| 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 |
| 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 | — | — | — |
| 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 | — | — | — |
| Aut1 RNAi | Aut1 depletion by RNAi form the first day of imaginal stage shortens lifespan by 28% on average in Drosophila and causes morphological behavioural features of premature aging [18219227]. | Fly | -28 | — | — |
| 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 |
| 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 | — | — | — |
| 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 |
| Bmcp knockout | Bmcp knockout flies live longer on low-calorie diets, have a decreased fertility, and gain less weight on high-calorie diets. Bmcp (ucp5) knockout mutants live longer than wild-type on low-calorie diets, but no longer on starvation or high-calorie diets. Ectopic neuronal expression of Bmcp transgene rescues starvation sensitive phenotype of Bmcp knockout mutants [16387864]. | Fly | — | — | — |
| BMH1 deletion | Deleting BMH1 extends chronological lifespan by 25% and is associated with activated stress response, decreased ROS levels and increased heat-shock-element-driven transcription activity. BMH1 deletion was non-additive with the genetic DR mimetic cdc25 and tor1. Water starvation (a form of extreme DR) extends chronological lifespan of BMH1 mutant even more as it does in wild-type [19805817].
| Yeast | +25 | — | — |
| BNA6 deletion | Deletion of BNA6 (alias QPT1) has no effect on replicative lifespan and is not required for lifespan extension by DR, but is lethal with mutation of NPT1 [11000115]. Deletion of BNA6 decreases chronological lifespan [17110466]. | Yeast | — | — | — |
| BRE5 deletion | Deletion of BRE5 increases mean replicative lifespan by 30% [16293764] and mean chronological lifespan in diploid cells [21447998] | Yeast | +30 | — | — |
GenAge
GenDR
