| YPT7 deletion | YPT7 deletion decreases replicative lifespan by 15% in the alpha strain [18340043]. Deletion of YPT7 cancels out replicative lifespan extension of 0.5% glucose restriction and results under DR also into a shorter replicative lifespan than under AL [18690010]. | Yeast | -15 | — | — |
| YHC3 deletion | YHC3 deletion decreases 10-20% shortened lifespan [16435200]. | Yeast | -10 to -20 | — | — |
| YGL235W deletion | YGL235W increases replicative lifespan by 20% in the alpha strain [19030232]. | Yeast | +20 | — | — |
| YDL180W deletion | YDL180W deletion impairs DR-mediated replicative lifespan extension, but does not change lifespan on AL significantly [22912585]. | Yeast | +5 | — | -6 |
| 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 | — | — | — |
| 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 | — | — | — |
| VPS20 deletion | VPS20 deletion decreases mean and maximum replicative lifespan by 16% and 19%, respectively, and additionally cancels out the DR-induced replicative lifespan extension [22912585]. | Yeast | -16 | — | -19 |
| VMA2 deletion | VMA2 deletion mutants have a reduced ΔΨ and mitochondrial morphology similar to aged cells. The restoration of the vacuolar acidity in daughter cells requires V-ATPase activity as it is eliminated in VMA2 deletion mutant cells [23172144]. VMA2 deletion mutation decreases the mean replicative lifespan by 80% in the alpha strain [18340043]. Deletion of VMA2 decreases mean, median and maximum replicative lifespan by 84%, 84% and 70%, respectively. DR (0.5% glucose restriction) does not extend the replicative lifespan of VMA2 and shortens it even more [23172144]. | Yeast | -80 to -83.9 | -84.1 | -70.0 |
| VAM7 deletion | VAM7 deletion decreases replicative lifespan under AL and blocked DR-mediated lifespan extension. Replicative lifespan decreases by 70% on DR in VAM7 deletion mutant [18690010]. | Yeast | — | — | — |
| VAC14 deletion | VAC14 mutants have a single vacuole and shortened lifespan on normal media [16293764]. | Yeast | — | — | — |
| ARO7 deletion | Under starvation/extreme DR deletion of ARO7 increases mean chronological lifespan and confers higher resistance to heat-shock, but made cell more sensitive to acetic acid and leads to growth defects. In W303-1A background ARO7 deletion causes an even more severe growth defect and mutants are short-lived [20657825]. | Yeast | — | — | — |
| VPS27 deletion | Under starvation conditions VPS27 deletion mutants have a dramatically reduced lifespan [20953148]. | Yeast | — | — | — |
| ATG16 deletion | Under AL atg16 mutation shortens chronological, but not replicative lifespan. 0.5% glucose DR extends chronological lifespan of atg16 mutants, but amino-acid DR does not extend the short chronological lifespan of atg16 mutants (similar to several other autophagy mutants). ADE4 deletion in atg16 mutants results only in a partial extension of chronological lifespan by 0.5% glucose DR. The long chronological lifespan of tor1 mutants requires ATG16 [20421943]. | Yeast | — | — | — |
| unc-76 mutation | unc-76(e911) allele extends male lifespan by about 50%, but has no effect on hermaphrodite lifespan [10747056].
unc-76 mutants are uncoordinated [4366476]. | Worm | +50 | — | — |
| TRM9 deletion | TRM9 deletion almost triples mean chronological lifespan under starvation/extreme DR, increases heat resistance, but reduces resistance to acetic acid. Similar effect were present in the BY746 background in SDC medium [20657825]. | Yeast | — | — | — |
| TOR1 Deletion | TOR1 deletion extends mean and maximum replicative lifespan by 21 and 25% [16293764] as well as chronological lifespan [21076178]. This lifespan extension is independent of SIR2 and additive with deletion of FOB1 [16293764]. Deletion of TOR1 fails to increase the replicative lifespan of a sir2 mutant [20947565]. Deletion of TOR1 substantially extends chronological lifespan, increasing median survival almost 3-fold (wild-type 4.5 days, tor1 null 12 days), i.e. by 167%. By 21 days in culture, the vast majority of wild-type cells had died (>99.9%), whereas many tor1 null cells remained viable. Deletion of TOR1 also extends the chronological lifespan of the relatively short-lived BY4742 strain, one of the two haploid genetic backgrounds of the widely used Yeast Knockout Collection available from Open Biosystems. Deletion of TOR1 fails to extend chronological lifespan in Petite strains that are unable to respire [17403371]. TOR1 deletion increases replicative lifespan by 30% in the alpha strain and 20% in a strain [19030232]. TOR1 deletion mutant have and increased mean and maximum replicative lifespan by 21% and 6%, respectively [21931558]. Deletion of TOR1 extends replicative lifespan as well as chronological lifespan [21076178] and glucose restriction fails to further extend the long replicative lifespan of tor1Delta [16293764; 16418483; 18225956]. Water starvation (extreme DR) further extends chronological lifespan of tor1 mutants [18225956]. | Yeast | +21 to +30 | +167 | +6 to +25 |
| ATG18 deletion | The replicative lifespan of ATG18 deletion mutant is not shorter than that of wild-type under DR [18690010]. | Yeast | — | — | — |
| OSH6 mutation | The CC domain of Osh6 is dispensable for longevity. Deletion of the CC domain leads Osh6 to the late endosome [Fusheng Tang, personal communication]. | Yeast | — | — | — |
| Terc deletion | Telomerase null mice exhibit age-dependent telomere shortening and shortened lifespan with succeeding generations. Median lifespan is reduced by 26% in G6 Terc(-/-) mice compared to wild-type or G1-G3 Terc(-/-) (18 months vs. 24 months). G6 Tec(-/-) display hair greying, hair loss, and ulcerative skin lesions, as well as impaired response to wound healing and hematoitopitic ablation, and an increased incidence of cancer [10089885].
Cells from Terc(-/-) mice (G4 and upward) exhibit chromosomes lacking detectable teloemre repeats, aneuplody, and end-to-end fusions [9335332]. | Mouse | — | -26 | — |
| tdp-1 mutation | tdp-1(ok803) mutation increases mean and maximum lifespan at 20 degree Celsius but not at 25 degree Celsius. tdp-1(ok803) reduce the lifespan of daf-2(e1370) mutants, but does not does not reduces the lifespan of daf-16(mu86) mutants [Vaccaro et al. 2012]. | Worm | — | — | — |
| TCO89 deletion | TCO89 deletion increases chronological lifespan, increases mitochondrial oxygen consumption, but decreases mitochondrial and cellular ROS in early stationary phase [21641548]. Deletion of TCO89 cancels out replicative lifespan extension by moderate DR [18690010]. | Yeast | — | — | — |
| TAE2 deletion | TAE2 deletion decreases replicative lifespan by 30% in the a strain [18340043]. | Yeast | -30 | — | — |
| SWH1 deletion | 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].
| Yeast | — | — | — |
| Rgn knockout | Survival among make animals lacking Rgn (alias SMP30) is 50% at 180 days compared to 100% among controls [N. Maruyama, unpublished data].
SMP30-/- mutant mice are indstuguishibale form their SMP30+/+ littermates in terms of development and fertilization capacity [12368201]. However, -/- mice were more susceptible to liver injury after treatment with anti-FAS antibody. SMP30-/- hepatocytes cultures in vitro are more susceptible to apoptosis induced by tumor-necrosis factor (TNF-alpha) plus actinomycin D (ActD) than SMP30+/+ hepatocytes.
| Mouse | — | — | — |
GenAge
GenDR
