My first exposure to research was as an undergraduate at George Fox University. My experiences there showed me the impact of a liberal arts education with an independent research experience. I am excited by research and teaching as a way to expand and share knowledge, but also to foster growth, perseverance, excellence, and community for my students.
I completed my PhD in Biological and Biomedical Sciences at Harvard University, studying cell signaling and metabolism. I became interested in the genetics underlying cellular processes and focused on the effects of genetic variation on enzyme function for my postdoc at the University of Washington. I continue to study how standing variation and new mutations affect function in budding yeast.
In my research and teaching, I aim to equip all students with knowledge and tools to think scientifically. I want my students to take ownership of their learning through research and exploration, but also emphasize their responsibility to engage in a diverse, conscientious, and ethical future of science, whether it is by participating directly in research or by being a knowledgeable citizen trained in critical thinking.
Complete list of publications on
Google Scholar.
I use budding yeast (Saccharomyces cerevisiae) to study how genetic changes affect protein function and cellular phenotypes. I have projects of interest for students wanting to study human and yeast genetics and genomics, evolution, cellular signaling in yeast, and science education and outreach. My research falls into two broad categories:
1.
Yeast as a tool to study the effect of human genetic variants on response to medications (pharmacogenetics). A key promise of precision medicine is that genetic information can be used to optimize drug prescribing and dosing, since up to half of all people will experience a variable response to one or more prescription drugs. However, while the increase in genetic sequencing has increased our awareness of variation in human genes, the functional effects of over 70% of variants are unknown. In order for genetic information to improve treatment, we must connect sequence variation to function. Many human genes can functionally replace yeast genes, and by engineering changes to these genes we can determine if the genetic change leads to a change in function that could impact drug response. We also use computational prediction tools and clinical evidence found by literature review, so that by combining all of this evidence we can interpret genetic variants as likely or unlikely to lead to variable drug responses.
2.
Experimental evolution to identify mechanisms by which yeast adapt to stressors. Since yeast cells grow and divide rapidly, we can measure change across many generations in just a few weeks. We grow yeast in increasing concentrations of a selective pressure and observe over time as growth improves due to selection for yeast harboring beneficial mutations. By sequencing the evolved yeast, we can draw connections between the affected genes and selective pressure, and form hypotheses to investigate further. We are particularly interested in adaptation to caffeine, which inhibits the master growth regulator TOR; by studying these mutations we can better understand TOR signaling in yeast.
In all of my research, connection to the broader scientific community is critical, and I aim to involve my students in these networks. I work closely with ClinGen to learn about best practices in human variant interpretation and ensure that our yeast data is accessible and clinically useful. I also work with yEvo (yeast evolution) Lab, which provides connections to other groups studying evolution of yeast and opportunities for outreach through authentic research experiences in high schools. I am excited to introduce more students to these communities so that they can interact with diverse scientists and role models.
