Interventions

  • Species: + -
  • name effect species mean median maximum
    esc mutation 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 [20018689]. Fly +47 to +60 +34
    Orco mutation Loss-of-function mutation in Orco (alias Or83b) results in olfactory defects, altered adult metabolism, enhanced stress resistance, and life-extension. Fully fed female homozygous Or83b null mutants exhibit a 56% increase in median lifespan and a 30% increase in maximum lifespan. Males are also significantly longer-lived, though to a smaller degree and maximum lifespan is not extended. Heterozygous mutants of both sexes show an intermediate longevity. Lifespan of homozygous Or83b null mutants is further increased by DR, but the relative increase in median and mean longevity is significantly greater when mutants were maintained in well-fed conditions [17272684]. Fly +56 +30
    Ablation of median neurosecretary cells Flies with an ablation of median neurosecretary cells (which eliminates Ilp2 expression) exhibit a significant increase in mean and maximum lifespan over that of control flies and an increase to oxidative stress and starvation. The mutants also exhibit increased storage of lipid and carbohydrate, reduced fecundity, and reduced tolerance of heat and cold [15708981]. The median and maximum lifespan of females is increased by 33.5% and 40%, respectively. In males the median and maximum lifespan is increased by 10.5% and 27%, respectively [15708981]. Fly +10.5 to +33.5 +27 to +40
    alpha-Man-I mutation 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% [19302370]. Fly +22 to +60 +15
    bwa mutation bwa (alias Dacer) inactivation increases Drosophila pre-adult development time and anti-oxidative stress capacity. Mean lifespan is increased by 16% in females, by 21% in males and by 19% in total. Maximum lifespan of females, males is also extended by 20 and 12%, respectively [20112046]. Fly +16 to +21 +12 to +20
    Sod mutation Sod mutant flies display infertility and a reduction in lifespan [2539600]. Fly
    sun mutation sun mutations increases lifespan and resistance to oxidative stress [15133470] Fly
    14-3-3epsilon mutation 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 [18665908]. Fly +25 to +49
    Akt1 mutation Akt1 homozygotous have a significantly decreased lifespan [11292874]. Heterozygous Akt1 animals form dwarfs [11292874]. Fly
    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
    E(z) mutation 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 [20018689]. Fly +33 to +76
    puc mutation Heterozygous loss-of-function mutations in puc (either pucA241.1 or pucE69) significantly extend median and maximum lifespan and increase resistance to oxidative stress. Heterzyogosity for puc only modestly extends lifespan in animals carrying a hypomorphic allele of the JNK kinase hep [14602080]. puc heterzyogotes do not differ signficantly from wild-type for body size, reproductive activity or developmental timing, but exhibit increased resistance to oxidative stress and starvation [14602080]. Fly
    Edem1 mutation The mean lifespan of Edem1 mutants of both male and female is increased by more than 30% [19302370]. Fly +30
    elav mutation elav mutation significantly decreases the lifespan. Median lifespan in males is 66% lower [20589912]. Fly
    Gr63a mutation 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 [20422037]. Fly +30
    aPKC transposition Insertion of a P-based vectors in the structural part of aPKC increase male and female lifespan [22661237]. Fly
    esg transposition Disruption of esg by insertion of the P{GT1} vector 300 bp downstream of its structural part increases male and female lifespan [22661237]. Fly
    insc transposition insc disruption through an insertion of the P{EPgy2} vector in ts structural part prolongs female lifespan [22661237]. Fly
    Lnk mutation 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 [20333234]. Fly -14 to -17.5
    Loco mutation 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 ad heat. Additional mutant have higher Manganese-containing superoxide dismutase (MnSOD) activity, increased fat content an diminished cAMP levels. Loco RGS domain is required for the regulation of longevity as deletion analysis suggest [21776417]. Fly +17 to +20
    pex16 mutation pex16 mutation lead to a reduced mean lifespan of one-third in females and on-fourth in males. The short lifespan can be rescued by the simultaneous overexpression of pex16 in the fat body and differentiated neurons [21826223]. Mutant flies lack normal peroxisomes, have an reduced adult body size (70%-85% smaller than controls) and rozy eyes, show locomotion defects in the development of the nervous system [21826223]. Fly -33 to -75
    Prx5 mutation dprx5(-/-) null mutants are comparatively more susceptible to oxidative stress, have higher incidence of apoptosis, and a shortened mean lifespan, but thee is no significant difference in maximum lifespan (10% survival) [21826223]. Fly
    Rbp9 mutation Rbp9 mutation significantly decreases longevity with a 33% reduction in median lifespan of males [20589912]. Fly -33
    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 [18219227]. Fly -23
    Cdk5 mutation Cdk5 loss-of-function mutations result in defective axon guidance, age-dependent behavioral deficits and reduced lifespan by about one third [17368005]. Fly
    Interventions are an extension of GenAge and GenDR.