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Title: The genetic basis of sexual antagonism in Drosophila melanogaster
Author: Hill, Mark Stephen
ISNI:       0000 0004 7226 9455
Awarding Body: UCL (University College London)
Current Institution: University College London (University of London)
Date of Award: 2017
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The divergent reproductive roles of males and females generate sexually antagonistic selection, with different trait values favoured in each sex. Responses to these selective pressures are however constrained by the sexes’ shared genome, leading to ’sexual antagonism, where, at a given locus, opposing alleles are favoured in males and females. Sexual antagonism is a taxonomically widespread and evolutionarily important phenomenon, but the identity and characteristics of the genetic loci underlying it remain almost entirely unknown. This thesis combines experimentation, bioinformatics and theory to identify, characterise, and explore the evolution of sexually antagonistic loci. In the introduction (chapter 1), I review the literature and integrate underlying theory and key empirical findings. I then identify the first putative antagonistic variants across the Drosophila melanogaster genome by comparing the sequences of haplotypes with contrasting sex-specific fitness profiles (chapter 2). I find a substantial excess of candidate SNPs, beyond the null expectation, and show that these SNPs are a non-random subset of the genetic variation in the LHM population. In chapter 3, I characterise the functional properties of antagonistic loci using a suite of bioinformatic analyses. Here, a prominent role of gene regulation emerges. I further describe an evolve-and-resequence experiment conducted to investigate the evolution of sexually antagonistic loci under sex-limited selection (chapter 4). Here, I was able to verify a subset of the sexually antagonistic loci identified in chapter 2. In chapter 5, I build a theoretical model to investigate when and where sexually antagonistic alleles invade in gene regulatory cascades. I find sexually antagonistic polymorphism can be displaced to higher levels of the regulatory hierarchy from where it initially arises. In the general discussion (chapter 6), I place these findings into context and provide a perspective on future research prospects.
Supervisor: Reuter, M. ; Fowler, K. Sponsor: Not available
Qualification Name: Thesis (Ph.D.) Qualification Level: Doctoral
EThOS ID:  DOI: Not available