A role for autophagy in the extension of lifespan by dietary restriction in C. elegans
What this study shows
Makes autophagy a necessary step between dietary restriction and a longer life, not a side effect of it: blocking autophagy genes abolishes the lifespan extension produced both by dietary restriction and by TOR inhibition. The paper is equally careful about what autophagy cannot do on its own, because autophagy still runs in animals lacking DAF-16/FOXO and yet those animals are not long-lived. Boundary: worms; necessity was shown, sufficiency was not.
Abstract
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In many organisms, dietary restriction appears to extend lifespan, at least in part, by down-regulating the nutrient-sensor TOR (Target Of Rapamycin). TOR inhibition elicits autophagy, the large-scale recycling of cytoplasmic macromolecules and organelles. In this study, we asked whether autophagy might contribute to the lifespan extension induced by dietary restriction in C. elegans. We find that dietary restriction and TOR inhibition produce an autophagic phenotype and that inhibiting genes required for autophagy prevents dietary restriction and TOR inhibition from extending lifespan.
Read the full abstract on PubMed →At a glance
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| Evidence type | A Animal model Marked A because it is an animal intervention or observation study measuring an organismal outcome (model: Caenorhabditis elegans); the code names the system studied -- animal work can be rigorous and still not be human data. |
| Study type | 4 - Animal Study |
| Model system | Caenorhabditis elegans |
| Journal | PLOS Genetics |
| Year | 2008 |
| Peer reviewed | Yes |
| Record last updated | 2026-10-01 |
| Source | DOI 10.1371/journal.pgen.0040024 · PMID 18282106 |
Where this study fits
How this study connects to the pathway map, open questions, people and other studies in the Atlas.
Pathway relations
Supports
mTORC1 inhibits LongevityStrongest evidence: A (Animal model) · settled in the literature · Status: Proposed
not tested in people
No human hard-endpoint evidence. This is the Atlas's flagged 'human endpoint desert'.
Open question
Mechanism-to-outcome gap · H4
Is autophagy actually REQUIRED for the mammalian lifespan benefit?Cited there as evidence. Evidence stands at: Lifespan in mice (sufficiency only).
People in the Atlas
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Showed in worms, alongside a 2007 report from Beth Levine's laboratory, that autophagy is required for dietary restriction to extend lifespan
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Showed in 1993 that a single-gene change doubles the lifespan of the worm C. elegans, which opened the study of nutrient-sensing pathways as ageing pathways
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Studies the biology of ageing in the roundworm C. elegans, including interventions that extend healthspan and the mechanisms that protect neurons from damage.
More: 3 other authors
No profile yet: Chandra A, Mitic LL, Onken B
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Topics
Plain-language answer: Is autophagy actually required for the lifespan benefit of mTOR inhibition?
Extracted findings
These fields were extracted from the paper with AI assistance and have not been checked against the source. Read them as a pointer into the paper, not as curated claims; where they disagree with the curated summary above, the curated summary stands.
| Intervention | Dietary restriction (eat-2), TOR RNAi, RNAi against autophagy genes; daf-2 mutants |
| Target | TOR / autophagy / PHA-4 / DAF-16 |
| Model | Caenorhabditis elegans |
| Effect | Autophagy is required for lifespan extension by dietary restriction and TOR inhibition but is not sufficient on its own. |
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