Reduction of nutrients in the diet extends the lifespan in flies [14-16].

The fat body in Drosophila acts as a nutrient sensor, which uses TOR signaling to generate humoral signal that modulates insulin signaling and growth in peripheral tissues [22].

TOR deficiency in nematode extends the lifespan [23].

Ubiquitously overexpression of UAS constructs (via the daughterless (da)-GAL-4 driver) containing dTSC1 or dTSC2 extends mean lifespan at 29°C by 14% and 12%, respectively.

Ubiquitous overexpression of the dominant-negative form of dS6K extends the lifespan.

Overexpression of dTsc2 and dTOR(FRB) at 25°C lead to a 20% and 26% increase in mean lifespan, respectively.

Overexpression of dTsc2 via a UAS promoter in the eye using the driver gmr-GAL4 or in the nervous system by using appI-GAL4 does not extend the lifespan. Using the drivers 24BGAL4 and PO188-GAL4, enhancer traps that are predominantly expressed in the muscle and fat results in mean lifespan extension of 27% and 37%, respectively, at 29°C.

Using DJ634-GAL4 to overexpress the dominant-negative form of TOR (UAS-dTOR(FRB)) or of S6k (UAS-UAS-dS6K(KQ)) also led to mean lifespan increases of 30% and 29%, respectively at 29°C.

Overexpression of the dominant-negative form of S6k protects flies from the deleterious effects of rich food.

Lifespan extension by TOR deficiency in C. elegans is not suppressible by a daf-16 mutation [23]. TOR mutant animals do not further extend lifespan in a daf-2 background [23],

TOR mutation does not further extend the lifespan of daf-2 mutants, but longevity conferred by TOR deficiency is not suppressed by daf-16 mutation

Lifespan extension by chico is semidominant [13]. Dominant effect on lifespan are observed with Inr, EcR, Indy and Rpd3, but their effect on lifespan can be uncoupled from other phenotypes such as decundity, stress resistance, or lipid accumulation.

DR in mice protects against age-related tumorgensis [38, 39].

Reduction of daf-2 levels in C. elegans nervous system is sufficient to extend lifespan [40, 41]. Lifespan extension due to mutations in IIS or germline ablation in C. elegans are dependent on daf-16 activity in the intestine (the fat-storage tissue in C. elegans) [41].

FIRKO mice live 18 longer [43].

Juvenile hormone and ecdysone are two endocrine signals that are implicated in regulating lifespan in conjunction with the insulin pathway in Drosophila [4].

This paper was retracted due to errors found in labeling of samples (Current Biology, Volume 14, Issue 19, 5 October 2004, Page 1789) [http://www.sciencedirect.com/science/article/pii/S0960982204007535].