Interventions

  • name effect species mean median maximum
    Coq7 overexpression Transgenic overexpression of mouse Coq7 reverts the extended lifespan of clk-1 mutants [11511092]. Worm
    Hsp70 locus overexpression Overexpression of the Hsp70 locus (containing Hsp70Bb and Hsp70Bc) in transgenic flies extends lifespan as much as 7.9% [9363888]. Fly +7.9
    tdp-1 overexpression tdp-1 overexpression strains have a reduced lifespan at 20 and 25 degree Celsius [Vaccaro et al. 2012]. Worm
    aak-2 constitutive active mutation A constitutive active mutation of aak-2 is sufficient to cause increase stress resistance as well as to significantly extend lifespan. Both increased stress resistance and extended lifespan is reverted in daf-16 knockdown by RNAi [17900900]. Worm
    clk-1 overexpression Overexpression of clk-1 shortens lifespan and is associated with increased mitochondrial activity [10202142]. Worm
    pha-4 overexpression pha-4 overexpression increases longevity of wild-type only slightly, but significant that of daf-16 mutants [17476212]. Worm
    Overexpression of constitutive nuclear DAF-16 Overexpression of constitutive nuclear forms of DAF-16 increases lifespan only slightly [11381260]. Worm
    wwp-1 overexpression wwp-1 overexpression extends lifespan by up to 20%. RNAi reduction of pha-4, but not of daf-16 suppresses increased longevity by wwp-1 overexpression [19553937]. Worm +20
    wwp-1 RNAi RNA interference of wwp-1 decreases median lifespan by 9% in wild-type animals and 24% in daf-2 mutants [18006689]. Loss of wwp-1 function by RNAi reduces lifespan at 25 degree Celsius, but not 20 degree Celsius. Reduced levels of wwp-1 completely suppress the extended longevity of eat-2 mutants. wwp-1 RNAi does not suppress the extended lifespan of isp-1 mutants and has only minor suppressive effects on lifespan of another mitochondrial mutant, clk-1, and in cyc-1 RNAi treated worms. RNAi depletion of wwp-1 has no effect on long lifespan of daf-2 mutants [19553937]. Worm -9
    aqp-1 overexpression Overexpression of aqp-1::GFP rescues short lifespan of aqp-1 deletion mutants and partially prevented glucose from shortening lifespan. Worm
    ubc-18 overexpression ubc-18 overexpression is unable to extend lifespan (possibly, UBC-18 is not limiting for WWP-1 function in lifespan) [19553937]. Worm
    AAT1 overexpression Overexpression of AAT1 extends replicative lifespan by 25% and does not synergize with 0.5% glucose restriction [18381895]. Yeast +25
    GUT2 overexpression Overexpression of GUT2 extends replicative lifespan by 25% and does not synergize with 0.5% glucose restriction [18381895]. Yeast +25
    HST2 overexpression HST2 overexpression extends replicative lifespan. 0.5% glucose restriction does not increase lifespan of sir2;fob1;hst2 triple mutants [16051752]. DR increases lifespan of all four sir2;fob1;hstX(X = sirtuin) triple mutants [16741098; 17129213]. Yeast
    LAT1 overexpression In contrast, overexpressing LAT1 extends replicative lifespan, and this lifespan extension was not further increased by 0.5% glucose restriction. Similar to DR, replicative lifespan extension by LAT1 overexpression largely requires mitochondrial respiration [17200108]. Overexpressing Lat1 extends lifespan (20% mean lifespan increase) and this lifespan extension is not further increased by DR. Similar to DR, lifespan extension by LAT1 overexpression largely requires mitochondrial respiration indicating mitochondrial metabolism plays an important role in DR. Interestingly, LAT1 overexpression does not require the Sir2 family to extend lifespan. Lat1 is also a limiting longevity factor in non-dividing cells in that overexpressing LAT1 extends cell survival during prolonged culture at stationary phase. Yeast +20
    MDH1 overexpression Overexpression of MDH1 extends replicative lifespan by 25% and does not synergize with 0.5% glucose restriction [18381895]. Yeast +25
    NDE1 NDE2 overexpression Overexpression of NDE1 and NDE2 increases intracellular NAD/NADH ratio by lowering NADH concentration and increases replicative lifespan by 20-25%. This lifespan extension is non-additive with 0.5% glucose restriction [14724176]. Yeast +20 to +25
    TSA1 activating mutation A gain-of-function allele of peroxiredoxin (thioredoxin peroxidase, Tsa1) causes a dominant oxidative stress-resistance and robust premature aging phenotype with reduced mean lifespan. These effect is not provoked by altered Tsa1 levels, nor can it be stimulated by deletion, haploinssufficiency or overexpression of wild-type allele [20729566]. Yeast
    ERG2 overexpression Overexpression of ERG2 with the promoter of ERG6 (Perg6-ERG2) extends replicative lifespan and this effect was overlapping with moderate DR, because DR can not extend the lifespan of this mutant [Tang et al., unpublished]. Yeast
    FRE6 deletion FRE6 deletion increases mean replicative lifespan by 14% and cancels out the lifespan extending effect of DR [22912585]. Yeast +14 -2
    wis1 constitutive active mutation Constitutive active mutation of wis1 extends chronological lifespan and there is no further beneficial effect of DR [20075862].
    atf1 overexpression Overexpressing atf1 is not sufficient to promote chronological lifespan extension in cells lacking sty1 [20075862].
    gpa2 constitutive active mutation Constitutive active mutation of gpa2 (alias git8) decreases chronological lifespan under AL (2% glucose) and almost completely cancels out the lifespan extending effect of DR (0.2% glucose) [19266076].
    git3 constitutive activative mutation Constitutive activation of the G-alpha subunit acting downstream of Git3 accelerates aging and inhibits the effect of DR [19266076].
    Pck1 overxpression Overexpression of Pck1 in skeletal muscle results in an increased number of mitochondria, markedly increase in activity, and extended lifespan by 30%. Transgenic mice ate 60% more than controls but had half the body weight and 10% of the body fat [17716967; Hakimi, Berger and Hanson, unpublished]. Pck1 overxpression leads to increased storage and utilization of fatty acids in muscle for energy purposes and mutants store up to 5-times more triglyceride in their skeletal muscle, and exhibit increased levels of physiological activity [18394430]. Mouse +30
    Interventions are an extension of GenAge and GenDR.