiment have a small effect on the estimate of the rate and effect of deleterious mutations, unless their rate is extremely large. Extrapolating our results to the wild-type mutation rate, we find that our estimate of the mutational effects is slightly larger and the inferred deleterious mutation rate slightly lower than previous estimates obtained for non-mutator E. coli .
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Sherer, Nicholas A., and Thomas E. Kuhlman. "Escherichia coli with a Tunable Point Mutation Rate for Evolution Experiments." G3: Genes|Genomes|Genetics 10, no. 8 (2020): 2671–81. http://dx.doi.org/10.1534/g3.120.401124.
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The mutation rate and mutations’ effects on fitness are crucial to evolution. Mutation rates are under selection due to linkage between mutation rate modifiers and mutations’ effects on fitness. The linkage between a higher mutation rate and more beneficial mutations selects for higher mutation rates, while the linkage between a higher mutation rate and more deleterious mutations selects for lower mutation rates. The net direction of selection on mutations rates depends on the fitness landscape, and a great deal of work has elucidated the fitness landscapes of mutations. However, tests of the effect of varying a mutation rate on evolution in a single organism in a single environment have been difficult. This has been studied using strains of antimutators and mutators, but these strains may differ in additional ways and typically do not allow for continuous variation of the mutation rate. To help investigate the effects of the mutation rate on evolution, we have genetically engineered a strain of Escherichia coli with a point mutation rate that can be smoothly varied over two orders of magnitude. We did this by engineering a strain with inducible control of the mismatch repair proteins MutH and MutL. We used this strain in an approximately 350 generation evolution experiment with controlled variation of the mutation rate. We confirmed the construct and the mutation rate were stable over this time. Sequencing evolved strains revealed a higher number of single nucleotide polymorphisms at higher mutations rates, likely due to either the beneficial effects of these mutations or their linkage to beneficial mutations.
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Stephan, Wolfgang. "The Rate of Compensatory Evolution." Genetics 144, no. 1 (1996): 419–26. http://dx.doi.org/10.1093/genetics/144.1.419.
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Abstract A two-locus model is presented to analyze the evolution of compensatory mutations occurring in stems of RNA secondary structures. Single mutations are assumed to be deleterious but harmless (neutral) in appropriate combinations. In proceeding under mutation pressure, natural selection and genetic drift from one fitness peak to another one, a population must therefore pass through a valley of intermediate deleterious states of individual fitness. The expected time for this transition is calculated using diffusion theory. The rate of compensatory evolution, kc, is then defined as the inverse of the expected transition time. When selection against deleterious single mutations is strong, kc, depends on the recombination fraction r between the two loci. Recombination generally reduces the rate of compensatory evolution because it breaks up favorable combinations of double mutants. For complete linkage, kc, is given by the rate at which favorable combinations of double mutantS are produced by compensatory mutation. For r > 0, kc, decreases exponentially with r. In contrast, kc, becomes independent of r for weak selection. We discuss the dynamics of evolutionary substitutions of compensatory mutants in relation to Wright'S shifting balance theory of evolution and use our results to analyze the substitution process in helices of mRNA secondary structures.
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Sniegowski, Paul. "Evolution: Setting the mutation rate." Current Biology 7, no. 8 (1997): R487—R488. http://dx.doi.org/10.1016/s0960-9822(06)00244-2.
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Lynch, Michael. "Evolution of the mutation rate." Trends in Genetics 26, no. 8 (2010): 345–52. http://dx.doi.org/10.1016/j.tig.2010.05.003.
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Schoen, Daniel J., and Stewart T. Schultz. "Somatic Mutation and Evolution in Plants." Annual Review of Ecology, Evolution, and Systematics 50, no. 1 (2019): 49–73. http://dx.doi.org/10.1146/annurev-ecolsys-110218-024955.
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Somatic mutations are common in plants, and they may accumulate and be passed on to gametes. The determinants of somatic mutation accumulation include the intraorganismal selective effect of mutations, the number of cell divisions that separate the zygote from the formation of gametes, and shoot apical meristem structure and branching. Somatic mutations can promote the evolution of diploidy, polyploidy, sexual recombination, outcrossing, clonality, and separate sexes, and they may contribute genetic variability in many other traits. The amplification of beneficial mutations via intraorganismal selection may relax selection to reduce the genomic mutation rate or to protect the germline in plants. The total rate of somatic mutation, the distribution of selective effects and fates in the plant body, and the degree to which the germline is sheltered from somatic mutations are still poorly understood. Our knowledge can be improved through empirical estimates of mutation rates and effects on cell lineages and whole organisms, such as estimates of the reduction in fitness of progeny produced by within- versus between-flower crosses on the same plant, mutation coalescent studies within the canopy, and incorporation of somatic mutation into theoretical models of plant evolutionary genetics.
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Krasovec, Marc, Rosalind E. M. Rickaby, and Dmitry A. Filatov. "Evolution of Mutation Rate in Astronomically Large Phytoplankton Populations." Genome Biology and Evolution 12, no. 7 (2020): 1051–59. http://dx.doi.org/10.1093/gbe/evaa131.
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Abstract Genetic diversity is expected to be proportional to population size, yet, there is a well-known, but unexplained lack of genetic diversity in large populations—the “Lewontin’s paradox.” Larger populations are expected to evolve lower mutation rates, which may help to explain this paradox. Here, we test this conjecture by measuring the spontaneous mutation rate in a ubiquitous unicellular marine phytoplankton species Emiliania huxleyi (Haptophyta) that has modest genetic diversity despite an astronomically large population size. Genome sequencing of E. huxleyi mutation accumulation lines revealed 455 mutations, with an unusual GC-biased mutation spectrum. This yielded an estimate of the per site mutation rate µ = 5.55×10−10 (CI 95%: 5.05×10−10 – 6.09×10−10), which corresponds to an effective population size Ne ∼ 2.7×106. Such a modest Ne is surprising for a ubiquitous and abundant species that accounts for up to 10% of global primary productivity in the oceans. Our results indicate that even exceptionally large populations do not evolve mutation rates lower than ∼10−10 per nucleotide per cell division. Consequently, the extreme disparity between modest genetic diversity and astronomically large population size in the plankton species cannot be explained by an unusually low mutation rate.
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Edlund, Jeffrey A., and Christoph Adami. "Evolution of Robustness in Digital Organisms." Artificial Life 10, no. 2 (2004): 167–79. http://dx.doi.org/10.1162/106454604773563595.
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We study the evolution of robustness in digital organisms adapting to a high mutation rate. As genomes adjust to the harsh mutational environment, the mean effect of single mutations decreases, up until the point where a sizable fraction (up to 30% in many cases) of the mutations are neutral. We correlate the changes in robustness along the line of descent to changes in directional epistasis, and find that increased robustness is achieved by moving from antagonistic epistasis between mutations towards codes where mutations are, on average, independent. We interpret this recoding as a breakup of linkage between vital sections of the genome, up to the point where instructions are maximally independent of each other. While such a recoding often requires sacrificing some replication speed, it is the best strategy for withstanding high rates of mutation.
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Komp Lindgren, Patricia, Åsa Karlsson, and Diarmaid Hughes. "Mutation Rate and Evolution of Fluoroquinolone Resistance in Escherichia coli Isolates from Patients with Urinary Tract Infections." Antimicrobial Agents and Chemotherapy 47, no. 10 (2003): 3222–32. http://dx.doi.org/10.1128/aac.47.10.3222-3232.2003.
