Spatial coupling of mTOR and autophagy augments secretory phenotypes
What this study shows
Protein synthesis and autophagic degradation are usually described as opposites that mTOR switches between, and this paper shows a compartment where the cell deliberately runs both at once. In senescent cells, autolysosomes and mTOR gather at one side of the Golgi (the TASCC), mTOR gets there in an amino-acid- and Rag-dependent way, and destroying that arrangement cuts interleukin-6/8 secretion. Boundary: cells, not organisms; it explains how the senescent secretory programme is fuelled, not whether blocking it helps an animal.
At a glance
| Evidence type | M Molecular — cells, biochemistry, structure Marked M because it is molecular or in-vitro work (model: Human and mouse cells (Ras-induced senescent fibroblasts, macrophages, podocytes)) rather than a whole-organism health-outcome study. That is often exactly where causal biology gets established -- the code says which system the finding was shown in, and nothing about how good the work is. |
| Study type | 5 - Mechanistic / In Vitro |
| Model system | Human and mouse cells (Ras-induced senescent fibroblasts, macrophages, podocytes) |
| Journal | Science |
| Year | 2011 |
| Peer reviewed | Yes |
| Record last updated | 2026-09-23 |
| Source | DOI 10.1126/science.1205407 · PMID 21512002 |