| Y46G5A.6 RNAi | RNA interference of Y46G5A.6 in adulthood shortens the extends lifespan of daf-2(mu150) mutants. Only a negligible or small reduction in the lifespan of wild-type worms occurs by knockdown of Y46G5A.6 [17392428]. | Worm | — | — | — |
| Y41E3.11 RNAi | Y41E3.11 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| Y37D8A.19 RNAi | Knockdown of Y37D8A.19 via RNAi started after the animal reached the late L4 stage has no significant effect on mean lifespan [22103665]. | Worm | — | — | — |
| xrn-1 RNAi | xrn-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| wwp-1 RNAi | RNA interference of wwp-1 decreases median lifespan by 9% in wild-type animals and 24% in daf-2 mutants [18006689]. Loss of wwp-1 function by RNAi reduces lifespan at 25 degree Celsius, but not 20 degree Celsius. Reduced levels of wwp-1 completely suppress the extended longevity of eat-2 mutants. wwp-1 RNAi does not suppress the extended lifespan of isp-1 mutants and has only minor suppressive effects on lifespan of another mitochondrial mutant, clk-1, and in cyc-1 RNAi treated worms. RNAi depletion of wwp-1 has no effect on long lifespan of daf-2 mutants [19553937].
| Worm | — | -9 | — |
| wwp-1 overexpression | wwp-1 overexpression extends lifespan by up to 20%. RNAi reduction of pha-4, but not of daf-16 suppresses increased longevity by wwp-1 overexpression [19553937]. | Worm | — | +20 | — |
| wwp-1 mutation | Loss of wwp-1 function by mutation reduces lifespan at 25 degree Celsius, but not 20 degree Celsius. Lifespan of wwp-1 mutants across entire food concentration range by bacterial dilution in liquid culture or on solid plates does not noticeable change. Reduced levels of wwp-1 completely suppress the extended longevity of eat-2 mutants [19553937].
| Worm | — | -9 | — |
| wts-1 RNAi | RNA interference of wts-1 in adulthood extends mean lifespan by 21% [17411345]. | Worm | +21 | — | — |
| WSC4 deletion | Deletion of WSC4 decreases replicative lifespan by 30% in the alpha strain [18340043]. | Yeast | -30 | — | — |
| wrn-1 RNAi | RNAi kockdown of wrn-1 shortens the lifespan, increases sensitivity to DNA damage, and accelerates aging phenoypes [15115755]. | Worm | — | — | — |
| wrn-1 mutation | A nonfunctional wrn-1 DNA helicase decreases the lifespan [23075628].
The expression of miR-124 in whole wrn-1 mutant worms is significantly reduced [23075628].
Supplementation of vitamin C normalizes the median lifespan of wnr-1 and mir-124 mutants [23075628]. | Worm | — | — | — |
| WRN mutation | Mutation in WRN causes Werner Syndrome which characteristics includes prematurely aged facies, scleroderma-like skin changes, cataracts, arteriosclerosis, subcutaneous calcification, and diabetes mellitus [McKusick et al. 1963; 5327241]. Inheritance is autosomal recessive and malignancy is frequent. THe frequency is 3 per million individuals in Japan [7460386].
Cells from a Werner heterozygote exit the cell cycle at a faster rate than do normal cells [8265666]. Loss of WRN promoter aberrant mitotic recombination [11316787]. | Human | — | — | — |
| Wrn mutation | Mice lacking the helicase domain fo the WRN ortholog exhibit many phenotypic features of Werner Syndrom, including a pro-oxidant status and a shorter mean lifespan. Mice with a deletion in the helicase domain [9789047] recapitulates most of the Werner syndrome phenotypes, including an abnormal hyaluronic acid excretion, higher reactive oxygen species levels, dyslipidemia, increased genomic instability, and cancer incidence. Wrn(Dehl/Dehl) mutant mice have a 10 - 15% decrease in their mean lifespan [12707040; 19741171]. | Mouse | -10 to -15 | — | — |
| WRKY6 deletion | Deletion of the WRKY6 promoter results in defects in root and leaf cell senescence [11722756]. | — | — | — | — |
| Wortmannin treatment | Treatment of Drosophila imago with 0.5 micromolar wortmannin increases median (by 5%) and maximum (by 39%) lifespan in males (p < 0.001), but the lifespan differences in females were statistical insignificant (p > 0.05) [22661237].
