|mrpl-37 ||— ||Knockdown of mrpl-37 increases lifespan by 41% . ||Nematode |
|mrpl-2 ||— ||Knockdown of mrpl-2 increases lifespan by 54% . ||Nematode |
|mrpl-1 ||— ||Knockdown of mrpl-1 increases lifespan by 57% . ||Nematode |
|ttll-9 ||Tubulin Tyrosine Ligase Like ||Knockdown of ttll-9 throughout the entire life increases the lifespan by 3% . ||Nematode |
|nkcc-1 ||Na-K-Cl Cotransporter homolog ||Knockdown of nkcc-1 throughout the entire life increases the lifespan by 23% . ||Nematode |
|mrps-5 ||— ||Knockdown of mrps-5 throughout the entire life increases the lifespan by 60%. mrps-5 RNAi prevents aging-associated functional decline and alters mitochondrial function. Knocking down mrps-5 after early development no longer affects nematode lifespan. When RNAi of mrps-5 was performed during the larval stages only, lifespan increases by 48%, whereas RNAi started from the L4 stage has no effect. mrps-5 RNAi results in fragmented mitochondria. mrps-5 RNAi increases lifespan by 40% in widltype, 37% in daf-16(mu86), 40% in sir-2.1(ok434) 69% in aak-2(ok524) and 112% in mev-1(kn1). Knockdown of cco-1 does not extend the lifespan of mrps-5 RNAi . ||Nematode |
|mir-277 ||— ||Constitutive miR-277 expression shortens lifespan and synthetically lethal with reduced insulin signaling, indicating that metabolic control underlies this phenotype. Transgenic inhibition with a miRNA sponge construct also shortens lifespan .
miR-277 is downregulated during adult life .
mir-277 controls branched-chain amino acid catabolism and as a result it can modulate the activity of TOR kinase . ||Fruit fly |
|snz ||snazarus ||Mutation in snz increases maximum lifespan of both sexes by up to 66%, while the median female lifespan is approximately 85% higher and that of males around 72% . ||Fruit fly |
|Loco ||locomotion defects ||Reduced expression of Loco due to hetero-deficient results in a 17-20% longer mean lifespan for both male and females, besides the fact that the homozygous deficiency of loco is lethal. Several of these long-lived mutants are more resistant to stresses such as starvation, oxidation and heat. Additionally, mutants have higher Manganese-containing superoxide dismutase (MnSOD) activity, increased fat content an diminished cAMP levels. Loco's RGS domain is required for the regulation of longevity as deletion analysis suggest . ||Fruit fly |
|Lnk ||— ||Loss of Lnk function results in increased median (14% in females and 17.5 in males) and maximum lifespan, reduced female fecundity and improves survival under conditions of oxidative stress and starvation. Heterozygousity does not result in any significant differences in lifespan in either males or females. Moreover, lifespan extension in one of the female homozygous mutant is fully rescued by the introduction of a Lnk genomic rescue construct . ||Fruit fly |
|LBR ||Lamin B receptor ||Overexpression of Lamin B receptor in the adult muscle and in the abdominal fat body results in a 54% and 46% reduction of mean lifespan, respectively . ||Fruit fly |
|kuk ||kugelkern ||Overexpression of kugelkern in the adult muscle results in a 60% reduction of mean lifespan . ||Fruit fly |
|CG3776 ||— ||Both overexpression and underexpression of CG3776 (alias Jhebp29) reduces the mean lifespan, where the reduction in males is slightly higher.
The lifespan of male flies with under- and overexpressed CG3776 is reduced by 38.8 and 42.6%, respectively when compared with Oregon R flies.The lifespan of female flies with under- and overexpressed CG3776 is reduced by 31.6 and 35%, respectively when compared to Oregon R flies.
Among the males and females, relatively to Oregon R and EP835/CyO, the age-specific survival of EP835/EP835 and EP835/Gal4 is reduced in both log-rank and Wilcoxon tests (P < 0.001); survival of EP835/EP835 and EP835/Gal4 differed using the log-rank-test (male: P<0.001; female: P=0.027) .
||Fruit fly |
|Gr63a ||Gustatory receptor 63a ||Gr63a loss-of-function in female flies leads to 30% extended mean lifespan, increased fat deposition, and enhanced resistance to some (but not all) environmental stresses. Lifespan of males is not extended .
