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N H Barton

Publications and source records attributed to N H Barton.

At least 55 records · Page 3Linked to original sources
PubMed1996

Natural selection and random genetic drift as causes of evolution on islands.

The evolutionary processes responsible for adaptation and speciation on islands differ in several ways from those on the mainland. Most attention has been given to the random genetic drift that arises when a population is founded from just a few colonizing genomes. Theoretical obstacles to "founder effect speciation' are discussed, together with recent proposals for avoiding them. It is argued that although certain kinds of epistasis can facilitate the evolution of strong reproductive isolation, this favours divergence by selection as much as by random drift.

Alleles↗
PubMed1996

Recombination load associated with selection for increased recombination.

Experiments on Drosophila suggest that genetic recombination may result in lowered fitness of progeny (a 'recombination load'). This has been interpreted as evidence either for a direct effect of recombination on fitness, or for the maintenance of linkage disequilibria by epistatic selection. Here we show that such a recombination load is to be expected even if selection favours increased genetic recombination. This is because of the fact that, although a modifier may suffer an immediate loss of fitness if it increases recombination, it eventually becomes associated with a higher additive genetic variance in fitness, which allows a faster response to direction selection. This argument applies to mutation-selection balance with synergistic epistasis, directional selection on quantitative traits, and ectopic exchange among transposable elements. Further experiments are needed to determine whether the selection against recombination due to the immediate load is outweighed by the increased additive variance in fitness produced by recombination.

Animals↗
PubMed1995

Genealogies and geography.

Any sample of genes traces back to a single common ancestor. Each gene also has other properties: its sequence, its geographic location and the phenotype and fitness of the organism that carries it. With sexual reproduction, different genes have different genealogies, which gives us much more information, but also greatly complicates population genetic analysis. We review the close relation between the distribution of genealogies and the classic theory of identity by descent in spatially structured populations, and develop a simple diffusion approximation to the distribution of coalescence times in a homogeneous two-dimensional habitat. This shows that when neighbourhood size is large (as in most populations) only a small fraction of pairs of genes are closely related, and only this fraction gives information about current rates of gene flow. The increase of spatial dispersion with lineage age is thus a poor estimator of gene flow. The bulk of the genealogy depends on the long-term history of the population; we discuss ways of inferring this history from the concordance between genealogies across loci.

Gene Frequency↗
PubMed1995

A general model for the evolution of recombination.

A general representation of multilocus selection is extended to allow recombination to depend on genotype. The equations simplify if modifier alleles have small effects on recombination. The evolution of such modifiers only depends on how they alter recombination between the selected loci, and does not involve dominance in modifier effects. The net selection on modifiers can be found explicitly if epistasis is weak relative to recombination. This analysis shows that recombination can be favoured in two ways: because it impedes the response to epistasis which fluctuates in sign, or because it facilitates the response to directional selection. The first mechanism is implausible, because epistasis must change sign over periods of a few generations: faster or slower fluctuations favour reduced recombination. The second mechanism requires weak negative epistasis between favourable alleles, which may either be increasing, or held in check by mutation. The selection (si) on recombination modifiers depends on the reduction in additive variance of log(fitness) due to linkage disequilibria (v1 < O), and on non-additive variance in log(fitness) (V'2, V'3.. for epistasis between 2, 3.. loci). For unlinked loci and pairwise epistasis, si = --(v1 +4V2/3)deltar, where deltar is the average increase in recombination caused by the modifier. The approximations are checked against exact calculations for three loci, and against Charlesworth's analyses of mutation/selection balance (1990), and directional selection (1993). The analysis demonstrates a general relation between selection on recombination and observable components of fitness variation, which is open to experimental test.

Biological Evolution↗
PubMed1995

Linkage and the limits to natural selection.

