Viktor I. Korolchuk
Showed that where lysosomes sit inside the cell tunes mTORC1 activity to nutrient supply. His Newcastle lab found that senescent cells can no longer switch mTORC1 off when nutrients or growth factors are withdrawn, and studies how autophagy and mitophagy decline with age
Professor of Cell Biology, Biosciences Institute, Newcastle University (since 2024) · Reader, Newcastle University (2017–2024) · Lecturer, Institute of Ageing and Health, Newcastle University (2011–2017) · postdoc, University of Cambridge (2003–2011, David Rubinsztein lab) · postdoc, University of Bristol (2000–2003) · PhD in Biochemistry, Institute of Biochemistry, National Academy of Sciences of Ukraine, Kyiv (2000)
Korolchuk Lab, Biosciences Institute, Newcastle University (Newcastle upon Tyne, England, United Kingdom) ↗ Lab lineagetrained under David C. Rubinsztein → Bluesky@korolchuklab.bsky.social ↗ ORCID0000-0002-4071-592X ↗
Portrait: Newcastle University
In 2011, working in David Rubinsztein's lab in Cambridge, Korolchuk showed that mTORC1 activity depends on a variable that had received little attention: where the lysosome physically sits in the cell. With nutrients available, lysosomes move out towards the cell periphery, close to the plasma-membrane signalling modules, and mTORC1 is active there. Starvation changes intracellular pH and pulls them into a cluster around the nucleus, mTORC1 output falls, and autophagy is released. The same positioning also sets how fast autophagosomes fuse with lysosomes — so one variable governs both the start and the finish of autophagic flux.
Since starting his own group at Newcastle in 2011, he has worked the other end of the same problem: what mTORC1 does in cells that have stopped dividing. His lab showed that in senescent human cells mTORC1 is constitutively active and deaf to the removal of serum or amino acids, and that the fault lies upstream — a depolarised plasma membrane, defective primary cilia, and an internal amino acid pool kept topped up by autophagy. Correct those inputs and the cells die, which makes persistent mTORC1 signalling a survival dependency of senescent cells rather than a side effect of senescence.
More recently the lab has tied rapamycin's effect on cellular ageing to mitochondrial housekeeping: healthy primary human cells run a high level of basal mitophagy that shuts down in senescence, and reactivating it turned out to be necessary for the anti-senescence effect of both rapamycin and NAD precursors. Alongside the research, Korolchuk is the human selector behind Autophagy and mTOR (bims-auttor), the weekly curated literature report on biomed.news that has been running since February 2019 — the same slice of the literature this Atlas curates.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2011 | M | Lysosomal positioning coordinates cellular nutrient responses KOR2011 First author: showed lysosomal positioning coordinates mTORC1 signalling with autophagic flux, adding a spatial axis to nutrient sensing. |
| 2017 | M | Persistent mTORC1 signaling in cell senescence results from defects in amino acid and growth factor sensing CAR2017 Senior author: explained why mTORC1 stays switched on in senescent cells, and that they depend on it to survive. |
| 2018 | A | Rapamycin improves healthspan but not inflammaging in nfκb1(-/-) mice. COR2018 Co-author: in nfkb1 mice rapamycin improved healthspan and lowered senescence markers without extending lifespan or reducing inflammaging. |
| 2021 | M | G3BPs tether the TSC complex to lysosomes and suppress mTORC1 signaling PRE2021 Co-author on the Cell study showing G3BP1/2 tether the TSC complex to lysosomes and thereby suppress mTORC1. |
| 2024 | M | Suppressed basal mitophagy drives cellular aging phenotypes that can be reversed by a p62-targeting small molecule KEL2024 Senior author: reactivation of basal mitophagy is required for the anti-senescence effect of rapamycin and NAD precursors. |
Co-authors in the Atlas 23
People with a profile here who share at least one study with Viktor I. Korolchuk.
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- Bernadette Carroll 3 shared studies First author of the study showing why mTORC1 stays switched on in senescent cells, and co-author on G3BP–TSC and senescence-mitophagy work; her own lab studies how nutrient sensing breaks down in ageing cells.
