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Local adaptation and sexual dimorphism are iconic evolutionary scenarios of intraspecific adaptive differentiation in the face of gene flow. Although theory has traditionally considered local adaptation and sexual dimorphism as conceptually distinct processes, emerging data suggest that they often act concurrently during evolutionary diversification. Here, I merge theories of local adaptation in space and sex-specific adaptation over time, and show that their confluence yields several new predictions about the roles of context-specific selection, migration, and genetic correlations, in adaptive diversification. I specifically revisit two influential predictions from classical studies of clinal adaptation and sexual dimorphism: (1) that local adaptation should decrease with distance from the species' range center and (2) that opposing directional selection between the sexes (sexual antagonism) should inevitably accompany the evolution of sexual dimorphism. I show that both predictions can break down under clinally varying selection. First, the geography of local adaptation can be sexually dimorphic, with locations of relatively high local adaptation differing profoundly between the sexes. Second, the intensity of sexual antagonism varies across the species' range, with subpopulations near the range center representing hotspots for antagonistic selection. The results highlight the context-dependent roles of migration versus sexual conflict as primary constraints to adaptive diversification.

Antagonistic selection between different fitness components (e.g., survival versus fertility) or different types of individuals in a population (e.g., females versus males) can potentially maintain genetic diversity and thereby account for the high levels of fitness variation observed in natural populations. However, the degree to which antagonistic selection can maintain genetic variation critically depends on the dominance relations between antagonistically selected alleles in diploid individuals. Conditions for stable polymorphism of antagonistically selected alleles are narrow, particularly when selection is weak, unless the alleles exhibit \"dominance reversals\"-in which each allele is partially or completely dominant in selective contexts in which it is favored and recessive in contexts in which it is harmful. Although theory predicts that dominance reversals should emerge under biologically plausible conditions, evidence for dominance reversals is sparse. In this primer, we review theoretical arguments and data supporting a role for dominance reversals in the maintenance of genetic variation. We then highlight an illuminating new study by Grieshop and Arnqvist, which reports a genome-wide signal of dominance reversals between male and female fitness in seed beetles.

Sex differences in the fitness effects of genetic variants can influence the rate of adaptation and the maintenance of genetic variation. For example, “sexually antagonistic” (SA) variants, which are beneficial for one sex and harmful for the other, can both constrain adaptation and increase genetic variability for fitness components such as survival, fertility, and disease susceptibility. However, detecting variants with sex-differential fitness effects is difficult, requiring genome sequences and fitness measurements from large numbers of individuals. Here, we develop new theory for studying sex-differential selection across a complete life cycle and test our models with genotypic and reproductive success data from approximately 250,000 UK Biobank individuals. We uncover polygenic signals of sex-differential selection affecting survival, reproductive success, and overall fitness, with signals of sex-differential reproductive selection reflecting a combination of SA polymorphisms and sexually concordant polymorphisms in which the strength of selection differs between the sexes. Moreover, these signals hold up to rigorous controls that minimise the contributions of potential confounders, including sequence mapping errors, population structure, and ascertainment bias. Functional analyses reveal that sex-differentiated sites are enriched in phenotype-altering genomic regions, including coding regions and loci affecting a range of quantitative traits. Population genetic analyses show that sex-differentiated sites exhibit evolutionary histories dominated by genetic drift and/or transient balancing selection, but not long-term balancing selection, which is consistent with theoretical predictions of effectively weak SA balancing selection in historically small populations. Overall, our results are consistent with polygenic sex-differential—including SA—selection in humans. Evidence for sex-differential selection is particularly strong for variants affecting reproductive success, in which the potential contributions of nonrandom sampling to signals of sex differentiation can be excluded.

Despite the pervasiveness of the world's biodiversity, no single species has a truly global distribution. In fact, most species have very restricted distributions. What limits species from expanding beyond their current geographic ranges? This has been classically treated by ecologists as an ecological problem and by evolutionary biologists as an evolutionary problem. Such a dichotomy is false-the problem of species' ranges sits firmly within the realm of evolutionary ecology. In support of this view, Polechová presents new theory that explains species' range limits with reference to two key factors central to both ecological and evolutionary theory-migration and population size. This new model sets the scene for empirical tests of range limit theory and builds the case for assisted gene flow as a key management tool for threatened species.