Overexpression of Gr63a has modest negative effect on lifespan . ||Fruit fly |
|esc ||extra sexcombs ||Males heterozygous for the null esc4 or the dominant negative esc9 mutation that are progeny of an out-cross to a O-R wild-type strain have median lifespan that is, respectively, 47% and 60% longer than the O-R control. When derived from an out-cross to a longer-lived C-S wild-type strain, heterozygous esc9 flies have a median lifespan that is 43% longer than the C-S control . ||Fruit fly |
|Edem1 ||— ||The mean lifespan of Edem1 mutants of both male and female is increased by more than 30% . ||Fruit fly |
|E(z) ||Enhancer of zeste ||Flies heterozygous for the protein null E(z)63 or the catalytically inactive E(z)731 mutation that are progeny of an out-cross to an Oregon-R (O-R) wild-type strain exhibit a substantially greater median lifespan than the O-R control (71% and 76%, respectively). When derived from an out-cross to a longer-lived Canton-S (C-S) wild-type strain, the median lifespan of E(z)63 heterozygous is 33% longer than the C-S control . ||Fruit fly |
|DNApol-gamma35 ||DNA polymerase gamma 35kD ||Overexpression of DNApol-gamma35 (DNA polymerase gamma) in the nervous system results in a decrease in the median lifespan ranging from 39% to 52% .
||Fruit fly |
|CG9172 ||— ||RNAi against CG9172 increases mean lifespan in females by up to 4-12% when applied in both development and adulthood, and up to 46% when applied in adult neurons only. For males the effect is variable . ||Fruit fly |
|CG18809 ||— ||RNAi of CG18809 results in a 7-19% increase in mean lifespan of females, while neural RNAi results in an increased mean lifespan of up to 12% in females. For males the results are variable . ||Fruit fly |
|CG17856 ||— ||RNAi of CG17856 results in an increase in mean lifespan of 13-18% in females. In the case of males and post-developmental experiments the results are variable . ||Fruit fly |
|alpha-Man-I ||alpha Mannosidase I ||alpha-Man-I mutant fly exhibit enhanced resistance to paraquat and starvation an a 60% increase in mean lifespan for both sexes. After outcrossing, the mutant exhibit, under normal conditions, an increase in mean lifespan of 22% for females and 38% for males. Maximum lifespan is increased by 15%. alpha-Man-I RNAi knockdown results in a 39% increase in mean lifespan . ||Fruit fly |
|14-3-3epsilon ||CG31196 gene product from transcript CG31196-RA ||Loss of 14-3-3ε results in increased stress-induced apoptosis, growth repression and extended lifespan of flies, in a foxo-dependent manner. Mean lifespan of males and females is increased by 25% and 49%, respectively. Increased 14-3-3ε expression also reverts foxo-induced growth defects. No effect of lifespan is observed when overexpressing 14-3-3ε in adipose tissue, indicating that endogenous foxo activity in this tissue is low under normal conditions . ||Fruit fly |
|GH1 ||Growth hormone 1 ||Transgenic mice overexpressing bovine GH1 are bigger than controls and display early onset of pathological changes in the kidneys such glomerulosis and glomerulonephritis as well as signs of premature aging such as a shortened lifespan, increased astrogliosis, shortened reproductive lifepsan and early onset of age-related changes in cognitive function, hypothalamic neurotransmitter turnover, and plasma corticosterone levels . ||Cattle |
|frh-1 ||FRataxin (involved in human Friedrich's ataxia) Homolog ||Complete absence of frataxin,the mitochondrial protein defective in individuals with Friedreich ataxia is lethal, while its partial deficiency extends animal lifespan in a p53 dependent manner. Frataxin knockdown via RNAi extends mean and maximum lifespan by 19 and 37%, respectively .
Substantial reduction of frataxin protein expression is required to extend lifespan, affect sensory neurons functionality, remodel lipid metabolism and trigger autophagy. Beclin and p53 genes are required to induce autophagy and concurrently reduce lipid storages and extend animal lifespan in response to frataxin suppression. Frataxin expression modulates autophagy in the absence of p53 . ||Nematode |