Marion Cornu
Physiologist from Michael Hall's Basel lab who showed in mice that mTORC1 in the liver controls body temperature, movement and fat metabolism through the hormone FGF21
Biozentrum, University of Basel, Michael N. Hall lab (2012–2018, most recent confirmed affiliation) · Center for Integrative Genomics, University of Lausanne (2014) · current position not confirmed
Portrait: LinkedIn
Marion Cornu is a co-author of two Atlas studies from Michael Hall's lab. In the first (2012), mice lacking rictor, the core subunit of mTORC2, only in the liver could not sense that they had eaten. Their livers kept making glucose and made less fat, and the animals had high blood sugar and insulin. Restoring the kinase Akt fixed both problems, which placed Akt as the main route from liver mTORC2 to these outputs. In the second (2013), a large-scale measurement of phosphorylated proteins in cells showed that mTORC1 turns on the production of pyrimidines, the building blocks of DNA and RNA.
Cornu's own first-author work looked at the opposite case, too much mTORC1 in the liver. In a 2014 PNAS study the team removed TSC1, a brake on mTORC1, from mouse liver. The mice moved less, had lower body temperature and less liver fat. Constant mTORC1 activity drained glutamine from the liver and blood and drove production of the hormone FGF21, which acted on the whole body. With Hall, Cornu also wrote a 2013 review on mTOR in aging, metabolism and cancer.
PubMed also lists Cornu in 2014 at the Center for Integrative Genomics of the University of Lausanne, on a study of insulin-producing beta cells, and in Basel on a 2018 Nature paper identifying the enzyme LHPP as a tumour suppressor in liver cancer. A current position could not be confirmed.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2012 | A | Hepatic mTORC2 activates glycolysis and lipogenesis through Akt, glucokinase, and SREBP1c HAG2012 Co-author: liver-specific loss of mTORC2 left mice unable to switch the liver to fed-state metabolism. |
| 2013 | M | Quantitative phosphoproteomics reveal mTORC1 activates de novo pyrimidine synthesis ROB2013 Co-author: phosphoproteomics showed that mTORC1 activates de novo pyrimidine synthesis. |
Co-authors in the Atlas 7
People with a profile here who share at least one study with Marion Cornu.
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- Michael N. Hall 2 shared studies Discovered TOR in yeast in 1991 and established it as a central controller of cell growth that responds to nutrients. His lab later showed that TOR works in two distinct complexes, TORC1 and TORC2, only one of which is blocked by rapamycin
- Aaron M. Robitaille Mass spectrometry scientist who, as a PhD student in Michael Hall's lab, used phosphoproteomics to show that mTORC1 switches on the cell's production of pyrimidines, and who now works on proteomics applications at Thermo Fisher Scientific
- Asami Hagiwara First author of a 2012 mouse study from Michael Hall's lab showing that liver mTORC2 tells the liver that the animal has eaten, by switching on sugar breakdown and fat production
- Charles Betz Traced mTORC2 to a specific address inside the cell — the mitochondria-ER contact site
- Markus A. Rüegg Neurobiologist at the Biozentrum of the University of Basel who studies how muscles and the nerve connections that drive them develop, age and fail, including the role of mTOR signalling in muscle.
- Mitsugu Shimobayashi Metabolism researcher who trained with Michael Hall in Basel on mTOR in fat tissue and now leads a group at KU Leuven studying how fat and liver control sugar and lipid storage
- Nadine Cybulski Cell biologist from Michael Hall's Basel lab who showed that mTORC2 in fat tissue helps control how big the whole body grows
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