The probability of fixation of a favorable mutation is reduced if selection at other loci causes inherited variation in fitness. A general method for calculating the fixation probability of an allele that can find itself in a variety of genetic backgrounds is applied to find the effect of substitutions, fluctuating polymorphisms, and deleterious mutations in a large population. With loose linkage, r, the effects depend on the additive genetic variance in relative fitness, var(W), and act by reducing effective population size by (N/Ne) = 1 + var(W)/2r2. However, tightly linked loci can have a substantial effect not predictable from Ne. Linked deleterious mutations reduce the fixation probability of weakly favored alleles by exp (-2U/R), where U is the total mutation rate and R is the map length in Morgans. Substitutions can cause a greater reduction: an allele with advantage s < scrit = (pi 2/6) loge (S/s) [var(W)/R] is very unlikely to be fixed. (S is the advantage of the substitution impeding fixation.) Fluctuating polymorphisms at many (n) linked loci can also have a substantial effect, reducing fixation probability by exp [square root of 2Kn var(W)/R] [K = -1/E((u-u)2/uv) depending on the frequencies (u,v) at the selected polymorphisms]. Hitchhiking due to all three kinds of selection may substantially impede adaptation that depends on weakly favored alleles.

Genetic Linkage↗
PubMed1994

Genetic and statistical analyses of strong selection on polygenic traits: what, me normal?

We develop a general population genetic framework for analyzing selection on many loci, and apply it to strong truncation and disruptive selection on an additive polygenic trait. We first present statistical methods for analyzing the infinitesimal model, in which offspring breeding values are normally distributed around the mean of the parents, with fixed variance. These show that the usual assumption of a Gaussian distribution of breeding values in the population gives remarkably accurate predictions for the mean and the variance, even when disruptive selection generates substantial deviations from normality. We then set out a general genetic analysis of selection and recombination. The population is represented by multilocus cumulants describing the distribution of haploid genotypes, and selection is described by the relation between mean fitness and these cumulants. We provide exact recursions in terms of generating functions for the effects of selection on non-central moments. The effects of recombination are simply calculated as a weighted sum over all the permutations produced by meiosis. Finally, the new cumulants that describe the next generation are computed from the non-central moments. Although this scheme is applied here in detail only to selection on an additive trait, it is quite general. For arbitrary epistasis and linkage, we describe a consistent infinitesimal limit in which the short-term selection response is dominated by infinitesimal allele frequency changes and linkage disequilibria. Numerical multilocus results show that the standard Gaussian approximation gives accurate predictions for the dynamics of the mean and genetic variance in this limit. Even with intense truncation selection, linkage disequilibria of order three and higher never cause much deviation from normality. Thus, the empirical deviations frequently found between predicted and observed responses to artificial selection are not caused by linkage-disequilibrium-induced departures from normality. Disruptive selection can generate substantial four-way disequilibria, and hence kurtosis; but even then, the Gaussian assumption predicts the variance accurately. In contrast to the apparent simplicity of the infinitesimal limit, data suggest that changes in genetic variance after 10 or more generations of selection are likely to be dominated by allele frequency dynamics that depend on genetic details.

Fourier Analysis↗
PubMed1993

Optimality, mutation and the evolution of ageing.

Evolutionary explanations of ageing fall into two classes. Organisms might have evolved the optimal life history, in which survival and fertility late in life are sacrificed for the sake of early reproduction and survival. Alternatively, the life history might be depressed below this optimal compromise by deleterious mutations: because selection against late-acting mutations is weaker, these will impose a greater load on late life. Evidence for the importance of both is emerging, and unravelling their relative importance presents experimentalists with a major challenge.

Adult↗
PubMed1993

Evolution of aging: testing the theory using Drosophila.

