Research
Current postdoctoral work
PhD work
The genetic basis of intralocus sexual conflict
The divergent reproductive roles of males and females generate sexually antagonistic selection, with opposing trait values favoured in each sex. Responses to these selective pressures are however constrained by the sexes' shared genome, leading to 'intralocus sexual conflict' (IASC) or 'sexual antagonism', where different alleles at given loci are favoured by selection in each sex. IASC is widespread among animals and plants and imposes an important evolutionary constraint on adaptation. However, despite our increasing understanding of the taxonomic prevalence of IASC and the traits affected, the genetic loci underlying this antagonism remain almost entirely unknown. To address this shortcoming I am combining experimental evolution, next-generation sequencing and bionformatics in a bid to identify causal sexually antagonistic loci across the Drosophila melanogaster genome.
The evolution of polymorphic gene expression in regulatory networks under sexually antagonistic selection
The widespread occurrence of sexual antagonism is somewhat at odds with classical population genetic theory which suggests that the conditions for invasion and maintenance of antagonistic alleles are highly restrictive, particularly under weak selection. This disparity suggests that classic models do not adequately capture the properties of antagonistic alleles nor of the fitness landscapes on which they evolve. To address this, I am collaborating with Dr. Alex Stewart and Dr. Max Reuter to develop a detailed biophysical model for the action of sexually antagonistic selection on gene expression. This was motivated by the fact that gene regulation sits at the core of sexual dimorphism and has previously been associated with sexual antagonism. In addition, we have a detailed understanding of transcription factor binding, allowing us to construct realistic fitness landscapes. This framework will allow us to gain a better understanding of the conditions in which antagonistic alleles invade and are maintained by selection as well a generate more specific insights into the expected distribution of these loci across regulatory networks.