Abstract
Recent years have seen a surge of interest in linking the theories of kin selection and sexual selection. In particular, there is a growing appreciation that kin selection, arising through demographic factors such as sex‐biased dispersal, may modulate sexual conflicts, including in the context of male–female arms races characterized by coevolutionary cycles. However, evolutionary conflicts of interest need not only occur between individuals, but may also occur within individuals, and sex‐specific demography is known to foment such intragenomic conflict in relation to social behavior. Whether and how this logic holds in the context of sexual conflict—and, in particular, in relation to coevolutionary cycles—remains obscure. We develop a kin‐selection model to investigate the interests of different genes involved in sexual and intragenomic conflict, and we show that consideration of these conflicting interests yields novel predictions concerning parent‐of‐origin specific patterns of gene expression and the detrimental effects of different classes of mutation and epimutation at loci underpinning sexually selected phenotypes.
Highlights
Recent years have seen a surge of interest in linking the theories of kin selection and sexual selection
We develop a kin-selection model to investigate the interests of different genes involved in sexual and intragenomic conflict, and we show that consideration of these conflicting interests yields novel predictions concerning parent-of-origin specific patterns of gene expression and the detrimental effects of different classes of mutation and epimutation at loci underpinning sexually selected phenotypes
We have investigated the potential for sex-biased dispersal to generate intragenomic conflict and, drive the evolution of genomic imprinting in the context of sexual conflict
Summary
MATHEMATICAL MODEL Following Rankin (2011) and Faria et al (2015), we consider an infinite diploid population divided into patches containing nm males and nf females, with multiple mating such that every female mates with every male in her patch, and vice versa. Male harm We investigate the interests of different classes of genes in relation to the male-harm phenotype by hypothetically granting control of this phenotype to a genic actor A, residing in the focal male’s genome, and determining when an increase in harm increases the gene’s inclusive fitness (Hamilton 1964; Gardner and Welch 2011; Gardner 2014). 2 (nf + nm) − mf (nf − 1) − mm (3nm − 2 − nf − mm (nm − 1)) + mf (nf (3 − mm) − nm (1 − mm) − 2) 2(nf(1 − mm)2 + nm(1 − mf)2 + (4 − mf − mm) (mf + mm) (nfnm)
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