Transposable elements (TEs) are mobile genetic elements that can self-replicate and insert elsewhere in the genome. This movement often comes with a fitness cost and yet TEs are tremendously common. They contribute more than 80% to the largest plant genomes, but are much less abundant in the smallest plant genomes. Combined, these observations raise the two central questions of this thesis. First, why are TEs so common, and the genomes so large, in some species but not others? Second, what prevents TEs from completely taking over and causing genomes to fail to produce functional individual organisms? In this thesis, I have used population and comparative genomics approaches on whole genome data from closely related plant species and syntheisising literature reviews to examine some of the evolutionary causes and consequences of TE proliferation in plants. In particular, I have investigated the role of mating system shifts, from outcrossing to self-fertilization and from sexual to asexual reproduction, in driving variation in TE abundance and genome size. I used the reference genome of Capsella rubella as an outgroup to show that the higher TE abundance and larger genome size of the outcrossing Arabidopsis lyrata compared to selfing A. thaliana is due to TE driven expansion in the outcrosser rather than genome loss in the selfer. I investigated three Capsella species of contrasting mating system and found that the evolution of self-fertilization may have different effects on TE evolution on short and on long timescales. I applied a phylogenetic comparative approach and whole genome sequencing to demonstrate that sex and TEs cannot explain the variation in genome size in evening primroses (Oenothera). Using transcriptome data I showed that the chromosomal distribution (sex chromosomes vs. autosomes) of nuclear gene with organellar origin in Rumex hastatulus is not consistent with either co-adaptation or sexual conflict hypotheses. Finally, I showed that studying the proliferation of TEs offers insights to the cardinal problem of social evolution of what prevents selfish behaviour at lower levels from destroying functionality of the group. Overall, my thesis is a contribution to understanding the evolutionary causes and consequences of TE proliferation.
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