Silencing the single worm TOR gene roughly doubled C. elegans lifespan, showing the longevity role of TOR inhibition is conserved across an enormous evolutionary distance.
| Evidence tier | C Animal in vivo |
| Study type | 4 - Animal Study |
| Model system | Caenorhabditis elegans (RNAi) |
| Journal | Nature |
| Year | 2003 |
| Peer reviewed | Yes |
| Source | DOI 10.1038/426620a · PMID 14668850 |
(Brief communication; no formal abstract in PubMed — editorial summary.) This report provides the first genetic evidence that the TOR kinase controls animal lifespan: RNAi inactivation of the Caenorhabditis elegans TOR ortholog (let-363/CeTOR) roughly doubles adult lifespan. The longevity effect operates largely in parallel to the insulin/IGF-1–DAF-16 pathway and is associated with a dauer-like shift in energy metabolism, establishing nutrient-sensing TOR signalling as an evolutionarily conserved regulator of ageing and laying the groundwork for later work on rapamycin and lifespan extension.
| Intervention | Genetic (RNAi of let-363/CeTOR) |
| Target | TOR (CeTOR) |
| Model | C. elegans |
| Effect | RNAi of C. elegans TOR roughly doubles adult lifespan, acting largely parallel to insulin/IGF-1-DAF-16 |