Data from: Meiotic drive influences the outcome of sexually antagonistic selection at a linked locus

Most meiotic drivers, such as the t-haplotype in Mus and the segregation distorter (SD) in Drosophila, act in a sex-specific manner, gaining a transmission advantage through one sex although suffering only the fitness costs associated with the driver in the other. Their inheritance is thus more likely through one of the two sexes, a property they share with sexually antagonistic alleles. Previous theory has shown that pairs of linked loci segregating for sexually antagonistic alleles are more likely to remain polymorphic and that linkage disequilibrium accrues between them. I probe this similarity between drive and sexual antagonism and examine the evolution of chromosomes experiencing these selection pressures simultaneously. Reminiscent of previous theory, I find that: the opportunity for polymorphism increases for a sexually antagonistic locus that is physically linked to a driving locus; the opportunity for polymorphism at a driving locus also increases when linked to a sexually antagonistic locus; and stable linkage disequilibrium accompanies any polymorphic equilibrium. Additionally, I find that drive at a linked locus favours the fixation of sexually antagonistic alleles that benefit the sex in which drive occurs. Further, I show that under certain conditions reduced recombination between these two loci is selectively favoured. These theoretical results provide clear, testable predictions about the nature of sexually antagonistic variation on driving chromosomes and have implications for the evolution of genomic architecture

drivecodePattenJEB

Contains Matlab code for all numerical analyses in Patten JEB 201

Reciprocally Imprinted Genes and the Response to Selection on One Sex

We explore the theoretical consequences of limiting selection to males for the evolution of imprinted genes. We find that the efficiency of male-limited selection depends on the pattern of imprinting at an imprinted locus. When selection is strong, the maternally expressed pattern of imprinting allows faster genetic change than the reciprocal, paternally expressed pattern. When selection is relatively weak, the pattern of imprinting that permits a greater rate of genetic response to selection depends on the frequency of the favored allele: the paternally expressed pattern permits faster genetic change than does the maternally expressed pattern at low frequencies of a favored allele; at higher frequencies of a favored allele, however, the maternally expressed pattern is again more conducive to a genetic response. To our knowledge, this is the first theoretical description of a difference between the two reciprocal patterns of imprinting. The selective efficiency bias we identify between the two patterns of imprinting has implications for natural and livestock populations, which we discuss

Regulatory links between imprinted genes:Evolutionary predictions and consequences

Genomic imprinting is essential for development and growth and plays diverse roles in physiology and behaviour. Imprinted genes have traditionally been studied in isolation or in clusters with respect to cis-acting modes of gene regulation, both from a mechanistic and evolutionary point of view. Recent studies in mammals, however, reveal that imprinted genes are often co-regulated and are part of a gene network involved in the control of cellular proliferation and differentiation. Moreover, a subset of imprinted genes acts in trans on the expression of other imprinted genes. Numerous studies have modulated levels of imprinted gene expression to explore phenotypic and gene regulatory consequences. Increasingly, the applied genome-wide approaches highlight how perturbation of one imprinted gene may affect other maternally or paternally expressed genes. Here, we discuss these novel findings and consider evolutionary theories that offer a rationale for such intricate interactions among imprinted genes. An evolutionary view of these trans-regulatory effects provides a novel interpretation of the logic of gene networks within species and has implications for the origin of reproductive isolation between species

Genetic conflicts and the case for licensed anthropomorphizing

The use of intentional language in biology is controversial. It has been commonly applied by researchers in behavioral ecology, who have not shied away from employing agential thinking or even anthropomorphisms, but has been rarer among researchers from more mechanistic corners of the discipline, such as population genetics. One research area where these traditions come into contact-and occasionally clash-is the study of genetic conflicts, and its history offers a good window to the debate over the use of intentional language in biology. We review this debate, paying particular attention to how this interaction has played out in work on genomic imprinting and sex chromosomes. In light of this, we advocate for a synthesis of the two approaches, a form of licensed anthropomorphizing. Here, agential thinking's creative potential and its ability to identify the fulcrum of evolutionary pressure are combined with the rigidity of formal mathematical modeling

Parental sex discrimination and intralocus sexual conflict

Intralocus sexual conflict occurs when populations segregate for alleles with opposing fitness consequences in the two sexes. This form of selection is known to be capable of maintaining genetic and fitness variation in nature, the extent of which is sensitive to the underlying genetics. We present a one-locus model of a haploid maternal effect that has sexually antagonistic consequences for offspring. The evolutionary dynamics of these maternal effects are distinct from those of haploid direct effects under sexual antagonism because the relevant genes are expressed only in females. Despite this, we find the same opportunity for sexually antagonistic polymorphism at the maternal effect locus as at a direct effect locus. Thus, sexually antagonistic maternal effects may underlie some natural genetic variation. The model we present permits alternative interpretations of how the genes are expressed and how the fitness variation is assigned, which invites a theoretical comparison to models of both imprinted genes and sex allocation