| C36H8.1 | — | RNA interference of C36H8.1 extends lifespan [15998808]. | Nematode |
| C42C1.3 | — | RNA interferenceof C42C1.3 increases mean lifespan by 60% [17608836]. | Nematode |
| C46G7.2 | — | RNA interference of C46G7.2 increases mean lifespan by 44% [17608836]. | Nematode |
| C47E12.2 | — | RNA interference of C47E12.2 increases mean lifespan by 36% [17608836]. | Nematode |
| C48E7.2 | — | RNA interference of C48E7.2 in adulthood results in a 26% increase in mean lifespan [17521386]. | Nematode |
| C56G2.1 | — | RNA interference of C56G2.1 in adulthood results in a 20% increase in mean lifespan [17411345]. | Nematode |
| SWH1 | — | SWH1 (alias OSH1) deletion mutants have an extended replicative lifespan (p=0.02) and DR does not increase the long lifespan of SWH1 deletion mutants [Xia et al. unpublished]. | Budding yeast |
| ovo | — | The dominant ovoD1 allele extends female lifespan by approximately 50%. It does not synergize or prevent life-extension caused by chico [10617470; 11292874].
ovoD1 mutants are sterile [Mevel-Ninio et al. 1991]. | Fruit fly |
| R02D3.3 | — | R02D3.3 RNAi in the adulthood extends mean and maximum lifespan by 13 and 22%, respectively [23144747]. | Nematode |
| mir-239 | — | Mutating mir-239 increases mean and maximum lifespan by 12 and 36%, respectively, whereas overexpressing mir-239 decreases mean and maximum lifespan by 13 and 17 - 33%, respectively [21129974]. | Nematode |
| p53 | — | Overexpression of wild-type p53 during adult life has no significant effect on lifespan. Expression of dominant-negative versions of p53 in adult neurons extends lifespan by 58% in females and by 32% in males and increases resistance to genotoxic stress and resistance to oxidative stress, but not to starvation or heat stress, while not affecting egg production or physical activity.
Dominant negative p53 expression cancels out lifespan extension effect of DR, low calorie-food (5% SY). Muscle or fat body specific expression of a dominant negative form of p53 as well as globally lack of p53 decreases lifespan [16303568]. Loss of p53 activity slightly shortens the lifespan. Mutants that lack p53 survive well up to 50 days, but mortality rate increases relative to wild-type at later ages. p53 mutant animals are extremely sensitive to irradiation [12935877].
Expression of dominant-negative (DN) form of p53 in adult neurons, but not in muscle or fat body cells, extends median lifespan by 19% and maximum lifespan by 8%. The lifespan of dietary-restricted flies is not further extended by simultaneously expressing DN-DMp53 in the nervous system, indicating that a decrease in Dmp53 activity may be part of the DR lifespan-extending effect. Selective expression of DN-Dmp53 in only the 14 insulin-producing cell (IPCs) in the brain extends lifespan to the same extent as expression in all neurons and this lifespan extension is not additive with DR [17686972].
| Fruit fly |
| CG17856 | — | RNAi of CG17856 results in an increase in mean lifespan of 13-18% in females. In the case of males and post-developmental experiments the results are variable [19747824]. | Fruit fly |
| CG18809 | — | RNAi of CG18809 results in a 7-19% increase in mean lifespan of females, while neural RNAi results in an increased mean lifespan of up to 12% in females. For males the results are variable [19747824]. | Fruit fly |
| CG5389 | — | RNAi of complex V subunit CG5389 results in increased mean longevity under standard laboratory food conditions (3% yeast) in males. RNAi started from the development results in a mild lifespan increase in both sexes (3-11% in females and 3-8% in males). Post-developmental RNAi and silencing limited to neurons has variable effects with reduction in lifespan of up to 9% [19747824]. Under rich media conditions CG5389 knockdown throughout development and adulthood increases mean lifespan by 26% and abolished the lifespan extension by DR (started in the adulthood) in males. Suppression of CG5389 only during the adulthood either via RNAi by tub-GS or via oligomycin (a specific inhibitor of complex V) feeding prevents an increase in longevity under DR (started in the adulthood) in males [19968629]. | Fruit fly |
| CG9172 | — | RNAi against CG9172 increases mean lifespan in females by up to 4-12% when applied in both development and adulthood, and up to 46% when applied in adult neurons only. For males the effect is variable [19747824]. | Fruit fly |
| Edem1 | — | The mean lifespan of Edem1 mutants of both male and female is increased by more than 30% [19302370]. | Fruit fly |
| CG3776 | — | Both overexpression and underexpression of CG3776 (alias Jhebp29) reduces the mean lifespan, where the reduction in males is slightly higher.
The lifespan of male flies with under- and overexpressed CG3776 is reduced by 38.8 and 42.6%, respectively when compared with Oregon R flies.The lifespan of female flies with under- and overexpressed CG3776 is reduced by 31.6 and 35%, respectively when compared to Oregon R flies.
Among the males and females, relatively to Oregon R and EP835/CyO, the age-specific survival of EP835/EP835 and EP835/Gal4 is reduced in both log-rank and Wilcoxon tests (P < 0.001); survival of EP835/EP835 and EP835/Gal4 differed using the log-rank-test (male: P<0.001; female: P=0.027) [18275960].
| Fruit fly |
| Lnk | — | Loss of Lnk function results in increased median (14% in females and 17.5 in males) and maximum lifespan, reduced female fecundity and improves survival under conditions of oxidative stress and starvation. Heterozygousity does not result in any significant differences in lifespan in either males or females. Moreover, lifespan extension in one of the female homozygous mutant is fully rescued by the introduction of a Lnk genomic rescue construct [20333234]. | Fruit fly |
| mir-277 | — | Constitutive miR-277 expression shortens lifespan and synthetically lethal with reduced insulin signaling, indicating that metabolic control underlies this phenotype. Transgenic inhibition with a miRNA sponge construct also shortens lifespan [23669073].
miR-277 is downregulated during adult life [23669073].
mir-277 controls branched-chain amino acid catabolism and as a result it can modulate the activity of TOR kinase [23669073]. | Fruit fly |
| mrps-5 | — | Knockdown of mrps-5 throughout the entire life increases the lifespan by 60%. mrps-5 RNAi prevents aging-associated functional decline and alters mitochondrial function. Knocking down mrps-5 after early development no longer affects nematode lifespan. When RNAi of mrps-5 was performed during the larval stages only, lifespan increases by 48%, whereas RNAi started from the L4 stage has no effect. mrps-5 RNAi results in fragmented mitochondria. mrps-5 RNAi increases lifespan by 40% in widltype, 37% in daf-16(mu86), 40% in sir-2.1(ok434) 69% in aak-2(ok524) and 112% in mev-1(kn1). Knockdown of cco-1 does not extend the lifespan of mrps-5 RNAi [23698443]. | Nematode |
| mrpl-1 | — | Knockdown of mrpl-1 increases lifespan by 57% [23698443]. | Nematode |
| mrpl-2 | — | Knockdown of mrpl-2 increases lifespan by 54% [23698443]. | Nematode |
| mrpl-37 | — | Knockdown of mrpl-37 increases lifespan by 41% [23698443]. | Nematode |
| rps-27 | Ribosomal Protein, Small subunit | Knockdown of rps-27 by RNAi extends mean and maximum lifespan by 50 and 44%, respectively [19293945]. | Nematode |
| shc-1 | SHC (Src Homology domain C-terminal) adaptor homolog | Loss of shc-1 function results in accelerated aging and enhanced senstivity ro heat, oxidative stress and heavy metals. | Nematode |
