The Genetic Basis Underlying the Evolution of Commensal Microbes to Opportunistic Pathogens

The complex and dynamic interactions between microbes and humans have been known to carry large implications on human health. The evolution of pathogenesis has been studied extensively in bacteria, but studies are lacking in eukaryotic species, particularly in fungi. Given their ability to sexually reproduce, the dynamics of evolution in fungal species could largely differ from those of bacteria. Furthermore, the amount of variation that a population originally evolves from — whether they are initially clonal or stem from a large amount of standing variation — can potentially affect their rate of adaptation. This project aims to study the evolution of pathogenesis in sexually and asexually reproducing populations of Saccharomyces cerevisiae by selecting for biofilm formation. In addition to comparing the rate of adaptation between asexual and sexual populations, we aim to compare populations evolved from initially clonal backgrounds and those with high standing genetic variation. Previous studies (McDonald, et. al., 2016 and Kosheleva and Desai, 2017) have shown that sexual reproduction can reduce linkage disequilibrium through the recombination of alleles. While most of those studies focused on growth as their phenotype of interest, we focused on biofilm formation as a proxy for pathogenicity. Five strains from diverse genetic and geographic backgrounds in addition to a synthetic mosaic strain constructed from those five backgrounds were evolved in an evolution experiment by a former lab mate. Genetic data was then analyzed to identify relevant mutations for pathogenicity and to compare the speed of adaptation between asexual and sexual populations from both initially clonal and highly recombinant populations. This project specifically focuses on one clonal strain from the European Wine background and the synthetic mosaic strain. We were able to confirm previous findings that sexual reproduction speeds that rate of adaptation in populations of clonal backgrounds. We were also able to identify a few patterns corresponding to Kosheleva and Desai’s (2017) findings that evolution in asexual populations are driven by clonal sweeps whereas, in sexual populations, evolution is driven by many linked variants that are weakly selected