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Fisher's Model (fisher + model)
Selected AbstractsNon-homogeneous infinitely many sites discrete-time model with exact coalescentMATHEMATICAL METHODS IN THE APPLIED SCIENCES, Issue 6 2010Adam Bobrowski Abstract Kingman's coalescent is among the most fertile concepts in mathematical population genetics. However, it only approximates the exact coalescent process associated with the Wright,Fisher model, in which the ancestry of a sample does not have to be a binary tree. The distinction between the approximate and exact coalescent becomes important when population size is small and time has to be measured in discrete units (generations). In the present paper, we explore the exact coalescent, with mutations following the infinitely many sites model. The methods used involve random point processes and generating functionals. This allows obtaining joint distributions of segregating sites in arbitrary intervals or collections of intervals, and generally in arbitrary Borel subsets of two or more chromosomes. Using this framework it is possible to find the moments of the numbers of segregating sites on pairs of chromosomes, as well as the moments of the average of the number of pairwise differences, in the form that is more general than usually. In addition, we demonstrate limit properties of the first two moments under a range of demographic scenarios, including different patterns of population growth. This latter part complements results obtained earlier for Kingman's coalescent. Finally, we discuss various applications, including the analysis of fluctuation experiments, from which mutation rates of biological cells can be inferred. Copyright © 2009 John Wiley & Sons, Ltd. [source] A GENERAL MULTIVARIATE EXTENSION OF FISHER'S GEOMETRICAL MODEL AND THE DISTRIBUTION OF MUTATION FITNESS EFFECTS ACROSS SPECIESEVOLUTION, Issue 5 2006Guillaume Martin Abstract The evolution of complex organisms is a puzzle for evolutionary theory because beneficial mutations should be less frequent in complex organisms, an effect termed "cost of complexity." However, little is known about how the distribution of mutation fitness effects (f(s)) varies across genomes. The main theoretical framework to address this issue is Fisher's geometric model and related phenotypic landscape models. However, it suffers from several restrictive assumptions. In this paper, we intend to show how several of these limitations may be overcome. We then propose a model of f(s) that extends Fisher's model to account for arbitrary mutational and selective interactions among n traits. We show that these interactions result in f(s) that would be predicted by a much smaller number of independent traits. We test our predictions by comparing empirical f(s) across species of various gene numbers as a surrogate to complexity. This survey reveals, as predicted, that mutations tend to be more deleterious, less variable, and less skewed in higher organisms. However, only limited difference in the shape of f(s) is observed from Escherichia coli to nematodes or fruit flies, a pattern consistent with a model of random phenotypic interactions across many traits. Overall, these results suggest that there may be a cost to phenotypic complexity although much weaker than previously suggested by earlier theoretical works. More generally, the model seems to qualitatively capture and possibly explain the variation of f(s) from lower to higher organisms, which opens a large array of potential applications in evolutionary genetics. [source] COMPENSATING FOR OUR LOAD OF MUTATIONS: FREEZING THE MELTDOWN OF SMALL POPULATIONSEVOLUTION, Issue 5 2000Art Poon Abstract We have investigated the reduction of fitness caused by the fixation of new deleterious mutations in small populations within the framework of Fisher's geometrical model of adaptation. In Fisher's model, a population evolves in an n -dimensional character space with an adaptive optimum at the origin. The model allows us to investigate compensatory mutations, which restore fitness losses incurred by other mutations, in a context-dependent manner. We have conducted a moment analysis of the model, supplemented by the numerical results of computer simulations. The mean reduction of fitness (i.e., expected load) scaled to one is approximately n/(n + 2Ne), where Ne is the effective population size. The reciprocal relationship between the load and Ne implies that the fixation of deleterious mutations is unlikely to cause extinction when there is a broad scope for compensatory mutations, except in very small populations. Furthermore, the dependence of load on n implies that pleiotropy plays a large role in determining the extinction risk of small populations. Differences and similarities between our results and those of a previous study on the effects of Ne and n are explored. That the predictions of this model are qualitatively different from studies ignoring compensatory mutations implies that we must be cautious in predicting the evolutionary fate of small populations and that additional data on the nature of mutations is of critical importance. [source] ADAPTATION AND THE COST OF COMPLEXITYEVOLUTION, Issue 1 2000H. Allen Orr Abstract., Adaptation is characterized by the movement of a population toward a many-character optimum, movement that results in an increase in fitness. Here I calculate the rate at which fitness increases during adaptation and describe the curve giving fitness versus time as a population approaches an optimum in Fisher's model of adaptation. The results identify several factors affecting the speed of adaptation. One of the most important is organismal complexity,complex organisms adapt more slowly than simple ones when using mutations of the same phenotypic size. Thus, as Fisher foresaw, organisms pay a kind of cost of complexity. However, the magnitude of this cost is considerably larger than Fisher's analysis suggested. Indeed the rate of adaptation declines at least as fast as n -1, where n is the number of independent characters or dimensions comprising an organism. The present results also suggest that one can define an effective number of dimensions characterizing an adapting species. [source] The role of hybridization in evolutionMOLECULAR ECOLOGY, Issue 3 2001N. H. Barton Abstract Hybridization may influence evolution in a variety of ways. If hybrids are less fit, the geographical range of ecologically divergent populations may be limited, and prezygotic reproductive isolation may be reinforced. If some hybrid genotypes are fitter than one or both parents, at least in some environments, then hybridization could make a positive contribution. Single alleles that are at an advantage in the alternative environment and genetic background will introgress readily, although such introgression may be hard to detect. ,Hybrid speciation', in which fit combinations of alleles are established, is more problematic; its likelihood depends on how divergent populations meet, and on the structure of epistasis. These issues are illustrated using Fisher's model of stabilizing selection on multiple traits, under which reproductive isolation evolves as a side-effect of adaptation in allopatry. This confirms a priori arguments that while recombinant hybrids are less fit on average, some gene combinations may be fitter than the parents, even in the parental environment. Fisher's model does predict heterosis in diploid F1s, asymmetric incompatibility in reciprocal backcrosses, and (when dominance is included) Haldane's Rule. However, heterosis arises only when traits are additive, whereas the latter two patterns require dominance. Moreover, because adaptation is via substitutions of small effect, Fisher's model does not generate the strong effects of single chromosome regions often observed in species crosses. [source] | ||||||||||