Índice
Literatura científica selecionada sobre o tema "Mutation rate evolution"
Crie uma referência precisa em APA, MLA, Chicago, Harvard, e outros estilos
Consulte a lista de atuais artigos, livros, teses, anais de congressos e outras fontes científicas relevantes para o tema "Mutation rate evolution".
Ao lado de cada fonte na lista de referências, há um botão "Adicionar à bibliografia". Clique e geraremos automaticamente a citação bibliográfica do trabalho escolhido no estilo de citação de que você precisa: APA, MLA, Harvard, Chicago, Vancouver, etc.
Você também pode baixar o texto completo da publicação científica em formato .pdf e ler o resumo do trabalho online se estiver presente nos metadados.
Artigos de revistas sobre o assunto "Mutation rate evolution"
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.
Texto completo da fonteResumo:
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 .
2
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.
Texto completo da fonteResumo:
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.
3
Stephan, Wolfgang. "The Rate of Compensatory Evolution." Genetics 144, no. 1 (1996): 419–26. http://dx.doi.org/10.1093/genetics/144.1.419.
Texto completo da fonteResumo:
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.
4
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.
Texto completo da fonte
5
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.
Texto completo da fonte
6
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.
Texto completo da fonteResumo:
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.
7
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.
Texto completo da fonteResumo:
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.
8
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.
Texto completo da fonteResumo:
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.
9
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.
Texto completo da fonteResumo:
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.
10
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.
Texto completo da fonteResumo:
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.