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ABSTRACT Escherichia coli strains from patients with uncomplicated urinary tract infections were examined by DNA sequencing for fluoroquinolone resistance-associated mutations in six genes: gyrA, gyrB, parC, parE, marOR, and acrR. The 54 strains analyzed had a susceptibility range distributed across 15 dilutions of the fluoroquinolone MICs. There was a correlation between the fluoroquinolone MIC and the number of resistance mutations that a strain carried, with resistant strains having mutations in two to five of these genes. Most resistant strains carried two mutations in gyrA and one mutation in parC. In addition, many resistant strains had mutations in parE, marOR, and/or acrR. No (resistance) mutation was found in gyrB. Thus, the evolution of fluoroquinolone resistance involves the accumulation of multiple mutations in several genes. The spontaneous mutation rate in these clinical strains varied by 2 orders of magnitude. A high mutation rate correlated strongly with a clinical resistance phenotype. This correlation suggests that an increased general mutation rate may play a significant role in the development of high-level resistance to fluoroquinolones by increasing the rate of accumulation of rare new mutations.
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Gerrish, Philip J., Alexandre Colato, and Paul D. Sniegowski. "Genomic mutation rates that neutralize adaptive evolution and natural selection." Journal of The Royal Society Interface 10, no. 85 (2013): 20130329. http://dx.doi.org/10.1098/rsif.2013.0329.
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When mutation rates are low, natural selection remains effective, and increasing the mutation rate can give rise to an increase in adaptation rate. When mutation rates are high to begin with, however, increasing the mutation rate may have a detrimental effect because of the overwhelming presence of deleterious mutations. Indeed, if mutation rates are high enough: (i) adaptive evolution may be neutralized, resulting in a zero (or negative) adaptation rate despite the continued availability of adaptive and/or compensatory mutations, or (ii) natural selection may be neutralized, because the fitness of lineages bearing adaptive and/or compensatory mutations—whether established or newly arising—is eroded by excessive mutation, causing such lineages to decline in frequency. We apply these two criteria to a standard model of asexual adaptive evolution and derive mathematical expressions—some new, some old in new guise—delineating the mutation rates under which either adaptive evolution or natural selection is neutralized. The expressions are simple and require no a priori knowledge of organism- and/or environment-specific parameters. Our discussion connects these results to each other and to previous theory, showing convergence or equivalence of the different results in most cases.
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Kondrashov, Alexey S. "Modifiers of mutation-selection balance: general approach and the evolution of mutation rates." Genetical Research 66, no. 1 (1995): 53–69. http://dx.doi.org/10.1017/s001667230003439x.
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SummaryA general approach is developed to estimate secondary selection at a modifier locus that influences some feature of a population under mutation-selection balance. The approach is based on the assumption that the properties of all available genotypes at this locus are similar. Then mutation-selection balance and weak associations between genotype distributions at selectable loci and the modifier locus are established rapidly. In contrast, changes of frequencies of the modifier genotypes are slow, and lead to only slow and small changes of the other features of the population. Thus, while these changes occur, the population remains in a state of quasi-equilibrium, where the mutation-selection balance and the associations between the selectable loci and the modifier locus are almost invariant. Selection at the modifier locus can be estimated by calculating quasiequilibrium values of these associations. This approach is developed for the situation where distributions of the number of mutations per genome within the individuals with a given modifier genotype are close to Gaussian. The results are used to study the evolution of the mutation rate. Because beneficial mutations are ignored, secondary selection at the modifier locus always diminishes the mutation rate. The coefficient of selection against an allele which increases the mutation rate by υ is approximately υδ2/[U(2−ρ)] = υŝ, where υ is the genomic deleterious mutation rate, δ is the selection differential of the number of mutations per individual in units of the standard deviation of the distribution of this number in the population, ρ is the ratio of variances of the number of mutations after and before selection, and ŝ is the selection coefficient against a mutant allele in the quasiequilibrium population. However, the decline of the mutation rate can be counterbalanced by the cost of fidelity, which can lead to an evolutionary equilibrium mutation rate.
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Johnson, Toby. "Beneficial Mutations, Hitchhiking and the Evolution of Mutation Rates in Sexual Populations." Genetics 151, no. 4 (1999): 1621–31. http://dx.doi.org/10.1093/genetics/151.4.1621.
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Abstract Natural selection acts in three ways on heritable variation for mutation rates. A modifier allele that increases the mutation rate is (i) disfavored due to association with deleterious mutations, but is also favored due to (ii) association with beneficial mutations and (iii) the reduced costs of lower fidelity replication. When a unique beneficial mutation arises and sweeps to fixation, genetic hitchhiking may cause a substantial change in the frequency of a modifier of mutation rate. In previous studies of the evolution of mutation rates in sexual populations, this effect has been underestimated. This article models the long-term effect of a series of such hitchhiking events and determines the resulting strength of indirect selection on the modifier. This is compared to the indirect selection due to deleterious mutations, when both types of mutations are randomly scattered over a given genetic map. Relative to an asexual population, increased levels of recombination reduce the effects of beneficial mutations more rapidly than those of deleterious mutations. However, the role of beneficial mutations in determining the evolutionarily stable mutation rate may still be significant if the function describing the cost of high-fidelity replication has a shallow gradient.
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Barton, N. H. "Mutation and the evolution of recombination." Philosophical Transactions of the Royal Society B: Biological Sciences 365, no. 1544 (2010): 1281–94. http://dx.doi.org/10.1098/rstb.2009.0320.
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Under the classical view, selection depends more or less directly on mutation: standing genetic variance is maintained by a balance between selection and mutation, and adaptation is fuelled by new favourable mutations. Recombination is favoured if it breaks negative associations among selected alleles, which interfere with adaptation. Such associations may be generated by negative epistasis, or by random drift (leading to the Hill–Robertson effect). Both deterministic and stochastic explanations depend primarily on the genomic mutation rate, U . This may be large enough to explain high recombination rates in some organisms, but seems unlikely to be so in general. Random drift is a more general source of negative linkage disequilibria, and can cause selection for recombination even in large populations, through the chance loss of new favourable mutations. The rate of species-wide substitutions is much too low to drive this mechanism, but local fluctuations in selection, combined with gene flow, may suffice. These arguments are illustrated by comparing the interaction between good and bad mutations at unlinked loci under the infinitesimal model.
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Singh, Tanya, Meredith Hyun, and Paul Sniegowski. "Evolution of mutation rates in hypermutable populations of Escherichia coli propagated at very small effective population size." Biology Letters 13, no. 3 (2017): 20160849. http://dx.doi.org/10.1098/rsbl.2016.0849.
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Mutation is the ultimate source of the genetic variation—including variation for mutation rate itself—that fuels evolution. Natural selection can raise or lower the genomic mutation rate of a population by changing the frequencies of mutation rate modifier alleles associated with beneficial and deleterious mutations. Existing theory and observations suggest that where selection is minimized, rapid systematic evolution of mutation rate either up or down is unlikely. Here, we report systematic evolution of higher and lower mutation rates in replicate hypermutable Escherichia coli populations experimentally propagated at very small effective size—a circumstance under which selection is greatly reduced. Several populations went extinct during this experiment, and these populations tended to evolve elevated mutation rates. In contrast, populations that survived to the end of the experiment tended to evolve decreased mutation rates. We discuss the relevance of our results to current ideas about the evolution, maintenance and consequences of high mutation rates.
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Nachman, Michael W., and Susan L. Crowell. "Estimate of the Mutation Rate per Nucleotide in Humans." Genetics 156, no. 1 (2000): 297–304. http://dx.doi.org/10.1093/genetics/156.1.297.
