Since the autosomal genome is shared between the sexes, sex-specific fitness optima present an evolutionary challenge. While sexually antagonistic selection might favor different alleles within females and males, segregation randomly reassorts alleles at autosomal loci between sexes each generation. This process of homogenization during transmission thus prevents between-sex allelic divergence generated by sexually antagonistic selection from accumulating across multiple generations. However, recent empirical studies have reported high male-female FST statistics. Here, we use a population genetic model to evaluate whether these observations could plausibly be produced by sexually antagonistic selection. To do this, we use both a single-locus model with nonrandom mate choice, and individual-based simulations to study the relationship between strength of selection, degree of between-sex divergence, and the associated genetic load. We show that selection must be exceptionally strong to create measurable divergence between the sexes and that the decrease in population fitness due to this process is correspondingly high. Individual-based simulations with selection genome-wide recapitulate these patterns and indicate that small sample sizes and sampling variance can easily generate substantial male-female divergence. We therefore conclude that caution should be taken when interpreting autosomal allelic differentiation between the sexes.
Sexual conflict is a specific class of intergenomic conflict that describes the reciprocal sex-specific fitness costs generated by antagonistic reproductive interactions. The potential for sexual conflict is an inherent property of having a shared genome between the sexes and, therefore, is an extreme form of an environment-dependent fitness effect. In this way, many of the predictions from environment-dependent selection can be used to formulate expected patterns of genome evolution under sexual conflict. However, the pleiotropic and transmission constraints inherent to having alleles move across sex-specific backgrounds from generation to generation further modulate the anticipated signatures of selection. We outline methods for detecting candidate sexual conflict loci both across and within populations. Additionally, we consider the ability of genome scans to identify sexually antagonistic loci by modeling allele frequency changes within males and females due to a single generation of selection. In particular, we highlight the need to integrate genotype, phenotype, and functional information to truly distinguish sexual conflict from other forms of sexual differentiation.
The ability to control both the means and timing of sexual reproduction provides a powerful tool to understand not only fertilization but also life history trade-offs resulting from sexual reproduction. However, precisely controlling fertilization has proved a major challenge across model systems. An ideal sterility induction system should be external, non-toxic, and reversible. Using the auxin-inducible degradation system targeting the spe-44 gene within the nematode Caenorhabditis elegans, we designed a means of externally inducing spermatogenesis arrest. We show that exposure to auxin during larval development induces both hermaphrodite self-sterility and male sterility. Moreover, male sterility can be reversed upon cessation of auxin exposure. The sterility induction system developed here has multiple applications in the fields of spermatogenesis and mating systems evolution. Importantly, this system is also a highly applicable tool for aging studies. In particular, we show that auxin-induced self-sterility is comparable to the commonly used chemically-induced FUdR sterility, while offering multiple benefits, including being less labor intensive, being non-toxic, and avoiding compound interactions with other experimental treatments.
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