Sue Menon
Showed insulin controls mTORC1 by moving the TSC complex on and off the lysosome
Research Investigator, Novartis · postdoctoral fellow, Manning Lab, Harvard T.H. Chan School of Public Health (2008–2013) · PhD, Yale University (2008)
Profile, Manning Lab (Harvard Chan) (Boston, Massachusetts, USA) ↗ Lab lineagetrained under Brendan D. Manning →
As a postdoc in Brendan Manning's lab, Sue Menon showed that insulin triggers the TSC complex to acutely dissociate from the lysosomal surface — where a pool of Rheb and mTORC1 resides — through Akt-mediated phosphorylation of TSC2, physically separating the brake (TSC) from the switch (Rheb) it otherwise keeps off. It gave a spatial explanation for how growth-factor and nutrient signals converge on the same lysosomal on/off switch without simply overriding each other.
Her other work in the Manning lab traced mTORC1's downstream reach into disease biology — including how chronic mTORC1 activation alone is sufficient to cause liver cancer in a mouse model, and how mTORC1 drives lipogenesis through SREBP1c — before she moved into industry research at Novartis.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2010 | M | Activation of a metabolic gene regulatory network downstream of mTOR complex 1 DUV2010 Co-author: mTORC1 switches on glycolysis, the pentose phosphate pathway and lipid synthesis through HIF1α and SREBP1/2 (cells). |
| 2014 | M | Spatial control of the TSC complex integrates insulin and nutrient regulation of mTORC1 at the lysosome MEN2014 Shows insulin triggers the TSC complex to dissociate from the lysosome, physically separating it from Rheb and mTORC1 — letting growth-factor and nutrient signals independently control the same switch. |
Co-authors in the Atlas 9
People with a profile here who share at least one study with Sue Menon.
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- Brendan D. Manning 2 shared studies Was among the groups that in 2002 identified TSC2 as a direct target of Akt (MAN2002), linking insulin and PI3K signalling to mTORC1, and later found TBC1D7 as the third subunit of the TSC complex. His lab has shown how mTORC1 turns growth signals into the synthesis of lipids and nucleotides
- Alexander J. Valvezan Showed as a Manning-lab postdoc that mTORC1 matches nucleotide production to demand, creating a weak point that can be targeted in tumours with TSC loss. His Rutgers lab found that mTORC1 activity rises and falls through the cell cycle and helps drive entry into mitosis
- George Talbott Research assistant in Brendan Manning's mTOR lab at Harvard in 2013 and 2014, who contributed to studies on where the TSC complex sits in the cell and how metformin reaches mTORC1
- Gerta Hoxhaj Studies how growth signalling through PI3K, AKT and mTOR rewires cell metabolism; as a Manning-lab postdoc she co-authored work on how metformin inhibits mTORC1 in the liver
- Christian C. Dibble Identified TBC1D7 as the third subunit of the TSC complex that controls mTORC1, as a Manning-lab graduate student. His lab at Beth Israel Deaconess studies how PI3K signalling and nutrient supply are integrated to control mTORC1 and cell metabolism
- Katrin Düvel First author of the study showing that mTORC1 switches on a metabolic gene program through HIF1α and SREBP, driving glycolysis, the pentose phosphate pathway and lipid synthesis
- Leon O Murphy Cell biologist who led autophagy and mTOR drug discovery at Novartis in Cambridge, Massachusetts, and is now Chief Scientific Officer of Casma Therapeutics, a company that develops drugs acting on the autophagy-lysosome system
- Lewis C. Cantley Co-discovered PI3K, the pathway that feeds into mTOR from growth factors
- Peter M Finan Biochemist and drug-discovery leader who started the PI 3-kinase drug discovery program at Novartis and ran its Developmental and Molecular Pathways group in Cambridge, Massachusetts, before moving into life-science venture investing
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