Frequency‐dependent (FD) selection is a central process maintaining genetic variation and mediating evolution of population fitness. FD selection has attracted interest from researchers in a wide range of biological subdisciplines, including evolutionary genetics, behavioural ecology and, more recently, community ecology. However, the implications of frequency dependence for applied biological problems, particularly maladaptation, biological conservation and evolutionary rescue remain underexplored. The neglect of FD selection in conservation is particularly unfortunate. Classical theory, dating back to the 1940s, demonstrated that frequency dependence can either increase or decrease population fitness. These evolutionary consequences of FD selection are relevant to modern concerns about population persistence and the capacity of evolution to alleviate extinction risks. But exactly when should we expect FD selection to increase versus decrease absolute fitness and population growth? And how much of an impact is FD selection expected to have on population persistence versus extinction in changing environments? The answers to these questions have implications for evolutionary rescue under climate change and may inform strategies for managing threatened populations. Here, we revisit the core theory of FD selection, reviewing classical single‐locus models of population genetic change and outlining short‐ and long‐run consequences of FD selection for the evolution of population fitness. We then develop a quantitative genetic model of evolutionary rescue in a deteriorating environment, with population persistence hinging upon the evolution of a quantitative trait subject to both frequency‐dependent and frequency‐independent natural selection. We discuss the empirical literature pertinent to this theory, which supports key assumptions of our model. We show that FD selection can promote population persistence when it aligns with the direction of frequency‐independent selection imposed by abiotic environmental conditions. However, under most scenarios of environmental change, FD selection limits a population's evolutionary responsiveness to changing conditions and narrows the rate of environmental change that is evolutionarily tolerable.

Adaptation is the central feature and leading explanation for the evolutionary diversification of life. Adaptation is also notoriously difficult to study in nature, owing to its complexity and logistically prohibitive timescale. Here, we leverage extensive contemporary and historical collections of Ambrosia artemisiifolia —an aggressively invasive weed and primary cause of pollen-induced hayfever—to track the phenotypic and genetic causes of recent local adaptation across its native and invasive ranges in North America and Europe, respectively. Large haploblocks—indicative of chromosomal inversions—contain a disproportionate share (26%) of genomic regions conferring parallel adaptation to local climates between ranges, are associated with rapidly adapting traits, and exhibit dramatic frequency shifts over space and time. These results highlight the importance of large-effect standing variants in rapid adaptation, which have been critical to A. artemisiifolia ’s global spread across vast climatic gradients. Ambrosia artemisiifolia is an invasive weed and primary cause of pollen-induced hayfever. Here, the authors report its chromosome-level phased genome assembly, examine genome-wide variation among modern and historic accessions, and identify large haploblocks underling rapid adaptation.

Sex differences in morphology, physiology, development, and behavior are widespread, yet the sexes inherit nearly identical genomes, causing most traits to exhibit strong and positive cross‐sex genetic correlations. In contrast to most other traits, estimates of cross‐sex genetic correlations for fitness and fitness components (rW fm ) are generally low and occasionally negative, implying that a substantial fraction of standing genetic variation for fitness might be sexually antagonistic (i.e., alleles benefitting one sex harm the other). Nevertheless, while low values of rW fm are often regarded as consequences of sexually antagonistic selection, it remains unclear exactly how selection and variation in quantitative traits interact to determine the sign and magnitude of rW fm , making it difficult to relate empirical estimates of cross‐sex genetic correlations to the evolutionary processes that might shape them. We present simple univariate and multivariate quantitative genetic models that explicitly link patterns of sex‐specific selection and trait genetic variation to the cross‐sex genetic correlation for fitness. We show that rW fm provides an unreliable signal of sexually antagonistic selection for two reasons. First, rW fm is constrained to be less than the cross‐sex genetic correlation for traits affecting fitness, regardless of the nature of selection on the traits. Second, sexually antagonistic selection is an insufficient condition for generating negative cross‐sex genetic correlations for fitness. Instead, negative fitness correlations between the sexes (rW fm <0) can only emerge when selection is sexually antagonistic and the strength of directional selection on each sex is strong relative to the amount of shared additive genetic variation in female and male traits. These results imply that empirical tests of sexual antagonism that are based on estimates of rW fm will be conservative and underestimate its true scope. In light of these theoretical results, we revisit current data on rW fm and sex‐specific selection and find that they are consistent with the theory.