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Abstract Many previous estimates of the mutation rate in humans have relied on screens of visible mutants. We investigated the rate and pattern of mutations at the nucleotide level by comparing pseudogenes in humans and chimpanzees to (i) provide an estimate of the average mutation rate per nucleotide, (ii) assess heterogeneity of mutation rate at different sites and for different types of mutations, (iii) test the hypothesis that the X chromosome has a lower mutation rate than autosomes, and (iv) estimate the deleterious mutation rate. Eighteen processed pseudogenes were sequenced, including 12 on autosomes and 6 on the X chromosome. The average mutation rate was estimated to be ~2.5 × 10−8 mutations per nucleotide site or 175 mutations per diploid genome per generation. Rates of mutation for both transitions and transversions at CpG dinucleotides are one order of magnitude higher than mutation rates at other sites. Single nucleotide substitutions are 10 times more frequent than length mutations. Comparison of rates of evolution for X-linked and autosomal pseudogenes suggests that the male mutation rate is 4 times the female mutation rate, but provides no evidence for a reduction in mutation rate that is specific to the X chromosome. Using conservative calculations of the proportion of the genome subject to purifying selection, we estimate that the genomic deleterious mutation rate (U) is at least 3. This high rate is difficult to reconcile with multiplicative fitness effects of individual mutations and suggests that synergistic epistasis among harmful mutations may be common.
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Pfenninger, Markus, Halina Binde Doria, Jana Nickel, Anne Thielsch, Klaus Schwenk, and Mathilde Cordellier. "Spontaneous rate of clonal single nucleotide mutations in Daphnia galeata." PLOS ONE 17, no. 4 (2022): e0265632. http://dx.doi.org/10.1371/journal.pone.0265632.
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Mutations are the ultimate source of heritable variation and therefore the fuel for evolution, but direct estimates of mutation rates exist only for few species. We estimated the spontaneous single nucleotide mutation rate among clonal generations in the waterflea Daphnia galeata with a short-term mutation accumulation approach. Individuals from eighteen mutation accumulation lines over five generations were deep sequenced to count de novo mutations that were not present in a pool of F1 individuals, representing the parental genotype. We identified 12 new nucleotide mutations in 90 clonal generational passages. This resulted in an estimated single nucleotide mutation rate of 0.745 x 10−9 (95% c.f. 0.39 x 10−9–1.26 x 10−9), which is slightly lower than recent estimates for other Daphnia species. We discuss the implications for the population genetics of Cladocerans.
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Eskier, Doğa, Gökhan Karakülah, Aslı Suner, and Yavuz Oktay. "RdRp mutations are associated with SARS-CoV-2 genome evolution." PeerJ 8 (July 21, 2020): e9587. http://dx.doi.org/10.7717/peerj.9587.
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COVID-19, caused by the novel SARS-CoV-2 virus, started in China in late 2019, and soon became a global pandemic. With the help of thousands of viral genome sequences that have been accumulating, it has become possible to track the evolution of the viral genome over time as it spread across the world. An important question that still needs to be answered is whether any of the common mutations affect the viral properties, and therefore the disease characteristics. Therefore, we sought to understand the effects of mutations in RNA-dependent RNA polymerase (RdRp), particularly the common 14408C>T mutation, on mutation rate and viral spread. By focusing on mutations in the slowly evolving M or E genes, we aimed to minimize the effects of selective pressure. Our results indicate that 14408C>T mutation increases the mutation rate, while the third-most common RdRp mutation, 15324C>T, has the opposite effect. It is possible that 14408C>T mutation may have contributed to the dominance of its co-mutations in Europe and elsewhere.
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Sung, W., M. S. Ackerman, S. F. Miller, T. G. Doak, and M. Lynch. "Drift-barrier hypothesis and mutation-rate evolution." Proceedings of the National Academy of Sciences 109, no. 45 (2012): 18488–92. http://dx.doi.org/10.1073/pnas.1216223109.
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Chintalapati, Manjusha, and Priya Moorjani. "Evolution of the mutation rate across primates." Current Opinion in Genetics & Development 62 (June 2020): 58–64. http://dx.doi.org/10.1016/j.gde.2020.05.028.
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Krasovec, Marc, Sophie Sanchez-Brosseau, and Gwenael Piganeau. "First Estimation of the Spontaneous Mutation Rate in Diatoms." Genome Biology and Evolution 11, no. 7 (2019): 1829–37. http://dx.doi.org/10.1093/gbe/evz130.
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Abstract Mutations are the origin of genetic diversity, and the mutation rate is a fundamental parameter to understand all aspects of molecular evolution. The combination of mutation–accumulation experiments and high-throughput sequencing enabled the estimation of mutation rates in most model organisms, but several major eukaryotic lineages remain unexplored. Here, we report the first estimation of the spontaneous mutation rate in a model unicellular eukaryote from the Stramenopile kingdom, the diatom Phaeodactylum tricornutum (strain RCC2967). We sequenced 36 mutation accumulation lines for an average of 181 generations per line and identified 156 de novo mutations. The base substitution mutation rate per site per generation is μbs = 4.77 × 10−10 and the insertion–deletion mutation rate is μid = 1.58 × 10−11. The mutation rate varies as a function of the nucleotide context and is biased toward an excess of mutations from GC to AT, consistent with previous observations in other species. Interestingly, the mutation rates between the genomes of organelles and the nucleus differ, with a significantly higher mutation rate in the mitochondria. This confirms previous claims based on indirect estimations of the mutation rate in mitochondria of photosynthetic eukaryotes that acquired their plastid through a secondary endosymbiosis. This novel estimate enables us to infer the effective population size of P. tricornutum to be Ne∼8.72 × 106.
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López-Cortegano, Eugenio, Rory J. Craig, Jobran Chebib, et al. "De Novo Mutation Rate Variation and Its Determinants in Chlamydomonas." Molecular Biology and Evolution 38, no. 9 (2021): 3709–23. http://dx.doi.org/10.1093/molbev/msab140.
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Abstract De novo mutations are central for evolution, since they provide the raw material for natural selection by regenerating genetic variation. However, studying de novo mutations is challenging and is generally restricted to model species, so we have a limited understanding of the evolution of the mutation rate and spectrum between closely related species. Here, we present a mutation accumulation (MA) experiment to study de novo mutation in the unicellular green alga Chlamydomonas incerta and perform comparative analyses with its closest known relative, Chlamydomonas reinhardtii. Using whole-genome sequencing data, we estimate that the median single nucleotide mutation (SNM) rate in C. incerta is μ = 7.6 × 10−10, and is highly variable between MA lines, ranging from μ = 0.35 × 10−10 to μ = 131.7 × 10−10. The SNM rate is strongly positively correlated with the mutation rate for insertions and deletions between lines (r > 0.97). We infer that the genomic factors associated with variation in the mutation rate are similar to those in C. reinhardtii, allowing for cross-prediction between species. Among these genomic factors, sequence context and complexity are more important than GC content. With the exception of a remarkably high C→T bias, the SNM spectrum differs markedly between the two Chlamydomonas species. Our results suggest that similar genomic and biological characteristics may result in a similar mutation rate in the two species, whereas the SNM spectrum has more freedom to diverge.
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Mawaribuchi, Shuuji, Michihiko Ito, Mitsuaki Ogata, et al. "Meiotic recombination counteracts male-biased mutation (male-driven evolution)." Proceedings of the Royal Society B: Biological Sciences 283, no. 1823 (2016): 20152691. http://dx.doi.org/10.1098/rspb.2015.2691.
