| ATG1 deletion | ATG1 deletion reduces chronological lifespan by 70% [19302372]. Deletion of ATG1 reduces replicative lifespan by 20% in the alpha strain [18340043]. | Yeast | -20 to -70 | — | — |
| ATG10 deletion | ATG10 deletion cancels out replicative lifespan extension by DR [18690010]. | Yeast | — | — | — |
| ATG11 deletion | ATG11 deletion extends replicative lifespan under AL and abrogates DR-lifespan extension [18690010]. | Yeast | — | — | — |
| ATG15 deletion | Deletion of ATG15 does not affect the lifespan significantly on AL, while DR shortens replicative lifespan of ATG15 deletion mutant by 28% [18690010]. | 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 | — | — | — |
| ATG17 deletion | ATG17 deletion decreases replicative lifespan under AL and blocks DR-lifespan extension. ATG17 mutant's replicative lifespan decreases by 70% on DR [18690010]. | Yeast | — | — | — |
| ATG18 deletion | The replicative lifespan of ATG18 deletion mutant is not shorter than that of wild-type under DR [18690010]. | Yeast | — | — | — |
| ATG2 deletion | ATG2 deletion prevents chronological lifespan extension induced by amino-acid DR [20421943]. | Yeast | — | — | — |
| ATG7 deletion | ATG7 deletion reduces chronological lifespan by 70% [19302372]. | Yeast | — | — | — |
| Atg7 knockout | Knockouts of Atg7 are short-lived with a 30% reduction in maximum lifespan and are hypersensitive to nutrient and oxidative stress [18056421; 19550147]. | Fly | — | — | -30 |
| Atg8a mutation | Mutations in Atg8a results in reduced lifespan and increased sensitivity to oxidative stress [18059160].
Atg8a mutation reduces the maximum lifespan by 25% under starvation conditions [17617737].
Loss-of-function mutation in atg8a reduces mean lifespan by 11 - 25% and maximum lifespan by 3 - 22% [17435236]. | Fly | -11 to -25 | — | -3 to -25 |
| ATH1 deletion | Deletion of ATH1 extend the mean chronological lifespan by 17% (at 30 degree Celsus in BY4742) [22783207].
ATH1 mutants have higher trehalose levels until the end of the post-diauxic growth phase, but reaches a plateau at the level of 50-70% of wild-type in the stationary phase [22783207]. | Yeast | +17 | — | — |
| Atm knockout | Atm-deficient mice are viable, retarded in growth, infertile (male produce no mature sperm and female no gametes), display neurological dysfunction, and exhibit severe defects in T cell maturation while going on to develop thymomas [8917548; 8689683]. The majority of mutant mice rapidly develop thymic lymphomas and die before 4 months of age [8843194].
Cells of Atm(-/-) mice exhibit slow growth also in culture and premature senescence, telomeres are extensively shortened in multiple tissues [8689683].
Mice mutant for Atm and Terc display progressive multi-organ system compromise and features of accelerated aging [12540856]. | Mouse | — | — | — |
| ATM mutation | Individuals with ataxia-telangiectasia (AT) have a decreased lifespan, with a maximum of 52 years [3864931]. | Human | — | — | — |
| ATP1 deletion | Deletion of ATP1 increases chronological lifespan by up to 50% [17492370], but decreases replicative lifespan by 70% in the alpha strain [18340043]. | Yeast | -70 to +50 | — | — |
| Atr knockout | Deletion of Atr in young adults eliminates 80-90% of proliferating cells and results in several age-related phenotypes accompanied by a depletion of stem and progenitor cells and exhaustion of tissue renewal and homeostatic capacity [18371340].
Atr mutant mice (so called Seckle mice) exhibit high levels of replicative stress during embryogenesis, when proliferation is widespread, but this is reduced to marginal amounts in postnatal life. In spite of this decrease, adult Seckel mice display accelerated aging, which is further aggravated in the absence of p53. Seckel mice die in less than half a year, exhibit pancytopenia, cachexia and signs of premature aging, including hair graying, kyphosis, osteoporosis, accumulation of fat in the bone marrow, decreased density of hair follicles and thinner epidermis [19620979]. | Mouse | — | — | — |
| AVO2 deletion | Deletion of AVO2 extends chronological lifespan [21641548]. | Yeast | — | — | — |
| 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 [23172144]. | Yeast | -20.6 | -22.4 | -11.8 |
| Bam mutation | Bam mutants have an extended lifespan due to germ cell loss. Lifespan of females is on average up to 50% higher and that of males on average s up to 27.8% higher [18434551]. | Fly | +27.8 to +50 | — | — |
| bar-1 mutation | BAR-1 may play a role in regulating daf-16 during dauer formation, particularly in conditions of oxidative stress as it directly interaction with DAF-16 and loss of bar-1 reduces activity of DAF-16 in dauer formation and lifespan. Deletion of bar-1 reduces mean (44%) and maximal (18%) lifespan, which is to a similar degree as seen to daf-16 mutants [15905404]. | Worm | -44 | — | -18 |
| BAS1 deletion | Deletion of BAS1 increases replicative lifespan by 30% in the alpha strain [16293764; 19030232]. | Yeast | +30 | — | — |
| Bax knockout | Inactivation of proapoptotic Bax extends fertile potential and minimized age-related health problems, including bone and muscle loss, excess fat deposition, alopecia, cataracts, deafness, increased anxiety, and selective attention deficit. Bax deficiency does not lead to an increase in tumor incidence. Despite the apparently increased quality of life of aging females lacing Bax, there is no significant differences in overall lifespan [17360389]. | Mouse | — | — | — |
| bchs mutation | Loss of function mutation in bchs results in a 40-45% decrease in mean lifespan and is associated with age-related neurodegenerative phenotype with reduced CNS size and altered morphology as well as accumulation of insoluble ubiquinated proteins and amyloid precursor-like proteins along with an increase in neuronal apoptosis. No pronounced developmental defects were observed and young adults have normal behaviours, indicating that the bchs gene is essential for normal adult survival and longevity [12598614].
bchs mutation reduces mean lifespan by 28 - 54% and maximum lifespan by 24 - 46% [17435236]. | Fly | -28 to -54 | — | -24 to -46 |
| BCY1 deletion | Disruption in BCY1 by mutation results decreases mean and maximum replicative lifespan by 37 and 16% and is associated with increased PKA activity [8195187]. | Yeast | -37 | — | -16 |
| BLM mutation | BLM mutation cuases Bloom syndrom. Individuals with Bloom syndrome have a shortend life expectancy []. Death is primary due to cancer, particulary leukemia and lymphoma [German, 1992]. Bloom syndrome is not a premature aging disease. Bloom syndrome characteristics are grwoth deficiency, sun-snesitivity, telangiectatic hypo- and hyperpigmented skin, predisposition to malignancy, and chromosomal instability [5770175]. | Human | — | — | — |
GenAge
GenDR
