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Yeast is an ideal system to empirically disentangle complex selective pressures and evolutionary tradeoffs: dynamics that influence evolution at all scales from ecosystems to disease progression. The Hays Lab's long-term research goal is to extend these topics to include environmental context: how does the environment in which these conflicts take place determine the ‘winners’ of molecular arms races, and shape the mutational spectra by which genomes adapt?
Using yeast’s unparalleled molecular and genomic resources, the Hays Lab is exploring the fundamental biology of host-parasite conflict. Understanding how biotic and abiotic pressures contribute to adaptive evolution at the molecular level has broad implications from conservation in a changing climate, to understanding infectious outbreaks and disease progression in individual patients.
Research areas:
each of the projects listed below encompasses the following research areas
Gene structure, function & regulation
Evolutionary and population genetics
Project 1. Biology and evolution of a rare eukaryotic plasmid
Project 1. Biology and evolution of a rare eukaryotic plasmid
Budding yeasts have plasmids! These plasmids are some of the few known to be naturally-occurring in eukaryotes. Like bacterial plasmids, they are extrachromosomal elements, and require host machinery for survival. We're interested in understanding more about how host cells and plasmids interact, and shape each others' evolution, with a particular focus on host protective mechanisms. We've built tools to explore host-plasmid compatibility (PMID 33063663), search for new plasmids, and aim to understand more about where these plasmids came from, what they are doing and how fungal genomes are evolving to suppress selfish elements.
Project 2. Transposons drive adaptation in nitrogen-starved yeast
Project 2. Transposons drive adaptation in nitrogen-starved yeast
Yeasts have retrotransposons! As in other eukaryotes, these selfish genetic elements can shape the structure and evolution of a host's genes and genome. Budding yeasts contain Ty elements which are LTR type transposons that use a 'copy and paste' lifestyle to spread in genomes. When new copies get inserted they can interrupt normal host function. We found previously (PMID 37192196) that Ty activity is increased under nitrogen starvation, and are now exploring more about the control of these retrotransposons under times of host stress and their role in adaptation.
Project 3. Evolution of novel resistance to killer yeast toxin, and killer counter-adaptation
Project 3. Evolution of novel resistance to killer yeast toxin, and killer counter-adaptation
Some yeasts are killers. They secrete protein toxins that can kill competing neighbor organisms, but protect themselves with an internal anti-toxin. In many yeasts, this toxin/antidote system is encoded on viral RNA genomes, not in the host genome. And these RNAs require an additional virus to survive. This system results in conflict within cells, between cells, and between viral genomes and is shaped by the microbial and environment context in which these interactions take place. We're using the abundant molecular tools and awesome power of yeast genetics to understand more about how each of the genomes in this complex conflict evolve, as selective pressures change around killers.
We hope in the long term to use these different systems to better understand the biology of fungal 'immune systems': how fungi protect themselves at the molecular level and adapt to biotic stressors. We hope that through understanding both shared and fungi-specific biology, we can shape future approaches in disease treatment and resistance.
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