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Meiotic recombination is believed to produce greater genetic variation despite the fact that deoxyribonucleic acid (DNA)-replication errors are a major source of mutations. In some vertebrates, mutation rates are higher in males than in females, which developed the theory of male-driven evolution (male-biased mutation). However, there is little molecular evidence regarding the relationships between meiotic recombination and male-biased mutation. Here we tested the theory using the frog Rana rugosa, which has both XX/XY- and ZZ/ZW-type sex-determining systems within the species. The male-to-female mutation-rate ratio ( α ) was calculated from homologous sequences on the X/Y or Z/W sex chromosomes, which supported male-driven evolution. Surprisingly, each α value was notably higher in the XX/XY-type group than in the ZZ/ZW-type group, although α should have similar values within a species. Interestingly, meiotic recombination between homologous chromosomes did not occur except at terminal regions in males of this species. Then, by subdividing α into two new factors, a replication-based male-to-female mutation-rate ratio ( β ) and a meiotic recombination-based XX-to-XY/ZZ-to-ZW mutation-rate ratio ( γ ), we constructed a formula describing the relationship among a nucleotide-substitution rate and the two factors, β and γ . Intriguingly, the β - and γ -values were larger and smaller than 1, respectively, indicating that meiotic recombination might reduce male-biased mutations.
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Boyce, Kylie J. "Mutators Enhance Adaptive Micro-Evolution in Pathogenic Microbes." Microorganisms 10, no. 2 (2022): 442. http://dx.doi.org/10.3390/microorganisms10020442.
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Adaptation to the changing environmental conditions experienced within a host requires genetic diversity within a microbial population. Genetic diversity arises from mutations which occur due to DNA damage from exposure to exogenous environmental stresses or generated endogenously through respiration or DNA replication errors. As mutations can be deleterious, a delicate balance must be obtained between generating enough mutations for micro-evolution to occur while maintaining fitness and genomic integrity. Pathogenic microorganisms can actively modify their mutation rate to enhance adaptive micro-evolution by increasing expression of error-prone DNA polymerases or by mutating or decreasing expression of genes required for DNA repair. Strains which exhibit an elevated mutation rate are termed mutators. Mutators are found in varying prevalence in clinical populations where large-effect beneficial mutations enhance survival and are predominately caused by defects in the DNA mismatch repair (MMR) pathway. Mutators can facilitate the emergence of antibiotic resistance, allow phenotypic modifications to prevent recognition and destruction by the host immune system and enable switching to metabolic and cellular morphologies better able to survive in the given environment. This review will focus on recent advances in understanding the phenotypic and genotypic changes occurring in MMR mutators in both prokaryotic and eukaryotic pathogens.
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Furió, Victoria, Andrés Moya, and Rafael Sanjuán. "The cost of replication fidelity in human immunodeficiency virus type 1." Proceedings of the Royal Society B: Biological Sciences 274, no. 1607 (2006): 225–30. http://dx.doi.org/10.1098/rspb.2006.3732.
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Mutation rates should be governed by at least three evolutionary factors: the need for beneficial mutations, the benefit of minimizing the mutational load and the cost of replication fidelity. RNA viruses show high mutation rates compared with DNA micro-organisms, and recent findings suggest that the cost of fidelity might play a role in the evolution of increased mutation rates. Here, by analysing previously published data from HIV-1 reverse transcriptase in vitro assays, we show a trade-off between enzymatic accuracy and the maximum rate of polymerization, thus providing a biochemical basis for the fitness cost of fidelity in HIV-1. This trade-off seems to be related to inefficient extension of mispairs, which increases fidelity at the expense of the polymerization rate. Since in RNA viruses fast replication is critical for survival, this could impose a high cost of fidelity and favour the evolution of high mutation rates.
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Ruan, Yongsen, Haiyu Wang, Bingjie Chen, Haijun Wen, and Chung-I. Wu. "Mutations Beget More Mutations—Rapid Evolution of Mutation Rate in Response to the Risk of Runaway Accumulation." Molecular Biology and Evolution 37, no. 4 (2019): 1007–19. http://dx.doi.org/10.1093/molbev/msz283.
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Abstract The rapidity with which the mutation rate evolves could greatly impact evolutionary patterns. Nevertheless, most studies simply assume a constant rate in the time scale of interest (Kimura 1983; Drake 1991; Kumar 2005; Li 2007; Lynch 2010). In contrast, recent studies of somatic mutations suggest that the mutation rate may vary by several orders of magnitude within a lifetime (Kandoth et al. 2013; Lawrence et al. 2013). To resolve the discrepancy, we now propose a runaway model, applicable to both the germline and soma, whereby mutator mutations form a positive-feedback loop. In this loop, any mutator mutation would increase the rate of acquiring the next mutator, thus triggering a runaway escalation in mutation rate. The process can be initiated more readily if there are many weak mutators than a few strong ones. Interestingly, even a small increase in the mutation rate at birth could trigger the runaway process, resulting in unfit progeny. In slowly reproducing species, the need to minimize the risk of this uncontrolled accumulation would thus favor setting the mutation rate low. In comparison, species that starts and ends reproduction sooner do not face the risk and may set the baseline mutation rate higher. The mutation rate would evolve in response to the risk of runaway mutation, in particular, when the generation time changes. A rapidly evolving mutation rate may shed new lights on many evolutionary phenomena (Elango et al. 2006; Thomas et al. 2010, 2018; Langergraber et al. 2012; Besenbacher et al. 2019).
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Scally, Aylwyn. "Mutation rates and the evolution of germline structure." Philosophical Transactions of the Royal Society B: Biological Sciences 371, no. 1699 (2016): 20150137. http://dx.doi.org/10.1098/rstb.2015.0137.
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Genome sequencing studies of de novo mutations in humans have revealed surprising incongruities in our understanding of human germline mutation. In particular, the mutation rate observed in modern humans is substantially lower than that estimated from calibration against the fossil record, and the paternal age effect in mutations transmitted to offspring is much weaker than expected from our long-standing model of spermatogenesis. I consider possible explanations for these discrepancies, including evolutionary changes in life-history parameters such as generation time and the age of puberty, a possible contribution from undetected post-zygotic mutations early in embryo development, and changes in cellular mutation processes at different stages of the germline. I suggest a revised model of stem-cell state transitions during spermatogenesis, in which ‘dark’ gonial stem cells play a more active role than hitherto envisaged, with a long cycle time undetected in experimental observations. More generally, I argue that the mutation rate and its evolution depend intimately on the structure of the germline in humans and other primates. This article is part of the themed issue ‘Dating species divergences using rocks and clocks'.
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Katz, Sophia, Sarit Avrani, Meitar Yavneh, Sabrin Hilau, Jonathan Gross, and Ruth Hershberg. "Dynamics of Adaptation During Three Years of Evolution Under Long-Term Stationary Phase." Molecular Biology and Evolution 38, no. 7 (2021): 2778–90. http://dx.doi.org/10.1093/molbev/msab067.
