Sex chromosomes in plants have often been contrasted with those in animals with the goal of identifying key differences that can be used to elucidate fundamental evolutionary properties. For example, the often homomorphic sex chromosomes in plants have been compared to the highly divergent systems in some animal model systems, such as birds, Drosophila and therian mammals, with many hypotheses offered to explain the apparent dissimilarities, including the younger age of plant sex chromosomes, the lesser prevalence of sexual dimorphism, or the greater extent of haploid selection. Furthermore, many plant sex chromosomes lack complete sex chromosome dosage compensation observed in some animals, including therian mammals, Drosophila, some poeciliids, and Anolis, and plant dosage compensation, where it exists, appears to be incomplete. Even the canonical theoretical models of sex chromosome formation differ somewhat between plants and animals. However, the highly divergent sex chromosomes observed in some animal groups are actually the exception, not the norm, and many animal clades are far more similar to plants in their sex chromosome patterns. This begs the question of how different are plant and animal sex chromosomes, and which of the many unique properties of plants would be expected to affect sex chromosome evolution differently than animals? in fact, plant and animal sex chromosomes exhibit more similarities than differences, and it is not at all clear that they differ in terms of sexual conflict, dosage compensation, or even degree of divergence. Overall, the largest difference between these two groups is the greater potential for haploid selection in plants compared to animals. This may act to accelerate the expansion of the non-recombining region at the same time that it maintains gene function within it. This article is part of the theme issue 'Sex determination and sex chromosome evolution in land plants'.

Male-female differences in many developmental mechanisms lead to the formation of two morphologically and physiologically distinct sexes. Although this is expected for traits with prominent differences between the sexes, such as the gonads, sex-specific processes also contribute to traits without obvious male-female differences, such as the intestine. Here, we review sex differences in developmental mechanisms that operate at several levels of biological complexity - molecular, cellular, organ and organismal - and discuss how these differences influence organ formation, function and whole-body physiology. Together, the examples we highlight show that one simple way to gain a more accurate and comprehensive understanding of animal development is to include both sexes.

Dosage compensation balances gene expression between the sexes in systems with diverged heterogametic sex chromosomes. Theory predicts that dosage compensation should rapidly evolve in tandem with the divergence of sex chromosomes to prevent the deleterious effects of dosage imbalances that occur as a result of sex chromosome divergence. Examples of complete dosage compensation, where gene expression of the entire sex chromosome is compensated, are rare, and have only been found in relatively ancient sex chromosome systems. Consequently, very little is known about the evolutionary dynamics of complete dosage compensationsystems.WithinthefamilyPoeciliidaethesubgenus Lebistessharethesamesexchromosomesystemwhichoriginated 18.48-26.08 Ma. In Poecilia reticulata and P. wingei, the Y chromosome has been largely maintained, whereas the Y in the closely related species P. picta and P. parae has rapidly degraded. We recently found P. picta to be the first example of complete dosage compensation in a fish. Here, we show that P. parae also has complete dosage compensation, thus complete dosage compensation likely evolved in the short (~3.7 Myr) interval after the split of the ancestor of these two species from P. reticulata, but before they diverged from each other. These data suggest that novel dosage compensation mechanisms can evolve rapidly, thus supporting the longstanding theoretical prediction that such mechanisms arise in tandem with rapidly diverging sex chromosomes. The Author(s) 2021.

The majority of the genome is shared between the sexes, and it is expected that the genetic architecture of most traits is shared as well. This common architecture has been viewed as a major source of constraint on the evolution of sexual dimorphism (SD). SD is nonetheless common in nature, leading to assumptions that it results from differential regulation of shared genetic architecture. Here, we study the effect of thousands of gene knockout mutations on 202 mouse phenotypes to explore how regulatory variation affects SD. We show that many traits are dimorphic to some extent, and that a surprising proportion of knockouts have sex-specific phenotypic effects. Many traits, regardless whether they are monomorphic or dimorphic, harbor cryptic differences in genetic architecture between the sexes, resulting in sexually discordant phenotypic effects from sexually concordant regulatory changes. This provides an alternative route to dimorphism through sex-specific genetic architecture, rather than differential regulation of shared architecture.

Genomic analysis of many nonmodel species has uncovered an incredible diversity of sex chromosome systems, making it possible to empirically test the rich body of evolutionary theory that describes each stage of sex chromosome evolution. Classic theory predicts that sex chromosomes originate from a pair of homologous autosomes and recombination between them is suppressed via inversions to resolve sexual conflict. The resulting degradation of the Y chromosome gene content creates the need for dosage compensation in the heterogametic sex. Sex chromosome theory also implies a linear process, starting from sex chromosome origin and progressing to heteromorphism. Despite many convergent genomic patterns exhibited by independently evolved sex chromosome systems, and many case studies supporting these theoretical predictions, emerging data provide numerous interesting exceptions to these long-standing theories, and suggest that the remarkable diversity of sex chromosomes is matched by a similar diversity in their evolution. For example, it is clear that sex chromosome pairs are not always derived from homologous autosomes. In addition, both the cause and the mechanism of recombination suppression between sex chromosome pairs remain unclear, and it may be that the spread of recombination suppression is a more gradual process than previously thought. It is also clear that dosage compensation can be achieved in many ways, and displays a range of efficacy in different systems. Finally, the remarkable turnover of sex chromosomes in many systems, as well as variation in the rate of sex chromosome divergence, suggest that assumptions about the inevitable linearity of sex chromosome evolution are not always empirically supported, and the drivers of the birth-death cycle of sex chromosome evolution remain to be elucidated. Here, we concentrate on how the diversity in sex chromosomes across taxa highlights an equal diversity in each stage of sex chromosome evolution.

