Masako Narita
Discovered, as first author, the TASCC, a compartment in senescent cells where mTOR and autophagy work side by side to fuel the secretion of inflammatory proteins
Principal Scientific Associate, Narita Group, Cancer Research UK Cambridge Institute, University of Cambridge
Narita Group, Cancer Research UK Cambridge Institute (Cambridge, England, United Kingdom) ↗ ORCID0000-0002-9774-4908 ↗
Portrait: Cancer Research UK Cambridge Institute
The textbook version says mTOR switches between building proteins and digesting them. NAR2011 found a place in the cell where both happen at once. In Ras-induced senescent cells, autolysosomes and mTOR gather on the trans side of the Golgi in a structure the paper named the TOR-autophagy spatial coupling compartment, or TASCC.
Two details make it more than an observation. mTOR's recruitment there is amino-acid- and Rag-dependent, which links the arrangement to the same machinery the Atlas draws for nutrient sensing. And disrupting mTOR's localisation to the TASCC suppresses interleukin-6 and interleukin-8 synthesis — so the compartment is how the senescent secretory programme is fuelled, with degradation supplying the amino acids that the synthesis consumes.
The same structure was seen during macrophage differentiation and in glomerular podocytes, both heavily secretory, which argues that it is a general solution to fast protein turnover rather than a quirk of senescence.
Milestones in the Atlas
| Year | Evidence | Study |
|---|---|---|
| 2011 | M | Spatial coupling of mTOR and autophagy augments secretory phenotypes NAR2011 First author: identified the TASCC, where autolysosomes and mTOR co-localise so that a senescent cell can degrade and secrete at the same time. |
Co-authors in the Atlas
People with a profile here who share at least one study with Masako Narita.
- Masashi Narita Studies what senescent cells do to the tissue around them, and showed that mTOR position, not just mTOR activity, sets their secretory output