Texte intégralRésumé :
Abstract Many bacterial species that cannot sporulate, such as the model bacterium Escherichia coli, can nevertheless survive for years, following exhaustion of external resources, in a state termed long-term stationary phase (LTSP). Here we describe the dynamics of E. coli adaptation during the first three years spent under LTSP. We show that during this time, E. coli continuously adapts genetically through the accumulation of mutations. For nonmutator clones, the majority of mutations accumulated appear to be adaptive under LTSP, reflected in an extremely convergent pattern of mutation accumulation. Despite the rapid and convergent manner in which populations adapt under LTSP, they continue to harbor extensive genetic variation. The dynamics of evolution of mutation rates under LTSP are particularly interesting. The emergence of mutators affects overall mutation accumulation rates as well as the mutational spectra and the ultimate spectrum of adaptive alleles acquired under LTSP. With time, mutators can evolve even higher mutation rates through the acquisition of additional mutation rate–enhancing mutations. Different mutator and nonmutator clones within a single population and time point can display extreme variation in their mutation rates, resulting in differences in both the dynamics of adaptation and their associated deleterious burdens. Despite these differences, clones that vary greatly in their mutation rates tend to coexist within their populations for many years, under LTSP.
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Amicone, Massimo, Vítor Borges, Maria João Alves, et al. "Mutation rate of SARS-CoV-2 and emergence of mutators during experimental evolution." Evolution, Medicine, and Public Health 10, no. 1 (2022): 142–55. http://dx.doi.org/10.1093/emph/eoac010.
Texte intégralRésumé :
Abstract Background and objectives To understand how organisms evolve, it is fundamental to study how mutations emerge and establish. Here, we estimated the rate of mutation accumulation of SARS-CoV-2 in vitro and investigated the repeatability of its evolution when facing a new cell type but no immune or drug pressures. Methodology We performed experimental evolution with two strains of SARS-CoV-2, one carrying the originally described spike protein (CoV-2-D) and another carrying the D614G mutation that has spread worldwide (CoV-2-G). After 15 passages in Vero cells and whole genome sequencing, we characterized the spectrum and rate of the emerging mutations and looked for evidences of selection across the genomes of both strains. Results From the frequencies of the mutations accumulated, and excluding the genes with signals of selection, we estimate a spontaneous mutation rate of 1.3 × 10−6 ± 0.2 × 10−6 per-base per-infection cycle (mean across both lineages of SARS-CoV-2 ± 2SEM). We further show that mutation accumulation is larger in the CoV-2-D lineage and heterogeneous along the genome, consistent with the action of positive selection on the spike protein, which accumulated five times more mutations than the corresponding genomic average. We also observe the emergence of mutators in the CoV-2-G background, likely linked to mutations in the RNA-dependent RNA polymerase and/or in the error-correcting exonuclease protein. Conclusions and implications These results provide valuable information on how spontaneous mutations emerge in SARS-CoV-2 and on how selection can shape its genome toward adaptation to new environments. Lay Summary: Each time a virus replicates inside a cell, errors (mutations) occur. Here, via laboratory propagation in cells originally isolated from the kidney epithelium of African green monkeys, we estimated the rate at which the SARS-CoV-2 virus mutates—an important parameter for understanding how it can evolve within and across humans. We also confirm the potential of its Spike protein to adapt to a new environment and report the emergence of mutators—viral populations where mutations occur at a significantly faster rate.
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Maddamsetti, Rohan, and Nkrumah A. Grant. "Divergent Evolution of Mutation Rates and Biases in the Long-Term Evolution Experiment with Escherichia coli." Genome Biology and Evolution 12, no. 9 (2020): 1591–603. http://dx.doi.org/10.1093/gbe/evaa178.
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Abstract All organisms encode enzymes that replicate, maintain, pack, recombine, and repair their genetic material. For this reason, mutation rates and biases also evolve by mutation, variation, and natural selection. By examining metagenomic time series of the Lenski long-term evolution experiment (LTEE) with Escherichia coli (Good BH, McDonald MJ, Barrick JE, Lenski RE, Desai MM. 2017. The dynamics of molecular evolution over 60,000 generations. Nature 551(7678):45–50.), we find that local mutation rate variation has evolved during the LTEE. Each LTEE population has evolved idiosyncratic differences in their rates of point mutations, indels, and mobile element insertions, due to the fixation of various hypermutator and antimutator alleles. One LTEE population, called Ara+3, shows a strong, symmetric wave pattern in its density of point mutations, radiating from the origin of replication. This pattern is largely missing from the other LTEE populations, most of which evolved missense, indel, or structural mutations in topA, fis, and dusB—loci that all affect DNA topology. The distribution of mutations in those genes over time suggests epistasis and historical contingency in the evolution of DNA topology, which may have in turn affected local mutation rates. Overall, the replicate populations of the LTEE have largely diverged in their mutation rates and biases, even though they have adapted to identical abiotic conditions.
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Orr, Adam J., Amanda Padovan, David Kainer, et al. "A phylogenomic approach reveals a low somatic mutation rate in a long-lived plant." Proceedings of the Royal Society B: Biological Sciences 287, no. 1922 (2020): 20192364. http://dx.doi.org/10.1098/rspb.2019.2364.
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Somatic mutations can have important effects on the life history, ecology, and evolution of plants, but the rate at which they accumulate is poorly understood and difficult to measure directly. Here, we develop a method to measure somatic mutations in individual plants and use it to estimate the somatic mutation rate in a large, long-lived, phenotypically mosaic Eucalyptus melliodora tree. Despite being 100 times larger than Arabidopsis, this tree has a per-generation mutation rate only ten times greater, which suggests that this species may have evolved mechanisms to reduce the mutation rate per unit of growth. This adds to a growing body of evidence that illuminates the correlated evolutionary shifts in mutation rate and life history in plants.
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Galtier, Nicolas, Richard W. Jobson, Benoît Nabholz, Sylvain Glémin, and Pierre U. Blier. "Mitochondrial whims: metabolic rate, longevity and the rate of molecular evolution." Biology Letters 5, no. 3 (2009): 413–16. http://dx.doi.org/10.1098/rsbl.2008.0662.
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The evolutionary rate of mitochondrial DNA (mtDNA) is highly variable across lineages in animals, and particularly in mammals. This variation has been interpreted as reflecting variations in metabolic rate: mitochondrial respiratory activity would tend to generate mutagenic agents, thus increasing the mutation rate. Here we review recent evidence suggesting that a direct, mechanical effect of species metabolic rate on mtDNA evolutionary rate is unlikely. We suggest that natural selection could act to reduce the (somatic) mtDNA mutation rate in long-lived species, in agreement with the mitochondrial theory of ageing.
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O'Brien, Siobhán, Antonio M. M. Rodrigues, and Angus Buckling. "The evolution of bacterial mutation rates under simultaneous selection by interspecific and social parasitism." Proceedings of the Royal Society B: Biological Sciences 280, no. 1773 (2013): 20131913. http://dx.doi.org/10.1098/rspb.2013.1913.
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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.
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Boezen, Dieke, Ghulam Ali, Manli Wang, et al. "Empirical estimates of the mutation rate for an alphabaculovirus." PLOS Genetics 18, no. 6 (2022): e1009806. http://dx.doi.org/10.1371/journal.pgen.1009806.
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Mutation rates are of key importance for understanding evolutionary processes and predicting their outcomes. Empirical mutation rate estimates are available for a number of RNA viruses, but few are available for DNA viruses, which tend to have larger genomes. Whilst some viruses have very high mutation rates, lower mutation rates are expected for viruses with large genomes to ensure genome integrity. Alphabaculoviruses are insect viruses with large genomes and often have high levels of polymorphism, suggesting high mutation rates despite evidence of proofreading activity by the replication machinery. Here, we report an empirical estimate of the mutation rate per base per strand copying (s/n/r) of Autographa californica multiple nucleopolyhedrovirus (AcMNPV). To avoid biases due to selection, we analyzed mutations that occurred in a stable, non-functional genomic insert after five serial passages in Spodoptera exigua larvae. Our results highlight that viral demography and the stringency of mutation calling affect mutation rate estimates, and that using a population genetic simulation model to make inferences can mitigate the impact of these processes on estimates of mutation rate. We estimated a mutation rate of μ = 1×10−7 s/n/r when applying the most stringent criteria for mutation calling, and estimates of up to μ = 5×10−7 s/n/r when relaxing these criteria. The rates at which different classes of mutations accumulate provide good evidence for neutrality of mutations occurring within the inserted region. We therefore present a robust approach for mutation rate estimation for viruses with stable genomes, and strong evidence of a much lower alphabaculovirus mutation rate than supposed based on the high levels of polymorphism observed.
