Evolution of Multicellular Drug Resistance. Cancer, microbial and protozoan infection therapies are challenged by the increasing resistance of the pathogens to the common drugs. Drug resistance, just as any physiological cellular stress response, evolves rapidly along with the changing host environment. One of the microbial cell traits underlying drug resistance is forming multicellular clusters, e.g. biofilms, flocs, and clumps. Our project focuses on revealing the genetic mechanisms controlling multicellular phenotypes in yeast and their impact on the emergence of drug resistance. I am interested in utilizing synthetic gene circuits to externally control the mitotic exit network.

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Synthetic Regulation of Tau/Amyloid Beta Interactions. Alzheimer's disease causal treatments have traditionally targeted a single protein target. The disease, however, still progresses due to multiple interactions of the pathological proteins with other molecules within the neural cell. In this project, we design the synthetic regulation of Tau- and amyloid beta-encoding genes in yeast cellular model to reveal the potential dose-dependent interaction between their protein products. Refer to more information to the leader of this project - Thomas Malachowski.

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Yeast Parkinson's Disease Model for Biotechnological Purposes. My undergraduate research focused on designing and describing a yeast model of production, metabolism, and degradation of human alpha-synuclein - a hallmark of Parkinson's disease. Specifically, the preferred intracellular tagging, pool control, and the debate of degradation via autophagal versus proteasomal system were addressed. The work laid foundation for a new branch in lab research dedicated to exploring oxidative stress responses upon heterologous aggregation-prone protein production in yeast.