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Abstract
The phylum Apicomplexa contains a very large group of mostly obligate intracellular parasites that are causative agents of devastating diseases including malaria, toxoplasmosis, and cryptosporidiosis. Apicomplexans have reductive streamlined genomes, with variable sizes and protein coding content. Differences in gene gain and loss patterns aid our understanding of the biology and evolution of parasitism. Gene gain and loss patterns were identified by an orthology clustering approach. Copy number variation in apicomplexan dynein motor complexes and sugar transporters was examined in detail. In this dissertation, I report phylum-wide identification of apicomplexan dyneins and sugar transporters, examination of trends in the evolution of respective gene family members, and characterization of whether identified trends correlate to the parasites biology. There are six phylogenetic subtypes of apicomplexan sugar transporters and twelve subtypes of dynein heavy chains. Variable copy number in dynein heavy chains appears to be a result of differential gene loss while in contrast sugar transporters appears to have evolved from gene expansions combined with differential gene retention. I found evidence correlating identified evolutionary trends to the biology of the parasites. Apicomplexans that do not build flagella have dispensed with flagellar axonemal dyneins. A retained flagellar dynein heavy chain protein is expressed and localized in Toxoplasma gondii non-flagellated tachyzoite stage, suggesting undiscovered or emergent dynein functions. A retained sugar transporter in Plasmodium falciparum might be sporozoite-specific. Here, I also use orthology analyses to define core conserved gene sets for diverse eukaryotic lineages. Existing core gene sets have many limitations when used to study diverse, non-model eukaryotes. Overall, the findings presented in this dissertation enhance our understanding of apicomplexan biology and eukaryotic evolution.