Elizabeth Bryda, PhD

Elizabeth Bryda, PhD
Professor
University of Missouri

Elizabeth Bryda earned a BS in Biology and Music from Tufts University, a MS in Microbiology and a PhD in Molecular Genetics at Rutgers University and went on to post-doctoral training in Mammalian Molecular Genetics at the Wadsworth Center.

While a faculty member at the Joan C. Edwards School of Medicine at Marshall University, she identified and characterized kidney and hearing loss genes in mouse models of polycystic kidney disease and Usher syndrome respectively. She relocated to the University of Missouri in 2003 and has continued to embrace comparative medicine approaches to studying human diseases using a variety of animal models from rodents to zebrafish and applying state-of-the art genetic engineering technologies.

She is currently a Professor of Veterinary Pathobiology in the College of Veterinary Medicine with adjunct appointments in the Division of Biological Sciences and School of Nursing and she serves as the Director of the MU Animal Modeling Core. Dr. Bryda is the Director of the NIH-funded Rat Resource and Research Center (RRRC) which serves as a repository for important rat genetic models as well as provides animals, embryonic cell lines and rat-related services to the global biomedical research community. She is a 2017 recipient of the Zoetis Award for Veterinary Research Excellence and a 2018 recipient of the Academy of Science-St. Louis James B. Eads Award for outstanding achievement in technology.

Animal Modeling in the Era of Precision Medicine

Comparative medicine and animal modeling allow us to understand genetics, disease, and basic biology across species.  Because genome editing can be performed in a quick and reliable manner in a variety of species using CRISPR/Cas9, this technology is transforming the ability to generate appropriate animal models to study human disorders.  Genetically engineered animals can be used effectively to dissect out various aspects of human disease, including identification of putative disease genes, re-creation and validation of potential disease-causing alleles observed in patients, and testing of targeted therapeutics.  Our recent studies to determine the genetic basis of cystic kidney disease in human patients illustrate the power of using CRISPR/Cas9 to generate informative animal models to validate the disease-causing nature of rare human variants.