Debasish Paul
Postdoctoral fellow in Steven Cappell's lab at the National Cancer Institute who studies how ubiquitin ligases time the start of the cell cycle, and who found that mTOR briefly switches off the APC/C to give cells a burst of glycolysis as they start to divide
Postdoctoral fellow, Cappell Lab, Laboratory of Cancer Biology and Genetics, Center for Cancer Research, National Cancer Institute (papers 2021–2025) · PhD on ubiquitin ligases
Debasish Paul is first author of PAU2025, a Nature paper about the moment a resting cell decides to divide. When a growth signal arrives, mTOR quickly adds a phosphate to CDH1, the helper protein of a large enzyme called APC/C that tags other proteins for destruction. This partly releases CDH1 and briefly switches APC/C off. One of APC/C's usual targets, the glycolysis enzyme PFKFB3, then builds up, and the cell burns more glucose for a while, until a slower-acting phosphatase turns APC/C back on. The study, in human cells, showed that this short pulse of glycolysis is needed for cells to enter the cell cycle.
The finding gives mTOR a new job: besides boosting protein synthesis, it times a metabolic switch by reaching into the cell-cycle machinery. Because many cancers have overactive mTOR, the circuit may also help explain how tumor cells keep their fuel supply high, although the paper itself did not test tumors.
Paul is a postdoctoral fellow in Steven Cappell's lab at the Center for Cancer Research of the National Cancer Institute in Bethesda, and the publication record places Paul there from at least 2021. That year the group showed that cells hit by DNA damage early in the cycle often keep going rather than stopping at the classic checkpoint. The lab uses time-lapse imaging of single living cells to follow cell-cycle decisions.
Paul's PhD was on ubiquitin ligases, enzymes that tag other proteins with a small protein called ubiquitin, often marking them for destruction. In the Cappell lab Paul studies how the activity of these enzymes rises and falls as a resting cell re-enters the cell cycle, focusing on the APC/C, and is building fluorescent biosensors that report ubiquitin ligase activity in living cells.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2025 | M | Transient APC/C inactivation by mTOR boosts glycolysis during cell cycle entry PAU2025 First author: showed that mTOR phosphorylates CDH1 to briefly inactivate APC/C, letting PFKFB3 build up and boost glycolysis as cells enter the cell cycle. |
Co-authors in the Atlas 2
People with a profile here who share at least one study with Debasish Paul.
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- John G. Albeck Measures mTORC1, AMPK and other metabolic signals in single living cells, following how they change over minutes and hours
- Steven D. Cappell Studies how single cells commit to dividing; showed that mTOR briefly switches off the APC/C to give cells a pulse of glycolysis at cell cycle entry
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