Sexual antagonism in haplodiploids. (21st December 2021)

• Record Type: Journal Article
• Authors: Hitchcock, Thomas J.; Gardner, Andy; Ross, Laura
• Is Part Of: Evolution. Volume 76:Number 2(2022)
• Page Start: 292
• Page End: 309
• Publication Date: 2021-12-21
• Subjects: Arrhenotoky -- haplodiploidy -- inbreeding -- intralocus sexual conflict -- paternal genome elimination -- sexually antagonistic alleles; Evolution -- Periodicals; Heredity -- Periodicals; Évolution (Biologie) -- Périodiques; Hérédité -- Périodiques; 338.47004094
• DOI: 10.1111/evo.14398
• Languages: English
• ISSNs: 0014-3820

Abstract

Abstract: 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.