Support teaching, research, and patient care.
Jesse is currently an Assistant Professor at Stanford University in the Department of Genetics and the Children’s Heart Center Basic Sciences and Engineering (BASE) Initiative, and is a recipient of the NHGRI Genomic Innovator Award. He co-leads a Functional Characterization Center at Stanford for the Impact of Genomic Variation on Function (IGVF) Consortium, and is an Associate Director of the Novo Nordisk Foundation Center for Genomic Mechanisms of Disease at the Broad Institute.Previously, Jesse was a Junior Fellow at the Harvard Society of Fellows and led a research group at the Broad Institute of MIT and Harvard. During his postdoctoral fellowship at the Broad Institute, Jesse developed large-scale CRISPR tools to map enhancer-gene regulation with Eric Lander and Nir Hacohen, and launched the Variants-to-Function (V2F) Initiative to connect genetic disease variants to their molecular and cellular functions. Jesse previously attended Stanford University, where he developed computational algorithms for analyzing gene expression with Russ Altman, and completed his PhD in the Harvard-MIT Division of Health Sciences and Technology, where he studied genome regulation by long noncoding RNAs with Eric Lander and Mitch Guttman. His research has been supported by the National Human Genome Research Institute, National Heart, Lung, and Blood Institute, Additional Ventures, Foundations for the National Institutes of Health, Harvard Society of Fellows, Fannie and John Hertz Foundation, and Department of Defense. Outside the lab, Jesse enjoys playing jazz/rock/funk, testing Chinese recipes, and surfing.
We are mapping the regulatory wiring of the genome to understand the genetic basis of heart diseases.The human genome encodes 2 million enhancers, which act in combination to regulate nearby genes. Each of the thousands of cell types in the human body has its own precise wiring that is difficult to resolve. Enhancers contain tens of thousands of DNA variants that affect human diseases — and therefore hold the key to understanding molecular mechanisms that control genetic risk for disease. We aim to map enhancer-gene connections in every cell type in the human body to connect disease variants to the genes, cell types, and pathways they control.Our approach:• We invent new single-cell methods combining genomics, biochemistry, and molecular biology.• We dissect molecular mechanisms of enhancer-gene communication. • We build computational models to map genome regulation. • We connect human genetic variants to biological mechanisms of disease by applying these tools in cellular and animal models.