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The loss of recombination between sex chromosomes has occurred repeatedly throughout nature, with important implications for their subsequent evolution. Explanations for this remarkable convergence have generally invoked only adaptive processes (e.g. sexually antagonistic selection); however, there is still little evidence for these hypotheses. Here we propose a model in which recombination on sex chromosomes is lost due to the neutral accumulation of sequence divergence adjacent to (and thus, in linkage disequilibriumwith) the sex determiner. Importantly, we include in our model the fact that sequence divergence, in any form, reduces the probability of recombination between any two sequences. Using simulations, we show that, under certain conditions, a region of suppressed recombination arises and expands outwards from the sex-determining locus, under purely neutral processes. Further, we show that the rate and pattern of recombination loss are sensitive to the pre-existing recombination landscape of the genome and to sex differences in recombination rates, with patterns consistent with evolutionary strata emerging under some conditions. We discuss the applicability of these results to natural systems. This article is part of the theme issue 'Challenging the paradigm in sex chromosome evolution: empirical and theoretical insights with a focus on vertebrates (Part I)'.

Sexual dimorphism is a substantial contributor to the diversity observed in nature, extending from elaborate traits to the expression level of individual genes. Sexual conflict and sexually antagonistic coevolution are thought to be central forces driving the dimorphism of the sexes and its diversity. We have substantial data to support this at the phenotypic level but much less at the genetic level, where distinguishing the role of conflict from other forms of sex-biased selection and from other processes is challenging. Here we discuss the powerful effects sexual conflict may have on genome evolution and critically evaluate the supporting evidence. Although there is much potential for sexual conflict to affect genome evolution, we have relatively little compelling evidence of a genomic signature of sexual conflict. A central obstacle is the mismatch between taxa in which we understand sexually antagonistic selection and those in which we understand genetics.

Sex differences in selection are ubiquitous in sexually reproducing organisms. When the genetic basis of traits is shared between the sexes, such sexually antagonistic selection (SAS) creates a potential constraint on adaptive evolution. Theory and laboratory experiments suggest that environmental variation and the degree of local adaptation may all affect the frequency and intensity of SAS. Here, we capitalize on a large database of over 700 spatially or temporally replicated estimates of sex-specific phenotypic selection from wild populations, combined with data on microclimates and geographical range information. We performed a meta-analysis to test three predictions from SAS theory, that selection becomes more concordant between males and females: (1) in more stressful environments, (2) in more variable environments and (3) closer to the edge of the species' range. We find partial empirical support for all three predictions. Within-study analyses indicate SAS decreases in extreme environments, as indicated by a relationship with maximum temperature, minimum precipitation and evaporative potential (PET). Across studies, we found that the average level of SAS at high latitudes was lower, where environmental conditions are typically less stable. Finally, we found evidence for reduced SAS in populations that are far from the centre of their geographical range. However, and notably, we also found some evidence of reduced average strength of selection in these populations, which is in contrast to predictions from classical theoretical models on range limit evolution. Our results suggest that environmental lability and species range position predictably influence sex-specific selection and sexual antagonism in the wild. This article is part of the theme issue ‘Linking local adaptation with the evolution of sex differences’.

Anisogamy predisposes the sexes to very different patterns of selection on shared traits. Selective differences between the sexes may manifest as changes in the direction or strength of selection acting on shared phenotypes. Although previous studies have found evidence for widespread differences in the direction of selection between the sexes, surprisingly little is known regarding potential differences in the magnitude of selection and whether such differences might be confined to specific components of fitness. We conducted a meta-analysis using 865 estimates of phenotypic selection from wild populations to characterize sex differences in the strength of selection and to ask whether different components of fitness exhibit differences in sex bias in the strength of selection. Overall, consistent with past results, we find evidence of male bias in the strength of selection, driven primarily by components of fitness related to mating success and we discuss several evolutionary implications.

The independent evolution of the sexes may often be constrained if male and female homologous traits share a similar genetic architecture. Thus, cross-sex genetic covariance is assumed to play a key role in the evolution of sexual dimorphism (SD) with consequent impacts on sexual selection, population dynamics, and speciation processes. We compiled cross-sex genetic correlations (rMF) estimates from 114 sources to assess the extent to which the evolution of SD is typically constrained and test several specific hypotheses. First, we tested if rMF differed among trait types and especially between fitness components and other traits. We also tested the theoretical prediction of a negative relationship between rMF and SD based on the expectation that increases in SD should be facilitated by sex-specific genetic variance. We show that rMF is usually large and positive but that it is typically smaller for fitness components. This demonstrates that the evolution of SD is typically genetically constrained and that sex-specific selection coefficients may often be opposite in sign due to sub-optimal levels of SD. Most importantly, we confirm that sex-specific genetic variance is an important contributor to the evolution of SD by validating the prediction of a negative correlation between rMF and SD.

Males and females share most of their genomes and express many of the same traits, yet the sexes often have markedly different selective optima for these shared traits. This sexually antagonistic (SA) selection generates intralocus sexual conflict that is thought to be resolved through the evolution of sexual dimorphism. However, we currently know little about the prevalence of SA selection, the components of fitness that generate sexual antagonism, or the relationship between sexual dimorphism and current SA selection. We reviewed published studies to address these questions, using 424 selection estimates representing 89 traits from 34 species. Males and females often differed substantially in the direction and magnitude of selection on shared traits, although statistically significant SA selection was relatively uncommon. Sexual selection generated stronger sexual antagonism than fecundity or viability selection, and these individual components of fitness tended to reinforce one another to generate even stronger sexual antagonism for net fitness. Traits exhibiting strong sexual dimorphism exhibited greater SA selection than did weakly dimorphic traits, although this pattern was not significant after we controlled for the inclusion of multiple traits nested within species. Our results suggest that intralocus sexual conflict often may persist despite the evolution of sexual dimorphism.