Evolutionary explanations of aging (or senescence) fall into two classes. First, organisms might have evolved the optimal life history, in which survival and fertility late in life are sacrificed for the sake of early reproduction or high pre-adult survival. Second, the life history might be depressed below this optimal compromise by the influx of deleterious mutations; since selection against late-acting mutations is weaker, deleterious mutations will impose a greater load on late life. We discuss ways in which these theories might be investigated and distinguished, with reference to experimental work with Drosophila. While genetic correlations between life history traits determine the immediate response to selection, they are hard to measure, and may not reflect the fundamental constraints on life history. Long term selection experiments are more likely to be informative. The third approach of using experimental manipulations suffers from some of the same problems as measures of genetic correlations; however, these two approaches may be fruitful when used together. The experimental results so far suggest that aging in Drosophila has evolved in part as a consequence of selection for an optimal life history, and in part as a result of accumulation of predominantly late-acting deleterious mutations. Quantification of these effects presents a major challenge for the future.

Aging↗
PubMed1991

Natural and sexual selection on many loci.

A method is developed that describes the effects on an arbitrary number of autosomal loci of selection on haploid and diploid stages, of nonrandom mating between haploid individuals, and of recombination. We provide exact recursions for the dynamics of allele frequencies and linkage disequilibria (nonrandom associations of alleles across loci). When selection is weak relative to recombination, our recursions provide simple approximations for the linkage disequilibria among arbitrary combinations of loci. We show how previous models of sex-independent natural selection on diploids, assortative mating between haploids, and sexual selection on haploids can be analyzed in this framework. Using our weak-selection approximations, we derive new results concerning the coevolution of male traits and female preferences under natural and sexual selection. In particular, we provide general expressions for the intensity of linkage-disequilibrium induced selection experienced by loci that contribute to female preferences for specific male traits. Our general results support the previous observation that these indirect selection forces are so weak that they are unlikely to dominate the evolution of preference-producing loci.

Animals↗
PubMed1990

Pleiotropic models of quantitative variation.

It is widely held that each gene typically affects many characters, and that each character is affected by many genes. Moreover, strong stabilizing selection cannot act on an indefinitely large number of independent traits. This makes it likely that heritable variation in any one trait is maintained as a side effect of polymorphisms which have nothing to do with selection on that trait. This paper examines the idea that variation is maintained as the pleiotropic side effect of either deleterious mutation, or balancing selection. If mutation is responsible, it must produce alleles which are only mildly deleterious (s approximately 10(-3)), but nevertheless have significant effects on the trait. Balancing selection can readily maintain high heritabilities; however, selection must be spread over many weakly selected polymorphisms if large responses to artificial selection are to be possible. In both classes of pleiotropic model, extreme phenotypes are less fit, giving the appearance of stabilizing selection on the trait. However, it is shown that this effect is weak (of the same order as the selection on each gene): the strong stabilizing selection which is often observed is likely to be caused by correlations with a limited number of directly selected traits. Possible experiments for distinguishing the alternatives are discussed.

Alleles↗
PubMed1989

Adaptation, speciation and hybrid zones.

Many species are divided into a mosaic of genetically distinct populations, separated by narrow zones of hybridization. Studies of hybrid zones allow us to quantify the genetic differences responsible for speciation, to measure the diffusion of genes between diverging taxa, and to understand the spread of alternative adaptations.

Adaptation, Physiological↗
PubMed1987

The frequency of shifts between alternative equilibria.

We derive a formula giving the frequency with which random drift shifts a population between alternative equilibria. This formula is valid when such shifts are rare (Ns much greater than 1), and applies over a wide range of mutation rates. When the number of mutations entering the population is low (4 N mu much less than 1), the rate of stochastic shifts reduces to the product of the mutation rate and the probability of fixation of a single mutation. However, when many mutations enter the population in each generation (4 N mu much greater than 1), the rate is higher than would be expected if mutations were established independently, and converges to that given by a gaussian approximation. We apply recent results on bistable systems to extend this formula to the general multidimensional case. This gives an explicit expression for the frequency of stochastic shifts, which depends only on the equilibrium probability distribution near the saddle point separating the alternative stable states. The plausibility of theories of speciation through random drift are discussed in the light of these results.

Adaptation, Biological↗