Dr. Casey Romanoski received her undergrad degree in 2004 from the Arizona International College at the University of Arizona where she concentrated in math and science. She then received her doctorate from UCLA in human genetics, working in the laboratory of Dr. Aldons (Jake) Lusis. In the Lusis Lab, Dr. Romanoski demonstrated that gene regulation in human endothelial cells is genetically and environmentally determined. She then completed her postdoctoral research at the Univeristy of California, San Diego, in the laboratory of Dr. Christopher Glass. There, she used natural genetic variation between inbred mouse strains to demonstrate the hierarchical and collaborative nature of enhancer activity in gene regulation. Throughout her training, Dr. Romanoski became very interested in the interdependence between genetic sequence and molecular traits, which is the foundation of her ongoing research. In 2016, she accepted a position as an Assistant Professor in the Department of Cellular and Molecular Medicine and BIO5 Fellow at the University of Arizona. Her research program uses experimental and computational approaches to better understand complex disease and human biology. A native Tucsonan, she is a proud Arizona Wildcat.
The overarching goal of my research program is to better understand the interaction between DNA variation and gene regulation. I study this interaction in settings of inflammation with application to complex diseases like atherosclerosis and hypertension. My research is predominantly focused on endothelial cells, which line blood vessels and are mediators of inflammation in the vessel wall. Using next-generation sequencing technologies, and a combination of experimental and computational approaches, we study how endothelial cells achieve context-appropriate expression patterns in healthy and inflammatory settings. By leveraging the interconnected relationship between DNA sequence, epigenetics, gene expression, and disease loci from genome-wide association studies, we aim to identify and interpret complex disease mechanisms.