In 2021 and 2022, Sabatini was fired from the Howard Hughes Medical Institute and resigned his positions at the Whitehead Institute and the Massachusetts Institute of Technology, following allegations of sexual harassment.[2][3][4] Sabatini denies the allegations.
Biography
David M. Sabatini was born and raised in
New York to
David D. Sabatini and 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, 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 graduated from Johns Hopkins.[5] In 2002 he became an assistant professor at MIT and a Member of the Whitehead Institute. He was promoted to tenured professor in 2006.
Sabatini is the scientific founder of Navitor,[7] Raze Therapeutics,[8] and KSQ Therapeutics.[9]
Allegations of sexual misconduct
In late 2021, following an investigation by an outside law firm of concerns surrounding sexual harassment, the
Howard Hughes Medical Institute fired Sabatini, and he resigned from the
Whitehead Institute.[2][10] Following this, MIT placed Sabatini on administrative leave while it conducted its own investigation.[11] MIT's investigation concluded that Sabatini had violated its policies on sexual relationships in the workplace. The investigation gave a recommendation to revoke tenure, at which time Sabatini resigned from his position at MIT.[3][11] Sabatini denies that the alleged behavior was sexual harassment, and he has filed a defamation lawsuit against the Whitehead Institute and two of its scientists.[3][12][4]
In 2022, Sabatini was under consideration for a position at the NYU Grossman School of Medicine.[13] After significant protests from students and some faculty over the sexual harassment allegations, he withdrew his name from consideration.[4][14][15]
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.[5] Although the TOR/DRR genes had been identified in 1993 as conferring rapamycin resistance in
budding yeast, the direct target of rapamycin and its mechanism of action in mammals was unknown.[20][21] 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.[5]
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.[22] For example, his lab discovered the
mTORC1[23] and
mTORC2[24] multi-protein complexes, the nutrient sensing Rag GTPase pathway upstream of mTORC1,[25] as well as the direct amino acid sensors Sestrin[26][27] and CASTOR.[28][29]
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[30] and the
CRISPR-Cas9 system.[31]
Sabatini DM, Erdjument-Bromage H, Lui M, Tempst P, Snyder SH (1994). "RAFT1: a mammalian protein that binds to FKBP12 in a rapamycin-dependent fashion and is homologous to yeast TORs". Cell. 78 (1): 35–43.
doi:
10.1016/0092-8674(94)90570-3.
PMID7518356.
S2CID33647539.
References
^Sabatini DM, Erdjument-Bromage H, Lui M, Tempst P, Snyder SH (July 1994). "RAFT1: a mammalian protein that binds to FKBP12 in a rapamycin-dependent fashion and is homologous to yeast TORs". Cell. 78 (1): 35–43.
doi:
10.1016/0092-8674(94)90570-3.
PMID7518356.
S2CID33647539.
^Kunz J, Henriquez R, Schneider U, Deuter-Reinhard M, Movva NR, Hall MN (1993). "Target of rapamycin in yeast, TOR2, is an essential phosphatidylinositol kinase homolog required for G1 progression". Cell. 73 (3): 585–96.
doi:
10.1016/0092-8674(93)90144-f.
PMID8387896.
S2CID42926249.
Arsenault, Mark; Irons, Meghan E.; Wen, Patricia (January 28, 2023). "Fate and the fallen star". Spotlight. The Boston Globe.
Part 1,
Part 2. Retrieved February 12, 2023