Most marine organisms have complex life histories, where the individual stages of a life cycle are often morphologically and ecologically distinct. Nevertheless, life‐history stages share a single genome and are linked phenotypically (by “carry‐over effects”). These commonalities across the life history couple the evolutionary dynamics of different stages and provide an arena for evolutionary constraints. The degree to which genetic and phenotypic links among stages hamper adaptation in any one stage remains unclear and yet adaptation is essential if marine organisms will adapt to future climates. Here, we use an extension of Fisher's geometric model to explore how both carry‐over effects and genetic links among life‐history stages affect the emergence of pleiotropic trade‐offs between fitness components of different stages. We subsequently explore the evolutionary trajectories of adaptation of each stage to its optimum using a simple model of stage‐specific viability selection with nonoverlapping generations. We show that fitness trade‐offs between stages are likely to be common and that such trade‐offs naturally emerge through either divergent selection or mutation. We also find that evolutionary conflicts among stages should escalate during adaptation, but carry‐over effects can ameliorate this conflict. Carry‐over effects also tip the evolutionary balance in favor of better survival in earlier life‐history stages at the expense of poorer survival in later stages. This effect arises in our discrete‐generation framework and is, therefore, unrelated to age‐related declines in the efficacy of selection that arise in models with overlapping generations. Our results imply a vast scope for conflicting selection between life‐history stages, with pervasive evolutionary constraints emerging from initially modest selection differences between stages. Organisms with complex life histories should also be more constrained in their capacity to adapt to global change than those with simple life histories.

Disruptive selection between males and females can generate sexual antagonism, where alleles improving fitness in one sex reduce fitness in the other. This type of genetic conflict arises because males and females carry nearly identical sets of genes: opposing selection, followed by genetic mixing during reproduction, generates a population genetic “tug-of-war” that constrains adaptation in either sex. Recent verbal models suggest that gene duplication and sex-specific cooption of paralogs might resolve sexual antagonism and facilitate evolutionary divergence between the sexes. However, this intuitive proximal solution for sexual dimorphism potentially belies a complex interaction between mutation, genetic drift, and positive selection during duplicate fixation and sex-specific paralog differentiation. The interaction of these processes—within the explicit context of duplication and sexual antagonism—has yet to be formally described by population genetics theory. Here, we develop and analyze models of gene duplication and sex-specific differentiation between paralogs. We show that sexual antagonism can favor the fixation and maintenance of gene duplicates, eventually leading to the evolution of sexually dimorphic genetic architectures for male and female traits. The timescale for these evolutionary transitions is sensitive to a suite of genetic and demographic variables, including allelic dominance, recombination, sex linkage, and population size. Interestingly, we find that female-beneficial duplicates preferentially accumulate on the X chromosome, whereas male-beneficial duplicates are biased toward autosomes, independent of the dominance parameters of sexually antagonistic alleles. Although this result differs from previous models of sexual antagonism, it is consistent with several findings from the empirical genomics literature.

Strict maternal inheritance renders the mitochondrial genome susceptible to accumulating mutations that harm males, but are otherwise benign or beneficial for females. This ‘mother's curse’ effect can degrade male survival and fertility if unopposed by counteracting evolutionary processes. Coadaptation between nuclear and mitochondrial genomes—with nuclear genes evolving to compensate for male-harming mitochondrial substitutions—may ultimately resolve mother's curse. However, males are still expected to incur a transient fitness cost during mito-nuclear coevolution, and it remains unclear how severe such costs should be. We present a population genetic analysis of mito-nuclear coadaptation to resolve mother's curse effects, and show that the magnitude of the ‘male mitochondrial load’—the negative impact of mitochondrial substitutions on male fitness components—may be large, even when genetic variation for compensatory evolution is abundant. We also find that the male load is surprisingly sensitive to population size: male fitness costs of mito-nuclear coevolution are particularly pronounced in both small and large populations, and minimized in populations of intermediate size. Our results reveal complex interactions between demography and genetic constraints during the resolution of mother's curse, suggesting potentially widespread species differences in susceptibility to mother's curse effects.