Sexual antagonism in sequential hermaphrodites.

Females and males may have distinct phenotypic optima, but share essentially the same complement of genes, potentially leading to trade-offs between attaining high fitness through female versus male reproductive success. Such sexual antagonism may be particularly acute in hermaphrodites, where both reproductive strategies are housed within a single individual. While previous models have focused on simultaneous hermaphroditism, we lack theory for how sexual antagonism may play out under sequential hermaphroditism, which has the additional complexities of age-structure. Here, we develop a formal theory of sexual antagonism in sequential hermaphrodites. First, we construct a general theoretical overview of the problem, then consider different types of sexually antagonistic and life-history trade-offs, under different modes of genetic inheritance (autosomal or cytoplasmic), and different forms of sequential hermaphroditism (protogynous, protoandrous or bidirectional). Finally, we provide a concrete illustration of these general patterns by developing a two-stage two-sex model, which yields conditions for both invasion of sexually antagonistic alleles and maintenance of sexually antagonistic polymorphisms.

Sex-biased demography modulates male harm across the genome.

Recent years have seen an explosion of theoretical and empirical interest in the role that kin selection plays in shaping patterns of sexual conflict, with a particular focus on male harming traits. However, this work has focused solely on autosomal genes, and as such it remains unclear how demography modulates the evolution of male harm loci occurring in other portions of the genome, such as sex chromosomes and cytoplasmic elements. To investigate this, we extend existing models of sexual conflict for application to these different modes of inheritance. We first analyse the general case, revealing how sex-specific relatedness, reproductive value and the intensity of local competition combine to determine the potential for male harm. We then analyse a series of demographically explicit models, to assess how dispersal, overlapping generations, reproductive skew and the mechanism of population regulation affect sexual conflict across the genome, and drive conflict between nuclear and cytoplasmic genes. We then explore the effects of sex biases in these demographic parameters, showing how they may drive further conflicts between autosomes and sex chromosomes. Finally, we outline how different crossing schemes may be used to identify signatures of these intragenomic conflicts.

Variable dosage compensation is associated with female consequences of an X-linked, male-beneficial mutation.

Recent theory has suggested that dosage compensation mediates sexual antagonism over X-linked genes. This process relies on the assumption that dosage compensation scales phenotypic effects between the sexes, which is largely untested. We evaluated this by quantifying transcriptome variation associated with a recently arisen, male-beneficial, X-linked mutation across tissues of the field cricket Teleogryllus oceanicus, and testing the relationship between the completeness of dosage compensation and female phenotypic effects at the level of gene expression. Dosage compensation in T. oceanicus was variable across tissues but usually incomplete, such that relative expression of X-linked genes was typically greater in females. Supporting the assumption that dosage compensation scales phenotypic effects between the sexes, we found tissues with incomplete dosage compensation tended to show female-skewed effects of the X-linked allele. In gonads, where expression of X-linked genes was most strongly female-biased, ovaries-limited genes were much more likely to be X-linked than were testes-limited genes, supporting the view that incomplete dosage compensation favours feminization of the X. Our results support the expectation that sex chromosome dosage compensation scales phenotypic effects of X-linked genes between sexes, substantiating a key assumption underlying the theoretical role of dosage compensation in determining the dynamics of sexual antagonism on the X.

Genomic Imprinting As a Window into Human Language Evolution.

Humans spend large portions of their time and energy talking to one another, yet it remains unclear whether this activity is primarily selfish or altruistic. Here, it is shown how parent-of-origin specific gene expression-or "genomic imprinting"-may provide an answer to this question. First, it is shown why, regarding language, only altruistic or selfish scenarios are expected. Second, it is pointed out that an individual's maternal-origin and paternal-origin genes may have different evolutionary interests regarding investment into language, and that this intragenomic conflict may drive genomic imprinting which-as the direction of imprint depends upon whether investment into language is relatively selfish or altruistic-may be used to discriminate between these two possibilities. Third, predictions concerning the impact of various mutations and epimutations at imprinted loci on language pathologies are derived. In doing so, a framework is developed that highlights avenues for using intragenomic conflicts to investigate the evolutionary drivers of language.

A gene's-eye view of sexual antagonism.

Females and males may face different selection pressures. Accordingly, alleles that confer a benefit for one sex often incur a cost for the other. Classic evolutionary theory holds that the X chromosome, whose sex-biased transmission sees it spending more time in females, should value females more than males, whereas autosomes, whose transmission is unbiased, should value both sexes equally. However, recent mathematical and empirical studies indicate that male-beneficial alleles may be more favoured by the X chromosome than by autosomes. Here we develop a gene's-eye-view approach that reconciles the classic view with these recent discordant results, by separating a gene's valuation of female versus male fitness from its ability to induce fitness effects in either sex. We use this framework to generate new comparative predictions for sexually antagonistic evolution in relation to dosage compensation, sex-specific mortality and assortative mating, revealing how molecular mechanisms, ecology and demography drive variation in masculinization versus feminization across the genome.

Paternal genome elimination promotes altruism in viscous populations.

Population viscosity has long been thought to promote the evolution of altruism. However, in the simplest scenarios, the potential for altruism is invariant with respect to dispersal-a surprising result that holds for haploidy, diploidy, and haplodiploidy (arrhenotoky). Here, we develop a kin-selection model to investigate how population viscosity affects the potential for altruism in species with male paternal genome elimination (PGE), exploring altruism enacted by both females and males, and both juveniles and adults. We find that (1) PGE promotes altruistic behaviors relative to the other inheritance systems, and to a degree that depends on the extent of paternal genome expression. (2) Under PGE, dispersal increases the potential for altruism in juveniles and decreases it in adults. (3) The genetics of PGE can lead to striking differences in sex-specific potentials for altruism, even in the absence of any sex differences in ecology.

Sexual antagonism in haplodiploids.

Females and males may face different selection pressures, such that alleles conferring a benefit in one sex may be deleterious in the other. Such sexual antagonism has received a great deal of theoretical and empirical attention, almost all of which has focused on diploids. However, a sizeable minority of animals display an alternative haplodiploid mode of inheritance, encompassing both arrhenotoky, whereby males develop from unfertilized eggs, and paternal genome elimination (PGE), whereby males receive but do not transmit a paternal genome. Alongside unusual genetics, haplodiploids often exhibit social ecologies that modulate the relative value of females and males. Here, we develop a series of evolutionary-genetic models of sexual antagonism for haplodiploids, incorporating details of their molecular biology and social ecology. We find that: (1) PGE promotes female-beneficial alleles more than arrhenotoky, and to an extent determined by the timing of elimination-and degree of silencing of-the paternal genome; (2) sib-mating relatively promotes female-beneficial alleles, as do other forms of inbreeding including limited male-dispersal, oedipal-mating, and the pseudo-hermaphroditism of Icerya purchasi; (3) resource competition between related females inhibits the invasion of female-beneficial alleles; and (4) sexual antagonism foments conflicts between parents and offspring, endosymbionts and hosts, and maternal- and paternal-origin genes.