Glyn Nelson
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
Specialist Experimental Scientific Officer and manager, Bioimaging Unit, Newcastle University · postdoc with Thomas von Zglinicki, Newcastle University · postdocs at the University of Liverpool and AstraZeneca · BSc and PhD, University of Edinburgh
Bioimaging Unit, Newcastle University (Newcastle upon Tyne, England, United Kingdom) ↗
Portrait: Newcastle University
Senescent cells have stopped dividing for good but stay alive and active, and they build up in aging tissues. Glyn Nelson is a co-author of two Newcastle studies in this Atlas that look at how mTORC1, the growth-control complex, behaves in these cells. The 2017 paper (CAR2017), on which Nelson is second author, found that mTORC1 stays switched on in senescent human fibroblasts and no longer responds when nutrients or growth factors are taken away. The fault lies upstream of mTORC1, in how the cells sense amino acids and growth signals. The 2024 paper (KEL2024) found that the routine clearing of damaged mitochondria shuts down as cells become senescent or old. Both studies were done in cultured human cells.
Nelson studied at the University of Edinburgh for a BSc and a PhD, then worked as a postdoc at AstraZeneca and at the University of Liverpool, and later joined Thomas von Zglinicki's group at Newcastle, which studies cell senescence. That research thread, on the signalling networks that start and maintain senescence, continues alongside Nelson's imaging role.
Nelson now manages Newcastle University's Bioimaging Unit, which gives researchers across the university access to light microscopes, training and image analysis help. Nelson also develops standard quality-control methods for light microscopy with the international QUAREP-LiMi initiative.
Milestones in the Atlas
A selection, not a full bibliography: only papers that meet the Atlas inclusion criteria.
| Year | Evidence | Study |
|---|---|---|
| 2017 | M | Persistent mTORC1 signaling in cell senescence results from defects in amino acid and growth factor sensing CAR2017 Second author: contributed to the study showing that mTORC1 stays active in senescent human cells because nutrient and growth-factor sensing upstream of it is faulty. |
| 2024 | M | Suppressed basal mitophagy drives cellular aging phenotypes that can be reversed by a p62-targeting small molecule KEL2024 Co-author: contributed to the study showing that basal mitophagy shuts down in senescent and aged human cells. |
Co-authors in the Atlas 6
People with a profile here who share at least one study with Glyn Nelson.
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- Bernadette Carroll 2 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.
- 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
- 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.
- Viktor I. Korolchuk 2 shared studies 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
- 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
- Satomi Miwa 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.
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