David M. Sabatini

As a graduate student in Solomon Snyder’s Lab at Johns Hopkins, Sabatini began working on understanding the molecular mechanism of rapamycin; a macrolide antibiotic discovered in the soil of Easter Island that has potent antifungal, immunosuppressive, and anti-tumorigenic properties. Although the TOR/DRR genes had been identified in 1993 as conferring rapymycin resistance in budding yeast, the direct target of rapamycin and its mechanism of action in mammals was unknown. In 1994, Sabatini used rapamycin and its binding partner FKBP12 to purify the mechanistic Target of Rapamycin (mTOR) protein from rat brain, showing it to be the direct target of rapamycin in mammals and the homolog of the yeast TOR/DRR genes.

Sabatini’s research interests have expanded in recent years to include cancer metabolism as well as technology development surrounding the use of high-throughput genetic screens in human cells, most notably through the use of RNA interference and the CRISPR-Cas9 system. As of 2016, Sabatini has authored over 250 publications and has an h-index of 100.

David M. Sabatini is an American scientist and Professor of Biology at the Massachusetts Institute of Technology as well as a member of the Whitehead Institute for Biomedical Research. He has been an investigator of the Howard Hughes Medical Institute since 2008 and was elected to the National Academy of Sciences in 2016. He is known for his important contributions in the areas of cell signaling and cancer metabolism, most notably the discovery and study of mTOR, a protein kinase that is an important regulator of cell and organismal growth that is deregulated in cancer, diabetes, as well as the aging process.

David M. Sabatini was born and raised in New York to Dr. David D. Sabatini and Dr. Zulema Sabatini, both Argentine immigrants from Buenos Aires. He obtained his B.S. from Brown University followed by both his MD and his Ph.D. at Johns Hopkins School of Medicine in Baltimore, Maryland, where he worked in the lab of Solomon H. Snyder. He joined the Whitehead Institute as a Whitehead Fellow in 1997, the same year he matriculated from Johns Hopkins. In 2002 he became an Assistant Professor at MIT and a Member of the Whitehead Institute. He was promoted to tenured professor in 2006.

Since starting his own lab at the Whitehead Institute in 1997, Sabatini has made numerous key contributions to the understanding of mTOR function, regulation, and importance in diseases such as cancer. For example, his lab discovered the mTORC1 and mTORC2 multi-protein complexes, the nutrient sensing Rag GTPase pathway upstream of mTORC1, as well as the direct amino acid sensors Sestrin and CASTOR.