scholarly journals Allele Based Inference on Evolution and Extinction; A Genetic Drift Approach

2019 ◽  
Vol 1 (4) ◽  
pp. 1-15
Author(s):  
S. Oluwafemi Oyamakin ◽  
Angela U. Chukwu ◽  
Wale-Orojo Oluwaseun A ◽  
Ogunjobi E. O

In other to present a series of stochastic models from population dynamics capable of describing rudimentary aspects of genetic evolution, we studied two-allele Wright–Fisher and the Moran models for evolution of the relative frequencies of two alleles at a diploid locus under random genetic drift in a population of fixed size “simplest form, selection, and random mutation”. Principal results were presented in qualitative terms, illustrated by Monte Carlo simulations from R and http://www.radford.edu/~rsheehy/Gen_flash/popgen. Moran and the Wright-Fisher Models exhibited the same fixation probabilities, only that the Moran model runs twice as fast as the Wright-Fisher Model. A clue that can help us to understand this result is provided by the variance in reproductive success in the two models. Genetic changes due to drift were neither directional nor predictable in any deterministic way. Nonetheless, genetic drift led to evolutionary change in the absence of mutation (P=0.5), natural selection or gene flow. In general, alleles drift to fixation is significantly faster in smaller populations. Probability of fixation of an allele A was approximately equivalent to the initial frequency of that allele. With the inclusion of selection in our model, probability of fixation of a favoured allele due to natural selection increased with increase in fitness advantage and population size. The time taken to reach fixation is much slower, in case of no selective advantage, than a fixation under mutation with selective advantage.

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Haoxuan Liu ◽  
Jianzhi Zhang

AbstractWhat determines the rate (μ) and molecular spectrum of mutation is a fundamental question. The prevailing hypothesis asserts that natural selection against deleterious mutations has pushed μ to the minimum achievable in the presence of genetic drift, or the drift barrier. Here we show that, contrasting this hypothesis, μ substantially exceeds the drift barrier in diverse organisms. Random mutation accumulation (MA) in yeast frequently reduces μ, and deleting the newly discovered mutator gene PSP2 nearly halves μ. These results, along with a comparison between the MA and natural yeast strains, demonstrate that μ is maintained above the drift barrier by stabilizing selection. Similar comparisons show that the mutation spectrum such as the universal AT mutational bias is not intrinsic but has been selectively preserved. These findings blur the separation of mutation from selection as distinct evolutionary forces but open the door to alleviating mutagenesis in various organisms by genome editing.


2018 ◽  
Author(s):  
Stephan Peischl ◽  
Kimberly J. Gilbert

AbstractUnderstanding the causes and consequences of range expansions or range shifts has a long history in evolutionary biology. Recent theoretical, experimental, and empirical work has identified two particularly interesting phenomena in the context of species range expansions: (i) gene surfing and the relaxation of natural selection, and (ii) spatial sorting. The former can lead to an accumulation of deleterious mutations at range edges, causing an expansion load and slowing down expansion. The latter can create gradients in dispersal-related traits along the expansion axis and cause an acceleration of expansion. We present a theoretical framework that treats spatial sorting and gene surfing as spatial versions of natural selection and genetic drift, respectively. This model allows us to study analytically how gene surfing and spatial sorting interact, and to derive the probability of fixation of pleiotropic mutations at the expansion front. We use our results to predict the co-evolution of mean fitness and dispersal rates, taking into account the effects of random genetic drift, natural selection and spatial sorting, as well as correlations between fitnessand dispersal-related traits. We identify a “rescue effect” of spatial sorting, where the evolution of higher dispersal rates at the leading edge rescues the population from incurring expansion load.


2017 ◽  
Author(s):  
Guillermo Rodrigo ◽  
Mario A. Fares

ABSTRACTGene duplication is a major source of functional innovations and genome complexity, albeit this evolutionary process requires the preservation of duplicates in the genomes for long time. However, the population genetic mechanisms governing this preservation, especially in the critical very initial phase, have remained largely unknown. Here, we demonstrate that gene duplication confers per se a weak selective advantage in scenarios of fitness trade-offs. Through a precise quantitative description of a model system, we show that a second gene copy enhances the information transfer from the environmental signal to the phenotypic response by reducing gene expression inaccuracies derived from pervasive molecular noise and suboptimal gene regulation. We then reveal that such a phenotypic accuracy yields a selective advantage in the order of 0.1% on average, which would allow the positive selection of gene duplication in populations with moderate or large sizes. This advantage is greater at higher noise levels and intermediate concentrations of the environmental molecule, when fitness trade-offs become more evident. Moreover, we show that the genome rearrangement rates greatly condition the eventual fixation of duplicated genes, either by natural selection or by random genetic drift. Overall, our theoretical results highlight an original adaptive value for cells carrying new-born duplicates, broadly analyze the selective conditions that determine their early fates in different organisms, and reconcile population genetics with evolution by gene duplication.SIGNIFICANCEGene duplication is considered a major driver for the evolution of biological complexity. However, it is still enigmatic to what extent natural selection and genetic drift have governed this evolutionary process. This work uncovers a selective advantage for genotypes carrying duplicates, called phenotypic accuracy, widely characterized thanks to a multi-scale mathematical model coupling gene regulation with population genetics. Importantly, the integrative results presented here provide a detailed mechanistic description for the fixation of duplicates, which allows making predictions about the genome architectures, and which is relevant to understand the origins of complexity.


