We investigate how protein folding, self-assembly, and cellular stress reshape the relationship between genotype and phenotype—creating heritable states that influence evolution, aging, drug resistance, and disease.
How do biological systems preserve stability while retaining the capacity for rapid change? We combine genetics, experimental evolution, cell biology, biochemistry, genomics, proteomics, and quantitative approaches to uncover how protein conformational states and molecular chaperones reveal, buffer, and generate heritable variation. How we approach this problem
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Stanford University School of Medicine
James H. Clark Center, W350
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Stanford, CA 94305
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j11nunez@stanford.edu
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