Low dose of wortmannin (5 microM) slightly increase the median and maximum lifespan [20017609]. | Fly | — | +5 | +39 |
| wnk-1 RNAi | RNA interference of wnk-1 decreases lifespan by 9% and suppresses lifespan extension by eat-2 mutation [22829775]. | Worm | -9 | — | — |
| wis1 constitutive active mutation | Constitutive active mutation of wis1 extends chronological lifespan and there is no further beneficial effect of DR [20075862]. | | — | — | — |
| Wings ablation/clipping | Flies on DR who could not move or had inhibited fat metabolism in their muscle and do not get an extended lifespan. Flies with ablated wings caused by overexpressing reaper (UAS-rpr) with a wing-sepcific Gal4 enhancer trap (1096-Gal4) exhibit only a 14% extension in lifespan compared to controls which exhibit a 61% extension upon DR. Clipped wing flies exhibit a modest 33% increase, while controls exhibit a 97% lifespan extension upon DR Lifespan reduction upon DR by curtailing movement is specific to control animals as lifespan is not futher reduced with Akh inhibition [22768842].
Control and clipped-wing flies exhibit a similiar level of fat synthesis and breakdown. Muscle specific RNAi of Akh, CG7834, or CG4389 results in a significant reduction in movement of flies upon DR [22768842]. | Fly | — | — | — |
| Whole-body Sirt1 deletion in the adulthood | Whole-body deletion of Sirt1 in the adulthood results in mice which are seemingly normal in every way. When mice were given low doses of resveratrol after Sirt1 was disabled, there were no discernible improvement in mitochondrial function or any paramenter, while mice with normal Sirt1 function given reservatrol showed dramatic increases in energy, mitochondrial biogenesis and function, AMPK activation and increased NAD+ levels in skeletal muscle. When mice lacking Sirt1 were given low doses of reserveratrol, AMPK was unaffected. When doses were significantly increased in these mice, AMPK was activated in a SIRT1-indepent manner, but still no benefit to mitochondrial function resulted [22560220]. | Mouse | — | — | — |
| wdr-23 RNAi | RNA interference of wdr-23 in adulthood extends mean lifespan by 24% [17411345]. | Worm | +24 | — | — |
| wah-1 RNAi | wah-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. RNAi against wah-1 started after the animal reaches the late L4 stage extends mean lifespan by 7-8% [22103665]. | Worm | +7 to +8 | — | — |
| W09C5.8 RNAi | RNAi against W09C5.8 increases mean and maximum lifespan by 62% and 50%, respectively [12447374]. Lifespan extension by RNAi of W09C5.8 is not suppressed by daf-16. Loss of W09C5.8 activity via RNAi can also result in a shortened lifespan, reduced fertility and defects in mitochondrial respiratory chain function [19074434].
W09C5.8 RNAi animals have lower ATP content and oxygen consumption [12447374]. | Worm | +62 | — | +50 |
| VPS8 deletion | Lack of VPS8 reduces lifespan under starvation conditions to a level similiar to that of wild-type cells incubated in synthetic complete medium and therefore blocked the lifespan-extending effect of DR [20657825]. | Yeast | — | — | — |
| VPS36 deletion | VPS36 deletion mutant had a chronological lifespan as long as wild type BY4741. Thus, Vps36 is not necessary for the starvation/extreme DR-dependent lifespan extension [20657825]. | Yeast | — | — | — |
| VPS30 deletion | VPS30 deletion prevents chronological lifespan extension induced by amino-acid DR [20421943]. | Yeast | — | — | — |
GenAge
GenDR