- Glyn Nelson 2 shared studies Microscopy specialist who manages Newcastle University's Bioimaging Unit and has worked for many years on the signalling networks that keep senescent cells in their arrested state
- Penny Lovat 2 shared studies Professor of Cellular Dermatology and Oncology at Newcastle University who studies autophagy in melanoma, and whose work on the autophagy protein AMBRA1 and the skin protein loricrin underlies a test, developed with AMLo Biosciences, to identify early melanomas at low risk of spreading
- Satomi Miwa 2 shared studies Mitochondrial biologist who contributed to Newcastle studies on rapamycin in NF-κB-driven ageing mice and on basal mitophagy as a brake on cellular senescence.
- Thomas von Zglinicki 2 shared studies Cell-senescence researcher who co-authored the Newcastle studies on stuck-on mTORC1 in senescent cells and on loss of basal mitophagy as a driver of cellular ageing.
- Alexander M Heberle Cell biologist and Junior Group Leader at the University of Innsbruck who studies how mTOR balances growth signalling and metabolism when cells are under stress, trained in Kathrin Thedieck's systems-biology group
- Aurelio A. Teleman Uses fruit-fly genetics and human cells to study how growth signalling through TOR controls cell and body size. His lab showed that starvation and other stresses move TSC2 to the lysosome to switch mTORC1 off
- Cahir O'Kane Fruit-fly geneticist at Cambridge who studies how the endoplasmic reticulum is built inside nerve fibres and how its failure causes hereditary spastic paraplegia, and who helped bring Drosophila models into David Rubinsztein's autophagy work
- Clara Correia-Melo Ageing biologist who showed with João Passos in Newcastle that rapamycin can improve healthspan in mice without lowering inflammation, and later studied metabolite sharing between cells in Markus Ralser's lab
- Constantinos Demetriades Showed as a postdoc in Aurelio Teleman's lab that starvation and other stresses pull TSC2 to the lysosome to switch mTORC1 off. His group, at the Max Planck Institute for Biology of Ageing in Cologne from 2017 and at ERIBA in Groningen since 2025, studies how cells sense nutrients and stress through mTORC1 and how this changes with age
- David C. Rubinsztein Showed that rapamycin induces autophagy to clear the toxic protein of Huntington's disease, and that where lysosomes sit inside a cell helps set mTORC1 activity
- Fiona Menzies Cell biologist who worked for many years in David Rubinsztein's Cambridge lab on autophagy and the clearance of disease proteins in neurodegeneration
- George Kelly Cell biologist from Viktor Korolchuk's group at Newcastle University who showed that the routine clearing of damaged mitochondria fails as human cells become senescent
- Gianluca Figlia Cell biologist who studied how mTORC1 senses nutrients in Aurelio Teleman's group at the German Cancer Research Center, including the finding that glutamine is sensed through the kinase GCN2, and who now works at the Institute of Neuropathology in Aachen
- João F. Passos Studies how senescent cells, mitochondria and telomeres contribute to ageing and age-related disease.
- Julian R. Sampson Clinical geneticist who led the consortium that identified the TSC2 gene and led trials of mTOR inhibitors in tuberous sclerosis, including the TRON trial of everolimus for cognition.
- Kathrin Thedieck Senior author of three Atlas studies that treat mTOR signalling as a dynamic network: TSC-independent mTORC2 activation, concurrent AMPK and mTOR activation by amino acids, and G3BP tethering of TSC to lysosomes.
- Laura Brohée Cell biologist who studied how lipid metabolism and the lysosome feed into mTORC1, first at the University of Liège and then at the Max Planck Institute for Biology of Ageing in Cologne
- Lukas A. Huber Cell biologist who studied the p14-MP1 scaffold on late endosomes, a complex later recognised as part of Ragulator (LAMTOR), the lysosomal platform that holds mTORC1 in place
- Mariana de Araujo Cell biologist in Lukas Huber's group in Innsbruck who solved the crystal structure of the Ragulator (LAMTOR) complex, the lysosomal platform on which mTORC1 is switched on
- Mirja Tamara Prentzell First author of the study showing that G3BP proteins anchor the TSC complex to lysosomes, a physical brake on mTORC1; earlier co-author on the dynamic insulin–mTOR network model.
- Ralf Baumeister Head of the Freiburg department that hosted the Thedieck group during the mTOR network modelling work; co-author on the dynamic mTOR model and the G3BP–TSC study.
- Vojo Deretic Studies how autophagy shapes infection, immunity and inflammation, including early work showing that autophagy restricts Mycobacterium tuberculosis, and how galectins and TRIM proteins control mTOR and AMPK.
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