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Boezen, Dieke, Ghulam Ali, Manli Wang, et al. "Empirical estimates of the mutation rate for an alphabaculovirus." PLOS Genetics 18, no. 6 (2022): e1009806. http://dx.doi.org/10.1371/journal.pgen.1009806.
Texte intégralRésumé :
Mutation rates are of key importance for understanding evolutionary processes and predicting their outcomes. Empirical mutation rate estimates are available for a number of RNA viruses, but few are available for DNA viruses, which tend to have larger genomes. Whilst some viruses have very high mutation rates, lower mutation rates are expected for viruses with large genomes to ensure genome integrity. Alphabaculoviruses are insect viruses with large genomes and often have high levels of polymorphism, suggesting high mutation rates despite evidence of proofreading activity by the replication machinery. Here, we report an empirical estimate of the mutation rate per base per strand copying (s/n/r) of Autographa californica multiple nucleopolyhedrovirus (AcMNPV). To avoid biases due to selection, we analyzed mutations that occurred in a stable, non-functional genomic insert after five serial passages in Spodoptera exigua larvae. Our results highlight that viral demography and the stringency of mutation calling affect mutation rate estimates, and that using a population genetic simulation model to make inferences can mitigate the impact of these processes on estimates of mutation rate. We estimated a mutation rate of μ = 1×10−7 s/n/r when applying the most stringent criteria for mutation calling, and estimates of up to μ = 5×10−7 s/n/r when relaxing these criteria. The rates at which different classes of mutations accumulate provide good evidence for neutrality of mutations occurring within the inserted region. We therefore present a robust approach for mutation rate estimation for viruses with stable genomes, and strong evidence of a much lower alphabaculovirus mutation rate than supposed based on the high levels of polymorphism observed.
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Gong, Yi, R. C. Woodruff, and J. N. Thompson. "Deleterious genomic mutation rate for viability in Drosophila melanogaster using concomitant sibling controls." Biology Letters 1, no. 4 (2005): 492–95. http://dx.doi.org/10.1098/rsbl.2005.0364.
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New deleterious mutations may reduce health and fitness and are involved in the evolution and maintenance of numerous biological processes. Hence, it is important to estimate the deleterious genomic mutation rate ( U ) in representative higher organisms. However, these estimated rates vary widely, mainly because of inadequate experimental controls. Here we describe an experimental design (the Binscy assay) with concomitant sibling controls and estimate U for viability in Drosophila melanogaster to be 0.31. This estimate, like most published studies, focuses on viability mutations and the overall deleterious genomic mutation rate would therefore be higher.
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Thornlow, Bryan P., Josh Hough, Jacquelyn M. Roger, Henry Gong, Todd M. Lowe, and Russell B. Corbett-Detig. "Transfer RNA genes experience exceptionally elevated mutation rates." Proceedings of the National Academy of Sciences 115, no. 36 (2018): 8996–9001. http://dx.doi.org/10.1073/pnas.1801240115.
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Transfer RNAs (tRNAs) are a central component for the biological synthesis of proteins, and they are among the most highly conserved and frequently transcribed genes in all living things. Despite their clear significance for fundamental cellular processes, the forces governing tRNA evolution are poorly understood. We present evidence that transcription-associated mutagenesis and strong purifying selection are key determinants of patterns of sequence variation within and surrounding tRNA genes in humans and diverse model organisms. Remarkably, the mutation rate at broadly expressed cytosolic tRNA loci is likely between 7 and 10 times greater than the nuclear genome average. Furthermore, evolutionary analyses provide strong evidence that tRNA genes, but not their flanking sequences, experience strong purifying selection acting against this elevated mutation rate. We also find a strong correlation between tRNA expression levels and the mutation rates in their immediate flanking regions, suggesting a simple method for estimating individual tRNA gene activity. Collectively, this study illuminates the extreme competing forces in tRNA gene evolution and indicates that mutations at tRNA loci contribute disproportionately to mutational load and have unexplored fitness consequences in human populations.
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Nyerges, Ákos, Bálint Csörgő, Gábor Draskovits, et al. "Directed evolution of multiple genomic loci allows the prediction of antibiotic resistance." Proceedings of the National Academy of Sciences 115, no. 25 (2018): E5726—E5735. http://dx.doi.org/10.1073/pnas.1801646115.
Texte intégralRésumé :
Antibiotic development is frequently plagued by the rapid emergence of drug resistance. However, assessing the risk of resistance development in the preclinical stage is difficult. Standard laboratory evolution approaches explore only a small fraction of the sequence space and fail to identify exceedingly rare resistance mutations and combinations thereof. Therefore, new rapid and exhaustive methods are needed to accurately assess the potential of resistance evolution and uncover the underlying mutational mechanisms. Here, we introduce directed evolution with random genomic mutations (DIvERGE), a method that allows an up to million-fold increase in mutation rate along the full lengths of multiple predefined loci in a range of bacterial species. In a single day, DIvERGE generated specific mutation combinations, yielding clinically significant resistance against trimethoprim and ciprofloxacin. Many of these mutations have remained previously undetected or provide resistance in a species-specific manner. These results indicate pathogen-specific resistance mechanisms and the necessity of future narrow-spectrum antibacterial treatments. In contrast to prior claims, we detected the rapid emergence of resistance against gepotidacin, a novel antibiotic currently in clinical trials. Based on these properties, DIvERGE could be applicable to identify less resistance-prone antibiotics at an early stage of drug development. Finally, we discuss potential future applications of DIvERGE in synthetic and evolutionary biology.
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Sniegowski, Paul D., and Philip J. Gerrish. "Beneficial mutations and the dynamics of adaptation in asexual populations." Philosophical Transactions of the Royal Society B: Biological Sciences 365, no. 1544 (2010): 1255–63. http://dx.doi.org/10.1098/rstb.2009.0290.
Texte intégralRésumé :
We discuss the dynamics of adaptive evolution in asexual (clonal) populations. The classical ‘periodic selection’ model of clonal evolution assumed that beneficial mutations are very rare and therefore substitute unfettered into populations as occasional, isolated events. Newer models allow for the possibility that beneficial mutations are sufficiently common to coexist and compete for fixation within populations. Experimental evolution studies in microbes provide empirical support for stochastic models in which both selection and mutation are strong effects and clones compete for fixation; however, the relative importance of competition among clones bearing mutations of different selective effects versus competition among clones bearing multiple mutations remains unresolved. We provide some new theoretical results, moreover, suggesting that population dynamics consistent with the periodic selection model can arise even in a deterministic model that can accommodate a very high beneficial mutation rate.
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Koch, Evan M., Rena M. Schweizer, Teia M. Schweizer, et al. "De Novo Mutation Rate Estimation in Wolves of Known Pedigree." Molecular Biology and Evolution 36, no. 11 (2019): 2536–47. http://dx.doi.org/10.1093/molbev/msz159.