Genetics ◽  
2003 ◽  
Vol 165 (4) ◽  
pp. 2249-2258 ◽  
Author(s):  
Mark M Iles ◽  
Kevin Walters ◽  
Chris Cannings

AbstractIt is well known that an allele causing increased recombination is expected to proliferate as a result of genetic drift in a finite population undergoing selection, without requiring other mechanisms. This is supported by recent simulations apparently demonstrating that, in small populations, drift is more important than epistasis in increasing recombination, with this effect disappearing in larger finite populations. However, recent experimental evidence finds a greater advantage for recombination in larger populations. These results are reconciled by demonstrating through simulation without epistasis that for m loci recombination has an appreciable selective advantage over a range of population sizes (am, bm). bm increases steadily with m while am remains fairly static. Thus, however large the finite population, if selection acts on sufficiently many loci, an allele that increases recombination is selected for. We show that as selection acts on our finite population, recombination increases the variance in expected log fitness, causing indirect selection on a recombination-modifying locus. This effect is enhanced in those populations with more loci because the variance in phenotypic fitnesses in relation to the possible range will be smaller. Thus fixation of a particular haplotype is less likely to occur, increasing the advantage of recombination.


1998 ◽  
Vol 60 (9) ◽  
pp. 681-683 ◽  
Author(s):  
Timothy J. Maret ◽  
Steven W. Rissing

2021 ◽  
Author(s):  
Charles H. Pence

Recent arguments concerning the nature of causation in evolutionary theory, now often known as the debate between the 'causalist' and 'statisticalist' positions, have involved answers to a variety of independent questions – definitions of key evolutionary concepts like natural selection, fitness, and genetic drift; causation in multi-level systems; or the nature of evolutionary explanations, among others. This Element offers a way to disentangle one set of these questions surrounding the causal structure of natural selection. Doing so allows us to clearly reconstruct the approach that some of these major competing interpretations of evolutionary theory have to this causal structure, highlighting particular features of philosophical interest within each. Further, those features concern problems not exclusive to the philosophy of biology. Connections between them and, in two case studies, contemporary metaphysics and philosophy of physics demonstrate the potential value of broader collaboration in the understanding of evolution.


Parasitology ◽  
1983 ◽  
Vol 86 (2) ◽  
pp. 335-344 ◽  
Author(s):  
D. J. Minchella ◽  
P. T. Loverde

SUMMARYA method of interrupting the life-cycle of the human blood fluke Schistosoma by increasing the proportion of genetically insusceptible intermediate host snails in natural populations was first proposed nearly 25 years ago. The method assumes that insusceptible snails will be at a selective advantage over susceptible snails when the schistosome parasite is present, and therefore natural selection will act to increase the proportion of alleles for insusceptibility. A major objection to the proposed technique is ‘If insusceptible snails are at a selective advantage, then why are they not predominant in natural populations that transmit disease?’ One explanation of this paradox is that insusceptibility may be associated with a disadvantageous character or a physiological defect. This study tests this hypothesis by measuring the relative reproductive success of susceptible and insusceptible snails under controlled conditions. Results indicate that insusceptible (unsuitable) snails are negatively affected in the presence of either susceptible snails or schistosome parasites. Furthermore, in the presence of both susceptible snails and schistosome parasites, insusceptible snails are selectively disadvantaged compared to susceptible snails. These results obtained under laboratory-controlled conditions suggest a plausible answer as to why insusceptible snails are not predominant in natural populations that transmit disease.


2018 ◽  
Author(s):  
Antonios Kioukis ◽  
Pavlos Pavlidis

The evolution of a population by means of genetic drift and natural selection operating on a gene regulatory network (GRN) of an individual has not been scrutinized in depth. Thus, the relative importance of various evolutionary forces and processes on shaping genetic variability in GRNs is understudied. Furthermore, it is not known if existing tools that identify recent and strong positive selection from genomic sequences, in simple models of evolution, can detect recent positive selection when it operates on GRNs. Here, we propose a simulation framework, called EvoNET, that simulates forward-in-time the evolution of GRNs in a population. Since the population size is finite, random genetic drift is explicitly applied. The fitness of a mutation is not constant, but we evaluate the fitness of each individual by measuring its genetic distance from an optimal genotype. Mutations and recombination may take place from generation to generation, modifying the genotypic composition of the population. Each individual goes through a maturation period, where its GRN reaches equilibrium. At the next step, individuals compete to produce the next generation. As time progresses, the beneficial genotypes push the population higher in the fitness landscape. We examine properties of the GRN evolution such as robustness against the deleterious effect of mutations and the role of genetic drift. We confirm classical results from Andreas Wagner’s work that GRNs show robustness against mutations and we provide new results regarding the interplay between random genetic drift and natural selection.