Evolutionary conflict arises from differences in the fitness interests of replicating entities and has its roots in relatedness asymmetries. Every replicator is related to itself by 100%, but in most cases is less related to other replicators, which generates selfishness and conflicts of interest. Since this basic condition is the norm at many levels of biological organization, conflict is rife in biological systems. Sexual conflict, on which we focus here, is the evolutionary conflict that occurs between males and females because of their divergent fitness interests. Sexual conflict occurs despite sexual reproduction requiring some level of cooperation between males and females because the fitness interests of the sexes are nevertheless never perfectly aligned. In other words, males and females may agree on where they are going, but not necessarily on how to get there. Sexual conflict is a vast topic with relevance to many areas of biology and so here we restrict our focus to matters we think are of broadest interest. Hosken et al. introduce sexual conflict.

The role of sex in biomedical studies has often been overlooked, despite evidence of sexually dimorphic effects in some biological studies. Here, we used high-throughput phenotype data from 14,250 wildtype and 40,192 mutant mice (representing 2,186 knockout lines), analysed for up to 234 traits, and found a large proportion of mammalian traits both in wildtype and mutants are influenced by sex. This result has implications for interpreting disease phenotypes in animal models and humans.

Sexual selection drives fundamental evolutionary processes such as trait elaboration and speciation. Despite this importance, there are surprisingly few examples of genes unequivocally responsible for variation in sexually selected phenotypes. This lack of information inhibits our ability to predict phenotypic change due to universal behaviours, such as fighting over mates and mate choice. Here, we discuss reasons for this apparent gap and provide recommendations for how it can be overcome by adopting contemporary genomic methods, exploiting underutilized taxa that may be ideal for detecting the effects of sexual selection and adopting appropriate experimental paradigms. Identifying genes that determine variation in sexually selected traits has the potential to improve theoretical models and reveal whether the genetic changes underlying phenotypic novelty utilize common or unique molecular mechanisms. Such a genomic approach to sexual selection will help answer questions in the evolution of sexually selected phenotypes that were first asked by Darwin and can furthermore serve as a model for the application of genomics in all areas of evolutionary biology.

Intralocus sexual conflict and intragenomic conflict both affect sex chromosome evolution and can in extreme cases even cause the complete turnover of sex chromosomes. Additionally, established sex chromosomes often become the focus of heightened conflict. This creates a tangled relationship between sex chromosomes and conflict with respect to cause and effect. To further complicate matters, sexual and intragenomic conflict may exacerbate one another and thereby further fuel sex chromosome change. Different magnitudes and foci of conflict offer potential explanations for lineage-specific variation in sex chromosome evolution and answer long-standing questions as to why some sex chromosomes are remarkably stable, whereas others show rapid rates of evolutionary change.

Polyandry is widespread in nature, and has important evolutionary consequences for the evolution of sexual dimorphism and sexual conflict. Although many of the phenotypic consequences of polyandry have been elucidated, our understanding of the impacts of polyandry and mating systems on the genome is in its infancy. Polyandry can intensify selection on sexual characters and generate more intense sexual conflict. This has consequences for sequence evolution, but also for sex-biased gene expression, which acts as a link between mating systems, sex-specific selection and the evolution of sexual dimorphism. We discuss this and the remarkable confluence of sexual-conflict theory and patterns of gene expression, while also making predictions about transcription patterns, mating systems and sexual conflict. Gene expression is a key link in the genotype-phenotype chain, and although in its early stages, understanding the sexual selection-transcription relationship will provide significant insights into this critical association.

Polyandry is widespread in nature, and has important evolutionary consequences for the evolution of sexual dimorphism and sexual conflict. Although many of the phenotypic consequences of polyandry have been elucidated, our understanding of the impacts of polyandry and mating systems on the genome is in its infancy. Polyandry can intensify selection on sexual characters and generate more intense sexual conflict. This has consequences for sequence evolution, but also for sex-biased gene expression, which acts as a link between mating systems, sex-specific selection and the evolution of sexual dimorphism. We discuss this and the remarkable confluence of sexual-conflict theory and patterns of gene expression, while also making predictions about transcription patterns, mating systems and sexual conflict. Gene expression is a key link in the genotype-phenotype chain, and although in its early stages, understanding the sexual selection-transcription relationship will provide significant insights into this critical association.

Sex chromosome dosage compensation was once thought to be required to balance gene expression levels between sex-linked and autosomal genes in the heterogametic sex. Recent evidence from a range of animals has indicated that although sex chromosome dosage compensation exists in some clades, it is far from a necessary companion to sex chromosome evolution, and is in fact rather rare in animals. This raises questions about why complex dosage compensation mechanisms arise in some clades when they are not strictly needed, and suggests that the role of sex-specific selection in sex chromosome gene regulation should be reassessed. We show there exists a tremendous diversity in the mechanisms that regulate gene dosage and argue that sexual conflict may be an overlooked agent responsible for some of the variation seen in sex chromosome gene dose regulation.