Texte intégralRésumé :
Abstract Knowledge of mutation rates is crucial for calibrating population genetics models of demographic history in units of years. However, mutation rates remain challenging to estimate because of the need to identify extremely rare events. We estimated the nuclear mutation rate in wolves by identifying de novo mutations in a pedigree of seven wolves. Putative de novo mutations were discovered by whole-genome sequencing and were verified by Sanger sequencing of parents and offspring. Using stringent filters and an estimate of the false negative rate in the remaining observable genome, we obtain an estimate of ∼4.5 × 10−9 per base pair per generation and provide conservative bounds between 2.6 × 10−9 and 7.1 × 10−9. Although our estimate is consistent with recent mutation rate estimates from ancient DNA (4.0 × 10−9 and 3.0–4.5 × 10−9), it suggests a wider possible range. We also examined the consequences of our rate and the accompanying interval for dating several critical events in canid demographic history. For example, applying our full range of rates to coalescent models of dog and wolf demographic history implies a wide set of possible divergence times between the ancestral populations of dogs and extant Eurasian wolves (16,000–64,000 years ago) although our point estimate indicates a date between 25,000 and 33,000 years ago. Aside from one study in mice, ours provides the only direct mammalian mutation rate outside of primates and is likely to be vital to future investigations of mutation rate evolution.
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ALÓS-FERRER, CARLOS, and ILJA NEUSTADT. "BEST-RESPONSE DYNAMICS IN A BIRTH-DEATH MODEL OF EVOLUTION IN GAMES." International Game Theory Review 12, no. 02 (2010): 197–204. http://dx.doi.org/10.1142/s021919891000260x.
Texte intégralRésumé :
We consider a model of evolution with mutations as in Kandori et al. (1993) [Kandori, M., Mailath, G.J., Rob, R., 1993. Learning, mutation, and long run equilibria in games. Econometrica 61, 29–56], where agents follow best-response decision rules as in Sandholm (1998) [Sandholm, W., 1998. Simple and clever decision rules for a model of evolution. Economics Letters 61, 165–170]. Contrary to those papers, our model gives rise to a birth-death process, which allows explicit computation of the long-run probabilities of equilibria for given values of the mutation rate and the population size. We use this fact to provide a direct proof of the stochastic stability of risk-dominant equilibria as the mutation rate tends to zero, and illustrate the outcomes of the dynamics for positive mutation rates.
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Jasieniuk, M., and B. D. Maxwell. "Populations genetics and the evolution of herbicide resistance in weeds." Comptes rendus 75, no. 4 (2005): 25–35. http://dx.doi.org/10.7202/706069ar.
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Numerous factors, including mutation, selection, inheritance, mating System, and gene flow are important in the evolution of herbicide resistance in weeds. Spontaneous gene mutation is believed to be the main source of genetic variation for resistance evolution in a geographic region in which resistance has not been detected previously. Despite mutation frequencies that are probably very low, the probability of occurrence of at least a single resistant mutant in a susceptible population may be high for weed species with high fecundities and large population sizes. Subsequent repeated treatments with herbicides having the same mode of action could lead to the rapid evolution of predominantly resistant populations. Rare dominantly inherited resistance mutations spread significantly more rapidly than recessive mutations in random mating populations, but at roughly the same rate in highly self-fertilizing species. Gene flow, through the movement of pollen or seed from resistant weed populations, may provide a source of resistance alleles to adjacent or nearby susceptible fields. Mathematical models indicate that the strength of selection imposed by a herbicide and the initial frequency of the resistant phenotype most strongly influence the rate of resistance evolution. The models predict that the most effective strategies to manage resistance are to reduce the intensity of selection by herbicide and to limit the migration of herbicide-resistant seed.
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Harris, Kelley. "Evidence for recent, population-specific evolution of the human mutation rate." Proceedings of the National Academy of Sciences 112, no. 11 (2015): 3439–44. http://dx.doi.org/10.1073/pnas.1418652112.
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As humans dispersed out of Africa they adapted to new environmental challenges, including changes in exposure to mutagenic solar radiation. Humans in temperate latitudes have acquired light skin that is relatively transparent to UV light, and some evidence suggests that their DNA damage response pathways have also experienced local adaptation. This raises the possibility that different populations have experienced different selective pressures affecting genome integrity. Here, I present evidence that the rate of a particular mutation type has recently increased in the European population, rising in frequency by 50% during the 40,000–80,000 y since Europeans began diverging from Asians. A comparison of SNPs private to Africa, Asia, and Europe in the 1000 Genomes data reveals that private European variation is enriched for the transition 5′-TCC-3′ → 5′-TTC-3′. Although it is not clear whether UV played a causal role in changing the European mutational spectrum, 5′-TCC-3′ → 5′-TTC-3′ is known to be the most common somatic mutation present in melanoma skin cancers, as well as the mutation most frequently induced in vitro by UV. Regardless of its causality, this change indicates that DNA replication fidelity has not remained stable even since the origin of modern humans and might have changed numerous times during our recent evolutionary history.
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Lynch, Michael. "The rate of polygenic mutation." Genetical Research 51, no. 2 (1988): 137–48. http://dx.doi.org/10.1017/s0016672300024150.
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SummaryBy application of the neutral model of phenotypic evolution, quantitative estimates of the rate of input of genetic variance by polygenic mutation can be extracted from divergence experiments as well as from the response of an inbred base population to selection. The analytical methods are illustrated through a survey of data on a diversity of organisms including Drosophila, Tribolium, mice, and several crop species. The mutational rate of introduction of genetic variance (Vm) scaled by the environmental variance (VE) is shown to vary between populations, species, and characters with a range of approximately 10−4 to 5 × 10−2. Vm/VE for Drosophila viability is somewhat below this range, while hybrid dysgenesis may temporarily inflate Vm/VE beyond 10−1. Potential sources of bias and error in the estimation of Vm are discussed, as are the practical implications of the observed limits to Vm/VE for projecting the long-term response to selection and for testing adaptational hypotheses.
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Gillooly, James F., Michael W. McCoy, and Andrew P. Allen. "Effects of metabolic rate on protein evolution." Biology Letters 3, no. 6 (2007): 655–60. http://dx.doi.org/10.1098/rsbl.2007.0403.
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Since the modern evolutionary synthesis was first proposed early in the twentieth century, attention has focused on assessing the relative contribution of mutation versus natural selection on protein evolution. Here we test a model that yields general quantitative predictions on rates of protein evolution by combining principles of individual energetics with Kimura's neutral theory. The model successfully predicts much of the heterogeneity in rates of protein evolution for diverse eukaryotes (i.e. fishes, amphibians, reptiles, birds, mammals) from different thermal environments. Data also show that the ratio of non-synonymous to synonymous nucleotide substitution is independent of body size, and thus presumably of effective population size. These findings indicate that rates of protein evolution are largely controlled by mutation rates, which in turn are strongly influenced by individual metabolic rate.
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Bachar, Amit, Elad Itzhaki, Shmuel Gleizer, Melina Shamshoom, Ron Milo, and Niv Antonovsky. "Point mutations in topoisomerase I alter the mutation spectrum in E. coli and impact the emergence of drug resistance genotypes." Nucleic Acids Research 48, no. 2 (2019): 761–69. http://dx.doi.org/10.1093/nar/gkz1100.