Evolutionary theory proposes that maternal inheritance of mitochondria will facilitate the accumulation of mitochondrial DNA (mtDNA) mutations that are harmful to males but benign or beneficial to females. Furthermore, mtDNA haplotypes sampled from across a given species distribution are expected to differ in the number and identity of these ‘male-harming’ mutations they accumulate. Consequently, it is predicted that the genetic variation which delineates distinct mtDNA haplotypes of a given species should confer larger phenotypic effects on males than females (reflecting mtDNA mutations that are male-harming, but female-benign), or sexually antagonistic effects (reflecting mutations that are male-harming, but female-benefitting). These predictions have received support from recent work examining mitochondrial haplotypic effects on adult life-history traits in Drosophila melanogaster . Here, we explore whether similar signatures of male-bias or sexual antagonism extend to a key physiological trait—metabolic rate. We measured the effects of mitochondrial haplotypes on the amount of carbon dioxide produced by individual flies, controlling for mass and activity, across 13 strains of D. melanogaster that differed only in their mtDNA haplotype. The effects of mtDNA haplotype on metabolic rate were larger in males than females. Furthermore, we observed a negative intersexual correlation across the haplotypes for metabolic rate. Finally, we uncovered a male-specific negative correlation, across haplotypes, between metabolic rate and longevity. These results are consistent with the hypothesis that maternal mitochondrial inheritance has led to the accumulation of a sex-specific genetic load within the mitochondrial genome, which affects metabolic rate and that may have consequences for the evolution of sex differences in life history. This article is part of the theme issue ‘Linking the mitochondrial genotype to phenotype: a complex endeavour’.

During the past few decades, fitness-centered and trait-centered definitions of natural selection have coexisted in the philosophical literature. The former render natural selection definitionally dependent on the presence of fitness differences, where “fitness” is understood as a distinct property from actual reproductive success. On the other hand, trait-centered definitions see selection as definitionally dependent on the presence of a causal relation between a trait (not necessarily fitness) and reproductive success. Interestingly, endorsers of these definitions have rarely–and usually only cursorily–critically engaged the views of the other camp. Therefore, a critical comparison of the two kinds of definitions is lacking in the literature. This paper starts filling this void by opening a discussion about which of the two kinds of definition is more appropriate. I first argue that fitness-centered definitions have difficulties in accommodating cases of opposing selection on correlated traits, whereas trait-centered views have no such problems. To do so, I revisit an old argument put forth by Elliott Sober and I show that recent attempts from the fitness-centered camp to reply to Sober’s charge are unsuccessful. I then show that fitness-centered views also have problems with a different type of case, namely opposing selection on a single trait; trait-centered views, on the other hand, may accommodate such cases if, as I propose here, we specify that the causal relation that figures prominently in them is understood as a relation of contributing causation. These arguments suggest that trait-centered definitions of selection are preferable to fitness-centered ones.

Mutations with beneficial effects in one sex can have deleterious effects in the other. Such ‘sexually antagonistic’ (SA) variants contribute to variation in life-history traits and overall fitness, yet their genomic distribution is poorly resolved. Theory predicts that SA variants could be enriched on the X chromosome or autosomes, yet current empirical tests face two formidable challenges: (i) identifying SA selection in genomic data is difficult; and (ii) metrics of SA variation show persistent biases towards the X, even when SA variants are randomly distributed across the genome. Here, we present an unbiased test of the theory that SA variants are enriched on the X. We first develop models for reproductive F ST—a metric for quantifying sex-differential (including SA) effects of genetic variants on lifetime reproductive success—that control for X-linked biases. Comparing data from approximately 250 000 UK Biobank individuals to our models, we find F ST elevations consistent with both X-linked and autosomal SA polymorphisms affecting reproductive success in humans. However, the extent of F ST elevations does not differ from a model in which SA polymorphisms are randomly distributed across the genome. We argue that the polygenic nature of SA variation, along with sex asymmetries in SA effects, might render X-linked enrichment of SA polymorphisms unlikely.

Frogs are ideal organisms for studying sex chromosome evolution because of their diversity in sex chromosome differentiation and sex-determination systems. We review 222 anuran frogs, spanning ~220 Myr of divergence, with characterized sex chromosomes, and discuss their evolution, phylogenetic distribution and transitions between homomorphic and heteromorphic states, as well as between sex-determination systems. Most (~75%) anurans have homomorphic sex chromosomes, with XY systems being three times more common than ZW systems. Most remaining anurans (~25%) have heteromorphic sex chromosomes, with XY and ZW systems almost equally represented. There are Y-autosome fusions in 11 species, and no W-/Z-/X-autosome fusions are known. The phylogeny represents at least 19 transitions between sex-determination systems and at least 16 cases of independent evolution of heteromorphic sex chromosomes from homomorphy, the likely ancestral state. Five lineages mostly have heteromorphic sex chromosomes, which might have evolved due to demographic and sexual selection attributes of those lineages. Males do not recombine over most of their genome, regardless of which is the heterogametic sex. Nevertheless, telomere-restricted recombination between ZW chromosomes has evolved at least once. More comparative genomic studies are needed to understand the evolutionary trajectories of sex chromosomes among frog lineages, especially in the ZW systems.