| pept-2 mutation | Deletion of pept-1 (alias opt-2 or pep-2) results in retarded development, reduced body size and extended reproductive lifespan. It also further extends (60%) the life-extension caused by daf-2 mutations [15155758].
pept-2 mutants exhibit a decrease in fat content. | Worm | — | — | — |
| Homozygous Prdx1 knockout | Homozygous Prdx1 knockout mice have a lifespan significant shorter than +/+ and +/- littermates and develop severe haemolytic anaemia and several malignant cancers (starting at about 9 months of age) [12891360] | Mouse | — | — | — |
| RAD1 mutation | Deletion of RAD1 has no effect on replicative lifespan [10207108]. | Yeast | — | — | — |
| RAD7 deletion | Deletion of RAD7 has no effect on replicative lifespan in PSY316 [10207108].
Mutation in RAD7 results in decrease repair of the non-transcribed strand in rDNA [8604332]. | 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Survival among make animals lacking Rgn (alias SMP30) is 50% at 180 days compared to 100% among controls [N. Maruyama, unpublished data].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 | — | — | — |
| RSR1 deletion | Deletion of RSR1 (alias BUD1) shortens replicative lifespan [9789734]. | Yeast | — | — | — |
| RTG2 deletion | RTG2 is required for replicative lifespan extension associated with the retrograde response, a pathway that signals the functional status of mitochondria to the nucleus to regulate the expression of several genes [11024000]. RTG2 is not required for replicative lifespan extension by DR [11024000].
RTG2 null mutants are not petite [8422683], but display various nutrient auxotrphies and alterations of carbohydrate metabolism [7727418]. | Yeast | — | — | — |
| SIM1 deletion | Disruption of SIM1 shortens mean (87.5%), but not maximum, lifespan without causing any other gross changes in cell cycle parameter or growth characteristics [8810036].
Cells bearing deletions in CLB1-4 are unable to undergo mitosis and normally arrest in G2. SIM1 disruption in clb1-4 mutant backgrounds will allow a second round of DNA synthesis without mitosis [8574583]. sim1delta;uth1delta double mutants exhibit various defects, including binucleated cells, benomyl sensitivity, heat shock sensitivity, inability to store glycogen, sensitivity to starvation and failure of spores to germinate [10612745]. | Yeast | — | — | — |
| SLT2 deletion | Deletion of SLT2 has no effect on replicative lifespan in W303 strain [12640455].
SLT2 deletion increases rDNA silencing and rDNA recombination and decreases silencing at the telomeres and HM loci [Ray et al., 2003] as well as results in decreased phosphorylation of Sir3 [12640455]. | 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 | — |
| Heterozyogus Trp53 truncation mutation | Mice heterozyogous for an allele of p53 that removes the 5' portion of the protein demonstrate decreased cancer, permature aging phenotypes, and shortened lifespan in the mixed inbred C57BL/6â129/Sv background. It has been proposed that the this allele of p53 results in increased activity/overexpression [11780111]. | Mouse | — | — | — |
| WRKY6 deletion | Deletion of the WRKY6 promoter results in defects in root and leaf cell senescence [11722756]. | — | — | — | — |
| ACH1 deletion | ACH1 deletion cells accumulate a high amount of extracellular acetic acid and display a reduced mean and maximum chronological lifespan. Maximum lifespan is reduced by 32%. Lifespan shortening is completely abrogated by alleviating the acid stress either by a DR regimen that prevents acetic acid production or by transferring chronologically aging mutant cells to water. Deletion of ACH1 is accompanied by reactive oxygen species accumulation, severe mitochondrial damage, and an early insurgence of apoptosis [22754872]. | Yeast | — | — | -32 |
| YKL069W deletion | Deletion of YKL069W increases sensitivity to oxidative stress and decreases replicative lifespan [19049972]. | Yeast | — | — | — |
| Acacb knockout | Acacb-null animals (alias Acc2-/-) exhibit upon regular diet an increase triglyceride breakdown, leaner phenotype, increased insulin sensitivity and no effect on lifespan [17923673]. | Mouse | — | — | — |
| git3 deletion | git3 encodes a G protein-coupled receptor for glucose. git3 deletion increases chronological lifespan in conditions where glucose consumption is not affected. The anti-aging effect of DR and git3 deletion mutation is accompanied by increased respiration and lower ROS production [19266076]. | | — | — | — |
| sty1 deletion | Deleting sty1 cancels out chronological lifespan extension and enhanced heat stress resistance by DR [20075862]. | | — | — | — |
| atf1 deletion | Deleting atf1 cancels out DR-mediated chronological lifespan extension and enhanced heat stress resistance[20075862]. | | — | — | — |
| HST1 deletion | Deletion of HST1 blocks the residual replicative lifespan extension by hxk2 mutant in a sir2;fob1;hst2 triple mutant background [16051752]. However, DR can increases the replicative lifespan to a similar extent in sir2;fob1;hst1;hst2 quadruple mutant cells as in sir2;fob1 double mutant cells under 0.5, 0.05 and 0.005% glucose conditions and even by hxk2 deletion mutant [16741098; 17129213]. | Yeast | — | — | — |
| PCK1 deletion | Loss of Pck1 activity blocks chronological lifespan extension caused by water starvation. Knockout of PCK1 dramatically reduces chronological lifespan in both water (extreme DR) and glucose-containing medium. Deletion of SIR2 does not alter the lifespan of PCK1 deletion mutant, pck1-K514R, and pck1-K514Q mutants [19303850]. | Yeast | — | — | — |
| GSH1 deletion | Deletion of GSH1 confers deficiency in glutathione biosynthesis and further increases chronological lifespan under 0.5% glucose restriction, but does not extend chronological lifespan under 2% glucose [18840459]. Therefore, GSH1 has a positive interaction with DR [18840459]. | Yeast | — | — | — |
| ERG3 deletion | Deletion of ERG3 decreases replicative lifespan under AL, cancels out replicative lifespan extension of 0.5% glucose DR and results under DR also into a shorter replicative lifespan than under AL [18690010]. | Yeast | — | — | — |
| SUR4 deletion | Deletion of SUR4 cancels out replicative lifespan extension of 0.5% glucose DR [18690010]. | Yeast | — | — | — |
| LCB4 deletion | Deletion of LCB4 increases replicative lifespan and cancels out replicative lifespan extension of 0.5% glucose DR [18690010]. | Yeast | — | — | — |
| NFU1 deletion | NFU1 mutation slightly shortens the chronological lifespan under AL and the chronological lifespan of NFU1 mutants is not extended by 0.5% glucose DR [20421943]. | Yeast | — | — | — |
GenAge
GenDR