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Abstract Identifying the molecular mechanisms that give rise to genetic variation is essential for the understanding of evolutionary processes. Previously, we have used adaptive laboratory evolution to enable biomass synthesis from CO2 in Escherichia coli. Genetic analysis of adapted clones from two independently evolving populations revealed distinct enrichment for insertion and deletion mutational events. Here, we follow these observations to show that mutations in the gene encoding for DNA topoisomerase I (topA) give rise to mutator phenotypes with characteristic mutational spectra. Using genetic assays and mutation accumulation lines, we find that point mutations in topA increase the rate of sequence deletion and duplication events. Interestingly, we observe that a single residue substitution (R168C) results in a high rate of head-to-tail (tandem) short sequence duplications, which are independent of existing sequence repeats. Finally, we show that the unique mutation spectrum of topA mutants enhances the emergence of antibiotic resistance in comparison to mismatch-repair (mutS) mutators, and leads to new resistance genotypes. Our findings highlight a potential link between the catalytic activity of topoisomerases and the fundamental question regarding the emergence of de novo tandem repeats, which are known modulators of bacterial evolution.
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Tanaka, Mark M., Carl T. Bergstrom, and Bruce R. Levin. "The Evolution of Mutator Genes in Bacterial Populations: The Roles of Environmental Change and Timing." Genetics 164, no. 3 (2003): 843–54. http://dx.doi.org/10.1093/genetics/164.3.843.
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Abstract Recent studies have found high frequencies of bacteria with increased genomic rates of mutation in both clinical and laboratory populations. These observations may seem surprising in light of earlier experimental and theoretical studies. Mutator genes (genes that elevate the genomic mutation rate) are likely to induce deleterious mutations and thus suffer an indirect selective disadvantage; at the same time, bacteria carrying them can increase in frequency only by generating beneficial mutations at other loci. When clones carrying mutator genes are rare, however, these beneficial mutations are far more likely to arise in members of the much larger nonmutator population. How then can mutators become prevalent? To address this question, we develop a model of the population dynamics of bacteria confronted with ever-changing environments. Using analytical and simulation procedures, we explore the process by which initially rare mutator alleles can rise in frequency. We demonstrate that subsequent to a shift in environmental conditions, there will be relatively long periods of time during which the mutator subpopulation can produce a beneficial mutation before the ancestral subpopulations are eliminated. If the beneficial mutation arises early enough, the overall frequency of mutators will climb to a point higher than when the process began. The probability of producing a subsequent beneficial mutation will then also increase. In this manner, mutators can increase in frequency over successive selective sweeps. We discuss the implications and predictions of these theoretical results in relation to antibiotic resistance and the evolution of mutation rates.
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Ho, Eddie K. H., Fenner Macrae, Leigh C. Latta, et al. "High and Highly Variable Spontaneous Mutation Rates in Daphnia." Molecular Biology and Evolution 37, no. 11 (2020): 3258–66. http://dx.doi.org/10.1093/molbev/msaa142.
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Abstract The rate and spectrum of spontaneous mutations are critical parameters in basic and applied biology because they dictate the pace and character of genetic variation introduced into populations, which is a prerequisite for evolution. We use a mutation–accumulation approach to estimate mutation parameters from whole-genome sequence data from multiple genotypes from multiple populations of Daphnia magna, an ecological and evolutionary model system. We report extremely high base substitution mutation rates (µ-n,bs = 8.96 × 10−9/bp/generation [95% CI: 6.66–11.97 × 10−9/bp/generation] in the nuclear genome and µ-m,bs = 8.7 × 10−7/bp/generation [95% CI: 4.40–15.12 × 10−7/bp/generation] in the mtDNA), the highest of any eukaryote examined using this approach. Levels of intraspecific variation based on the range of estimates from the nine genotypes collected from three populations (Finland, Germany, and Israel) span 1 and 3 orders of magnitude, respectively, resulting in up to a ∼300-fold difference in rates among genomic partitions within the same lineage. In contrast, mutation spectra exhibit very consistent patterns across genotypes and populations, suggesting the mechanisms underlying the mutational process may be similar, even when the rates at which they occur differ. We discuss the implications of high levels of intraspecific variation in rates, the importance of estimating gene conversion rates using a mutation–accumulation approach, and the interacting factors influencing the evolution of mutation parameters. Our findings deepen our knowledge about mutation and provide both challenges to and support for current theories aimed at explaining the evolution of the mutation rate, as a trait, across taxa.
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Garvin, Michael R., and Anthony J. Gharrett. "Evolution: are the monkeys’ typewriters rigged?" Royal Society Open Science 1, no. 2 (2014): 140172. http://dx.doi.org/10.1098/rsos.140172.
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Evolution is presumed to proceed by random mutations, which increase an individual’s fitness. Increased fitness produces a higher survival rate for those individuals within populations and drives the variants to fixation over large timescales to produce new species. We recently identified positively selected sites in mitochondrial complex I in numerous, diverse taxa. In one taxon, a simple sequence repeat (SSR) encompassed the positively selected sites. We hypothesized a model in which: (i) slip-strand mis-pairing during replication due to the SSR increases the mutation rate at these sites, and (ii) a functional constraint at the protein level maintains the SSR and therefore a higher mutation rate at this site over large time scales to drive evolution. We tested this model by identifying SSRs in a mitochondrial-encoded protein in species from our previous work and determined that nearly all of the positively selected sites encompass an SSR. Furthermore, we show that our proposed model accounts for most of the mutations at neutral sites but it is probably the predominant mechanism at positively selected sites. This suggests that evolution does not proceed by simple random processes but is guided by physical properties of the DNA itself and functional constraint of the proteins encoded by the DNA.
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Nicholson, Michael D., David Cheek, and Tibor Antal. "Sequential mutations in exponentially growing populations." PLOS Computational Biology 19, no. 7 (2023): e1011289. http://dx.doi.org/10.1371/journal.pcbi.1011289.
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Stochastic models of sequential mutation acquisition are widely used to quantify cancer and bacterial evolution. Across manifold scenarios, recurrent research questions are: how many cells are there with n alterations, and how long will it take for these cells to appear. For exponentially growing populations, these questions have been tackled only in special cases so far. Here, within a multitype branching process framework, we consider a general mutational path where mutations may be advantageous, neutral or deleterious. In the biologically relevant limiting regimes of large times and small mutation rates, we derive probability distributions for the number, and arrival time, of cells with n mutations. Surprisingly, the two quantities respectively follow Mittag-Leffler and logistic distributions regardless of n or the mutations’ selective effects. Our results provide a rapid method to assess how altering the fundamental division, death, and mutation rates impacts the arrival time, and number, of mutant cells. We highlight consequences for mutation rate inference in fluctuation assays.
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Otto, S. P., and M. E. Orive. "Evolutionary consequences of mutation and selection within an individual." Genetics 141, no. 3 (1995): 1173–87. http://dx.doi.org/10.1093/genetics/141.3.1173.
Texte intégralRésumé :
Abstract Whether in sexual or asexual organisms, selection among cell lineages during development is an effective way of eliminating deleterious mutations. Using a mathematical analysis, we find that relatively small differences in cell replication rates during development can translate into large differences in the proportion of mutant cells within the adult, especially when development involves a large number of cell divisions. Consequently, intraorganismal selection can substantially reduce the deleterious mutation rate observed among offspring as well as the mutation load within a population, because cells rather than individuals provide the selective "deaths" necessary to stem the tide of deleterious mutations. The reduction in mutation rate among offspring is more pronounced in organisms with plastic development than in those with structured development. It is also more pronounced in asexual organisms that produce multicellular rather than unicellular offspring. By effecting the mutation rate, intraorganismal selection may have broad evolutionary implications; as an example, we consider its influence on the evolution of ploidy levels, finding that cell-lineage selection is more effective in haploids and tends to favor their evolution.