Aneil F. Agrawal

ESTIMATING NONLINEAR SELECTION GRADIENTS USING QUADRATIC REGRESSION COEFFICIENTS: DOUBLE OR NOTHING?

Abstract The use of regression analysis has been instrumental in allowing evolutionary biologists to estimate the strength and mode of natural selection. Although directional and correlational selection gradients are equal to their corresponding regression coefficients, quadratic regression coefficients must be doubled to estimate stabilizing/disruptive selection gradients. Based on a sample of 33 papers published in Evolution between 2002 and 2007, at least 78% of papers have not doubled quadratic regression coefficients, leading to an appreciable underestimate of the strength of stabilizing and disruptive selection. Proper treatment of quadratic regression coefficients is necessary for estimation of fitness surfaces and contour plots, canonical analysis of the γ matrix, and modeling the evolution of populations on an adaptive landscape.

PURGING THE GENOME WITH SEXUAL SELECTION: REDUCING MUTATION LOAD THROUGH SELECTION ON MALES

Healthy males are likely to have higher mating success than unhealthy males because of differential expression of condition-dependent 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.

How much do genetic covariances alter the rate of adaptation

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.

Evolution of Sex: Why Do Organisms Shuffle Their Genotypes?

Sexual processes alter associations among alleles. To understand the evolution of sex, we need to know both the short-term and long-term consequences of changing these genetic associations. Ultimately, we need to identify which evolutionary forces--for example, selection, genetic drift, migration--are responsible for building the associations affected by sex.

Higher rates of sex evolve in spatially heterogeneous environments

The evolution and maintenance of sexual reproduction has puzzled biologists for decades. Although this field is rich in hypotheses, experimental evidence is scarce. Some important experiments have demonstrated differences in evolutionary rates between sexual and asexual populations; other experiments have documented evolutionary changes in phenomena related to genetic mixing, such as recombination and selfing. However, direct experiments of the evolution of sex within populations are extremely rare (but see ref. 12). Here we use the rotifer, Brachionus calyciflorus, which is capable of both sexual and asexual reproduction, to test recent theory predicting that there is more opportunity for sex to evolve in spatially heterogeneous environments. Replicated experimental populations of rotifers were maintained in homogeneous environments, composed of either high- or low-quality food habitats, or in heterogeneous environments that consisted of a mix of the two habitats. For populations maintained in either type of homogeneous environment, the rate of sex evolves rapidly towards zero. In contrast, higher rates of sex evolve in populations experiencing spatially heterogeneous environments. The data indicate that the higher level of sex observed under heterogeneity is not due to sex being less costly or selection against sex being less efficient; rather sex is sufficiently advantageous in heterogeneous environments to overwhelm its inherent costs. Counter to some alternative theories for the evolution of sex, there is no evidence that genetic drift plays any part in the evolution of sex in these populations.

The evolution of sex is favoured during adaptation to new environments

In experiments with a facultatively sexual rotifer, populations adapting to novel environments evolve higher rates of sex because sexual mixing quickly assembles well-adapted genotypes.

On Indirect Genetic Effects in Structured Populations

Indirect genetic effects (IGEs) occur when the phenotype of an individual, and possibly its fitness, depends, at least in part, on the genes of its social partners. The effective result is that environmental sources of phenotypic variance can themselves evolve. Simple models have shown that IGEs can alter the rate and direction of evolution for traits involved in interactions. Here we expand the applicability of the theory of IGEs to evolution in metapopulations by including nonlinear interactions between individuals and population genetic structure. Although population subdivision alone generates some dramatic and nonintuitive evolutionary dynamics for interacting phenotypes, the combination of nonlinear interactions with subdivision reveals an even greater importance of IGEs. The presence of genetic structure links the evolution of interacting phenotypes and the traits that influence their expression (“effector traits”) even in the absence of genetic correlations. When nonlinear social effects occur in subdivided populations, evolutionary response is altered and can even oppose the direction expected due to direct selection. Because population genetic structure allows for multilevel selection, we also investigate the role of IGEs in determining the response to individual and group selection. We find that nonlinear social effects can cause interference between levels of selection even when they act in the same direction. In some cases, interference can be so extreme that the actual evolutionary response to multilevel selection is opposite in direction to that predicted by summing selection at each level. This theoretical result confirms empirical data that show higher levels of selection cannot be ignored even when selection acts in the same direction at all levels.

Environmental duress and epistasis: how does stress affect the strength of selection on new mutations?

To an evolutionary geneticist, the most important property of a new mutation is its effect on fitness. Stress is a reduction in fitness that can also alter the selection on new mutations. Although the effects of environmental and genetic stresses are typically studied separately, it is useful to consider them from the same perspective. Here we evaluate the common perception that stress increases selection. We consider various conceptual paradigms for thinking about selection and stress, and then review the empirical data. We reject the notion that stress typically increases selection. Instead, we find that different types of stresses affect selection differently, though the underlying mechanisms are, as yet, unclear in most cases.

Inferences about the distribution of dominance drawn from yeast gene knockout data.

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.

PARASITES AND THE EVOLUTION OF SELF‐FERTILIZATION

Abstract.— Assuming all else is equal, an allele for selfing should spread when rare in an outcrossing population and rapidly reach fixation. Such an allele will not spread, however, if self‐fertilization results in inbreeding depression so severe that the fitness of selfed offspring is less that half that of outcrossed offspring. Here we consider an ecological force that may also counter the spread of a selfing allele: coevolution with parasites. Computer simulations were conducted for four different genetic models governing the details of infection. Within each of these models, we varied both the level of selfing in the parasite and the level of male‐gamete discounting in the host (i.e., the reduction in outcrossing fitness through male function due to the selfing allele). We then sought the equilibrium level of host selfing under the different conditions. The results show that, over a wide range of conditions, parasites can select for host reproductive strategies in which both selfed and outcrossed progeny are produced (mixed mating). In addition, mixed mating, where it exits, tends to be biased toward selfing.