Healthy males are likely to have higher mating success than unhealthy males because of differential expression of conditiondependent traits such as mate searching intensity, fighting ability, display vigor, and some types of exaggerated morphological characters. We therefore expect that most new mutations that are deleterious for overall fitness may also be deleterious for male mating success. From this perspective, sexual selection is not limited to influencing those genes directly involved in exaggerated morphological traits but rather affects most, if not all, genes in the genome. If true, sexual selection can be an important force acting to reduce the frequency of deleterious mutations and, as a result, mutation load. We review the literature and find various forms of indirect evidence that sexual selection helps to eliminate deleterious mutations. However, direct evidence is scant, and there are almost no data available to address a key issue: is selection in males stronger than selection in females? In addition, the total effect of sexual selection on mutation load is complicated by possible increases in mutation rate that may be attributable to sexual selection. Finally, sexual selection affects population fitness not only through mutation load but also through sexual conflict, making it difficult to empirically measure how sexual selection affects load. Several lines of enquiry are suggested to better fill large gaps in our understanding of sexual selection and its effect on genetic load. K E Y W O R D S : Condition, male mating success, mean fitness, mutation load, sexual selection, vigor.

No abstract

Genetically correlated traits do not evolve independently, and the covariances between traits affect the rate at which a population adapts to a specified selection regime. To measure the impact of genetic covariances on the rate of adaptation, we compare the rate fitness increases given the observed G matrix to the expected rate if all the covariances in the G matrix are set to zero. Using data from the literature, we estimate the effect of genetic covariances in real populations. We find no net tendency for covariances to constrain the rate of adaptation, though the quality and heterogeneity of the data limit the certainty of this result. There are some examples in which covariances strongly constrain the rate of adaptation but these are balanced by counter examples in which covariances facilitate the rate of adaptation; in many cases, covariances have little or no effect. We also discuss how our metric can be used to identify traits or suites of traits whose genetic covariances to other traits have a particularly large impact on the rate of adaptation.

The maintenance of sexual reproduction is a problem in evolutionary theory because, all else being equal, asexual populations have a twofold fitness advantage over their sexual counterparts and should rapidly outnumber a sexual population because every individual has the potential to reproduce. The twofold cost of sex exists because of anisogamy or gamete dimorphism-egg-producing females make a larger contribution to the zygote compared with the small contribution made by the sperm of males, but both males and females contribute 50% of the genes. Anisogamy also generates the conditions for sexual selection, a powerful evolutionary force that does not exist in asexual populations. The continued prevalence of sexual reproduction indicates that the 'all else being equal' assumption is incorrect. Here I show that sexual selection can mitigate or even eliminate the cost of sex. If sexual selection causes deleterious mutations to be more deleterious in males than females, then deleterious mutations are maintained at lower equilibrium frequency in sexual populations relative to asexual populations. The fitness of sexual females is higher than asexuals because there is no difference in the fecundity of sexual females and asexuals of the same genotype, but the equilibrium frequency of deleterious mutations is lower in sexual populations. The results are not altered by synergistic epistasis in males.

No abstract

Data from several thousand knockout mutations in yeast (Saccharomyces cerevisiae) were used to estimate the distribution of dominance coefficients. We propose a new unbiased likelihood approach to measuring dominance coefficients. On average, deleterious mutations are partially recessive, with a mean dominance coefficient $0.2. Alleles with large homozygous effects are more likely to be more recessive than are alleles of weaker effect. Our approach allows us to quantify, for the first time, the substantial variance and skew in the distribution of dominance coefficients. This heterogeneity is so great that many population genetic processes analyses based on the mean dominance coefficient alone will be in substantial error. These results are applied to the debate about various mechanisms for the evolution of dominance, and we conclude that they are most consistent with models that depend on indirect selection on homeostatic gene expression or on the ability to perform well under periods of high demand for a protein.

Many multicellular eukaryotes have reasonably high per-generation mutation rates. Consequently, most populations harbor an abundance of segregating deleterious alleles. These alleles, most of which are of small effect individually, collectively can reduce substantially the fitness of individuals relative to what it would be otherwise; this is mutation load. Mutation load can be lessened by any factor that causes more mutations to be removed per selective death, such as inbreeding, synergistic epistasis, population structure, or harsh environments. The ecological effects of load are not clear-cut because some conditions (such as selection early in life, sexual selection, reproductive compensation, and intraspecific competition) reduce the effects of load on population size and persistence, but other conditions (such as interspecific competition and load on resource use efficiency) can cause small amounts of load to have strong effects on the population, even extinction. We suggest a series of studies to improve our understanding of the effects of mutation load.

Whether the changes brought about by sexual selection are, on the whole, congruent or incongruent with the changes favored by natural selection is a fundamentally important question in evolutionary biology. Although a number of theoretical models have assumed that sexual selection reinforces natural selection [1, 2], others assume these forces are in opposition [3-5]. Empirical results have been mixed (see reviews in [1, 6-8]) and the reasons for the differences among studies are unclear. Variable outcomes are expected if populations differ in their evolutionary histories and therefore harbor different amounts and types of segregating genetic variation. Here, we constructed populations of Drosophila melanogaster that differed in this regard to directly test this hypothesis. In well-adapted populations, sexually successful males sired unfit daughters, indicating sexual and natural selection are in conflict. However, in populations containing an influx of maladaptive alleles, attractive males sired offspring of high fitness, suggesting that sexual selection reinforces natural selection. Taken together, these results emphasize the importance of evolutionary history on the outcome of sexual selection. Consequently, studies based on laboratory populations, cultured for prolonged periods under homogeneous conditions, may provide a skewed perspective on the relationship between sexual and natural selection.