2016 ◽  
Author(s):  
Stephen R. Doyle ◽  
Catherine Bourguinat ◽  
Hugues C. Nana-Djeunga ◽  
Jonas A. Kengne-Ouafo ◽  
Sébastien D.S. Pion ◽  
...  

ABSTRACTBackgroundTreatment of onchocerciasis using mass ivermectin administration has reduced morbidity and transmission throughout Africa and Central/South America. Mass drug administration is likely to exert selection pressure on parasites, and phenotypic and genetic changes in several Onchocerca volvulus populations from Cameroon and Ghana - exposed to more than a decade of regular ivermectin treatment - have raised concern that sub-optimal responses to ivermectin’s anti-fecundity effect are becoming more frequent and may spread.Methodology/Principal FindingsPooled next generation sequencing (Pool-seq) was used to characterise genetic diversity within and between 108 adult female worms differing in ivermectin treatment history and response. Genome-wide analyses revealed genetic variation that significantly differentiated good responder (GR) and sub-optimal responder (SOR) parasites. These variants were not randomly distributed but clustered in ~31 quantitative trait loci (QTLs), with little overlap in putative QTL position and gene content between countries. Published candidate ivermectin SOR genes were largely absent in these regions; QTLs differentiating GR and SOR worms were enriched for genes in molecular pathways associated with neurotransmission, development, and stress responses. Finally, single worm genotyping demonstrated that geographic isolation and genetic change over time (in the presence of drug exposure) had a significantly greater role in shaping genetic diversity than the evolution of SOR.Conclusions/SignificanceThis study is one of the first genome-wide association analyses in a parasitic nematode, and provides insight into the genomics of ivermectin response and population structure of O. volvulus. We argue that ivermectin response is a polygenically-determined quantitative trait in which identical or related molecular pathways but not necessarily individual genes likely determine the extent of ivermectin response in different parasite populations. Furthermore, we propose that genetic drift rather than genetic selection of SOR is the underlying driver of population differentiation, which has significant implications for the emergence and potential spread of SOR within and between these parasite populations.Author summaryOnchocerciasis is a human parasitic disease endemic across large areas of Sub-Saharan Africa, where more that 99% of the estimated 100 million people globally at-risk live. The microfilarial stage of Onchocerca volvulus causes pathologies ranging from mild itching to visual impairment and ultimately, irreversible blindness. Mass administration of ivermectin kills microfilariae and has an anti-fecundity effect on adult worms by temporarily inhibiting the development in utero and/or release into the skin of new microfilariae, thereby reducing morbidity and transmission. Phenotypic and genetic changes in some parasite populations that have undergone multiple ivermectin treatments in Cameroon and Ghana have raised concern that sub-optimal response to ivermectin’s anti-fecundity effect may increase in frequency, reducing the impact of ivermectin-based control measures. We used next generation sequencing of small pools of parasites to define genome-wide genetic differences between phenotypically characterised good and sub-optimal responder parasites from Cameroon and Ghana, and identified multiple genomic regions differentiating the response types. These regions were largely different between parasites from both countries but revealed common molecular pathways that might be involved in determining the extent of response to ivermectin’s anti-fecundity effect. These data reveal a more complex than previously described pattern of genetic diversity among O. volvulus populations that differ in their geography and response to ivermectin treatment.


Author(s):  
Christian M. Reidys

The fundamental mechanisms of biological evolution have fascinated generations of researchers and remain popular to this day. The formulation of such a theory goes back to Darwin (1859), who in the The Origin of Species presented two fundamental principles: genetic variability caused by mutation, and natural selection. The first principle leads to diversity and the second one to the concept of survival of the fittest, where fitness is an inherited characteristic property of an individual and can basically be identified with its reproduction rate. Wright [530, 531] first recognized the importance of genetic drift in evolution in improving the evolutionary search capacity of the whole population. He viewed genetic drift merely as a process that could improve evolutionary search. About a decade later, Kimura proposed [317] that the majority of changes that are observed in evolution at the molecular level are the results of random drift of genotypes. The neutral theory of Kimura does not deny that selection plays a role, but claims that no appreciable fraction of observable molecular change can be caused by selective forces: mutations are either a disadvantage or, at best, neutral in present day organisms. Only negative selection plays a major role in the neutral evolution, in that deleterious mutants die out due to their lower fitness. Over the last few decades, there has been a shift of emphasis in the study of evolution. Instead of focusing on the differences in the selective value of mutants and on population genetics, interest has moved to evolution through natural selection as an abstract optimization problem. Given the tremendous opportunities that computer science and the physical sciences now have for contributing to the study of biological phenomena, it is fitting to study the evolutionary optimization problem in the present volume. In this chapter, we adopt the following framework: assuming that selection acts exclusively upon isolated phenotypes, we introduce the following compositum of mappings . . . Genotypes→ Phenotypes →Fitness . . . . We will refer to the first map as to the genotype-phenotype map and call the preimage of a given phenotype its neutral network. Clearly, the main ingredients here are the phenotypes and genotypes and their respective organization. In the following we will study various combinatorial properties of phenotypes and genotypes for RNA folding maps.


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