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Kerry Geiler-Samerotte is an evolutionary cell biologist and assistant professor in the Center for Mechanisms of Evolution and School of Life Sciences at Arizona State University.
Geiler-Samerotte and her research team investigate how basic features of cells constrain or influence the way cells can evolve. To do this, the lab quantifies the impact of mutations on cell physiology and growth across fine environmental gradients. A major goal is to understand and predict when and why the impacts of a mutation change across contexts. Research in the Geiler-Samerotte lab combines high-throughput, high-precision laboratory experiments in yeast with computational and mathematical approaches.
Assistant professor Geiler-Samerotte earned a BS from Cornell University in 2004 in Ecology and Evolutionary Biology, advised by Rick Harrison. She earned her PhD from Harvard University in 2011 in Organismal and Evolutionary Biology, co-advised by Daniel Hartl and D. Allan Drummond. Her postdoctoral work was completed with Mark Siegal (New York University) and Dmitri Petrov (Stanford University).
Organisms are comprised of interacting parts. Even within single cells, networks of proteins regulate basic functions. The impact of perturbing one part of an organism for example, via genetic mutation can often be modified by perturbation to other parts. This creates obstacles for scientists: how do we predict traits from genetic data when the same mutation can have different impacts? This also presents challenges during evolution: how does an organism adapt or evolve when changing one trait can influence many other traits, resulting in complex tradeoffs? To quantify the spectrum of effects that a specific perturbation may have on an organism, the Geiler-Samerotte lab measures how yeast cells respond to subtle genetic or environmental changes. Then, we study how cellular responses change when multiple perturbations are combined or when the magnitude of a perturbation is systematically varied. Our research provides insight about how interactions between small-effect genetic variants shape the evolution of complex traits.