Oliver's mTOR Atlas Evidence Platform
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Spatial coupling of mTOR and autophagy augments secretory phenotypes

Narita Masako, Young AR, Arakawa S, Samarajiwa SA, Nakashima T, Yoshida S, Hong S, Berry LS, Reichelt S, Ferreira M, Tavare S, Inoki K · 2011 · Science · Atlas ID NAR2011

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.

Abstract

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Protein synthesis and autophagic degradation are regulated in an opposite manner by mammalian target of rapamycin (mTOR), whereas under certain conditions it would be beneficial if they occurred in unison to handle rapid protein turnover. We observed a distinct cellular compartment at the trans side of the Golgi apparatus, the TOR-autophagy spatial coupling compartment (TASCC), where (auto)lysosomes and mTOR accumulated during Ras-induced senescence.

Read the full abstract on PubMed →

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 type5 - Mechanistic / In Vitro
Model systemHuman and mouse cells (Ras-induced senescent fibroblasts, macrophages, podocytes)
JournalScience
Year2011
Peer reviewedYes
Record last updated2026-09-23
SourceDOI 10.1126/science.1205407 · PMID 21512002

Cite this paper

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Narita Masako, Young, A. R., Arakawa, S., Samarajiwa, S. A., Nakashima, T., Yoshida, S., Hong, S., Berry, L. S., Reichelt, S., Ferreira, M., Tavare, S., Inoki, K., Shimizu, S., & Narita Masashi (2011). Spatial coupling of mTOR and autophagy augments secretory phenotypes. Science. https://doi.org/10.1126/science.1205407

@article{NAR2011,
  author       = {Narita Masako and Young, A. R. and Arakawa, S. and Samarajiwa, S. A. and Nakashima, T. and Yoshida, S. and Hong, S. and Berry, L. S. and Reichelt, S. and Ferreira, M. and Tavare, S. and Inoki, K. and Shimizu, S. and Narita Masashi},
  title        = {{Spatial coupling of mTOR and autophagy augments secretory phenotypes}},
  journal      = {Science},
  year         = {2011},
  doi          = {10.1126/science.1205407},
  note         = {PMID: 21512002},
}

Cite this Atlas record

The record is the Atlas's own work — the evidence label, the extracted findings and the links. It is cited as part of the dataset, not as the paper.

Barton, O. (2026). Oliver's mTOR Atlas (record NAR2011) [Data set]. https://mtor-atlas.org/study/NAR2011/ · Dataset DOI 10.5281/zenodo.22059963

@misc{atlas_NAR2011,
  author       = {Barton, Oliver},
  title        = {{Oliver's mTOR Atlas}, record NAR2011},
  howpublished = {Data set},
  year         = {2026},
  url          = {https://mtor-atlas.org/study/NAR2011/},
  doi          = {10.5281/zenodo.22059963}
}