|SNF4Agamma deletion ||Deletion of SNF4Agamma from the first day of the imaginal stage shortens mean lifespan by 23% and causes morphological and behavioural features of premature aging . ||Fly ||-23 ||— ||— |
|GCN4 Deletion ||Deletion of GCN4 increases the replicative lifespan by 10% in the alpha strain .
GCN4 deletion decreases the lifespan in the alpha and a strain .
The chronological lifespan of GCN4 deletion is strongly decreased in the a strain . ||Yeast ||+10 ||— ||— |
|tert knockout ||First-generation tert(-/-) zebrafish die prematurely with shorter telomeres. tert(-/-) fish develop degenerative phenotypes, including premature infertility, gastrointestinal atrophy, and sarcopenia. tert(-/-) mutants have impaired cell proliferation, accumulation of DNA damage markers, and a p53 response leading to early apoptosis, followed by accumulation of senescence cells. Apoptosis is primarily observed in the proliferative niche and germ cells. Cell proliferation, but not apoptosis, is rescued in tp53(-/-)tert(-/-) mutants, underscoring p53 as mediator of telomerase deficiency and consequent telomere instability [http://denigma.de/url/3p]. ||Zebra ||— ||— ||— |
|Fxn disruption ||Disruption results in reduced lifespan, increased oxidative stress, impaired respiration, and the development of hepatic tumors . ||— ||— ||— ||— |
|Foxm1 deletion ||Deletion of Foxm1 causes age-related deterioration in liver regeneration . ||Mouse ||— ||— ||— |
|Fgf23 knockout ||Fgf23 knockouts have a short lifespan and display premature aging-like symptoms including kyphosis, muscle wasting, osteopenia, emphysema, uncoordinated movement, atherosclerosis, and atrophy of the intestinal villi, skin, thymus, and spleen .
Lack of Fgf23 activities results in extensive premature aging-like features and early mortality of Fgf-23(-/-) mice, while restoring the systemic effects of FGF-23 significantly ameliorates these phenotypes, with the resultant effect being improved growth, restored fertility, and significantly prolonged survival of double mutants . ||Mouse ||— ||— ||— |
|Efemp1 knockout ||Efemp1 knockout mice exhibited an early onset of aging-associated phenotypes including a 20% shorted median lifespan and 30% shorter maximum lifespan, decreased body mass, lordokyphosis, reduced hair growth, and atrophy . ||Mouse ||— ||+20 ||+30 |
|Cdkn1a knockout ||Deletion of Cdkna1 (alias p21) prolongs the lifespan of telomerase-deficient mice with dysfunctional telomeres and improves the repopulation capacity and self-renewal of hematopoietic stem cells .
The p21(-/-) strains like the Cdkn1a(tmi/Tyj) exhibits enormous regenerative capacities as it closes ear holes similar to MRL mice [20231440; 21722344]. ||Mouse ||— ||— ||— |
|Casp-2 deficiency ||Loss of caspase-2 resulted in a shortened (10%) maximum lifespan and in enhanced aging-related traits such as impaired hair growth, increased bone loss, and reduced body fat content . ||Mouse ||— ||— ||-10 |
|Brca1 deletion ||Deletion of Brca1 causes senescence in mutant embryos and cultured cells and tumorigenesis and signs of premature aging in adults . Brca1 heterozygous seem to have shortened lifespan with 70% of tumor incidence. Lymphoma, but not ovarian and mammary gland tumors, occurs commonly in these animals. After a whole-body exposure to ionizing radiation, Brca1 heterozygous mice have a 3-5-fold higher incidence to ovarian tumors, but not lymphoma, when compared with Brca1(+/+) mice . ||Mouse ||— ||— ||— |
|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  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 ||— ||— |
|AVT1 deletion ||Deletion of AVT1 accelerates the development of age-induced mitochondrial dysfunction without effecting the kinetics of vacuolar acidity decline and prevents the suppression of mitochondrial dysfunction by VMA1 and VPH2 overexpression without affecting vacuolar acidity. AVT1 deletion decreases mean, median and maximum lifespan by 21, 22, and 12%, respectively . ||Yeast ||-20.6 ||-22.4 ||-11.8 |
|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 . VMA2 deletion mutation decreases the mean replicative lifespan by 80% in the alpha strain . 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 . ||Yeast ||-80 to -83.9 ||-84.1 ||-70.0 |
|HAC1 deletion ||Deletion of HAC1 decreases mean, median and maximum replicative lifespan by 10, 8 and 5%, respectively . ||Yeast ||+10.3 ||+8.3 ||+5.3 |
|Scgdelta deletion ||Deletion of Scgdelta has detrimental effects on the flight muscles of adult animals and heart function. Median lifespan is reduced 15-30% . ||Fly ||— ||-15 to -30 ||— |
|AVO2 deletion ||Deletion of AVO2 extends chronological lifespan . ||Yeast ||— ||— ||— |
|YOL092W deletion ||Deletion of YOL092W decreases mean and maximum replicative lifespan by 36 and 21%, respectively. Lifespan of YOL092Y deletion mutants is extended by 0.5% glucose restriction . ||Yeast ||-36 ||— ||-21 |
|OSH6 deletion ||OSH6 deletion does not affect lifespan under normal conditions, but it abrogates the lifespan extension by 0.5% glucose restriction [Xia et al. unpublished]. ||Yeast ||— ||— ||— |
|OSH4 deletion ||Deletion of OSH4 decreases mean replicative lifespan by 18% [Xia et al., unpublished]. ||Yeast ||— ||— ||— |
|VAC14 deletion ||VAC14 mutants have a single vacuole and shortened lifespan on normal media . ||Yeast ||— ||— ||— |
|ZDS1 deletion ||Deletion of ZDS1 increases replicative lifespan by 37% in a SIR3-dependent manner .
Null mutation in ZDS1 causes 100-fold decrease in telomeric silencing, a nine-fold increase in rDNA silencing, reduces rDNA recombination, and decreases Sir3 phosphorylation . ||Yeast ||+37 ||— ||— |
|SKN1 deletion ||Chronological lifespan increased by 60% for single skn1 and double ipt1-skn1 deletion . ||Yeast ||+60 ||— ||— |
|TOS8 ||Deletion of TOS8 increases replicative lifespan increased by 35% in the alpha strain . ||Yeast ||+35 ||— ||— |
|WSC4 deletion ||Deletion of WSC4 decreases replicative lifespan by 30% in the alpha strain . ||Yeast ||-30 ||— ||— |
|YHF1 deletion ||Deletion of YFH1 decreases replicative lifespan by 50% . ||Yeast ||-50 ||— ||— |