David Schatz is a molecular geneticist and immunologist recognized for his work on the genetics of antibody and T cell receptor gene assembly and diversification. He is known particularly for the discovery of the recombination activating genes, RAG1 and RAG2, and for insights into the biochemical function, regulation, and evolution of the RAG proteins and the genome targeting of somatic hypermutation. Schatz was born and grew up in Charlottesville, Virginia, where he attended the public schools. He graduated from Yale University with a B.S.-M.S. degree in molecular biophysics and biochemistry and then spent two years as a Rhodes Scholar at Oxford University, earning a B.A. in philosophy and politics. Schatz earned his Ph.D. in biology from the Massachusetts Institute of Technology in 1990 and joined the faculty of Yale School of Medicine in the Department of Immunobiology in 1991. He is currently Professor and Chair of the Department of Immunobiology and was an investigator of the Howard Hughes Medical Institute from 1991-2017. Schatz is a fellow of the American Association for the Advancement of Science and a member of the National Academy of Sciences, the National Academy of Medicine, and the American Academy of Arts and Sciences.

Research Interests

David Schatz's laboratory is interested in the mechanism, regulation, and evolution of V(D)J recombination and somatic hypermutation, the reactions that assemble and refine the genes that encode the immunoglobulin and T-cell receptors employed by B and T lymphocytes. They have provided insights into the biochemical mechanism of action of the RAG1 and RAG2 proteins, which initiate V(D)J recombination, and have contributed to our understanding of how V(D)J recombination is regulated in vivo. They identified the pattern of RAG binding at antigen receptor genes and elsewhere the genome, resulting in the "recombination center" model for V(D)J recombination. They discovered the ability of RAG to perform DNA transposition and provided evidence linking RAG1 and RAG2 to DNA transposases from evolutionarily diverse eukaryotes, with implications for models of the evolution of the adaptive immune system. In the area of somatic hypermutation, they performed a seminal sequence analysis of non-immunoglobulin genes in germinal center B cells, thereby defining the magnitude of the activation induced deaminase (AID) "off-target" problem. In addition, they identified and characterized the key DNA sequences responsible for targeting SHM to immunoglobulin loci, with implications for the origins of germinal center B cell lymphomas.

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Primary Section

Section 43: Immunology and Inflammation