Interventions

  • name effect species mean median maximum
    T08A11.2 RNAi T08A11.2 RNAi in the adulthood extends the lifespan [New longevity regulators]. Worm
    Y41E3.11 RNAi Y41E3.11 RNAi in the adulthood extends the lifespan [New longevity regulators]. Worm
    ins-17 RNAi ins-17 RNAi in the adulthood extends the lifespan [New longevity regulators]. Worm
    pie-1 RNAi pie-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. Worm
    srh-20 RNAi srh-20 RNAi in the adulthood extends the lifespan [New longevity regulators]. Worm
    dcn-1 RNAi dcn-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. Worm
    R144.2 RNAi R144.2 RNAi in the adulthood extends the lifespan [New longevity regulators]. Worm
    beta-transducin RNAi beta-transducin RNAi in the adulthood extends the lifespan [New longevity regulators]. Worm
    F54E2.1 RNAi RNAi against F54E2.1 started after the animal reached the late L4 stage does not affect lifespan significantly [22103665]. Worm
    faah-1 overexpression faah-1 overexpression reduces eicosapentaenoyl ethanolamide (EPEA), palmitoleyol ethanolamide, linoleyol ethanolamide, as well as arachidonoyl ethanolamide (AEA) levels, delays development, increases thermal stress resistance, and was associated with mean and maximum adult lifespan extension by 19 and 35%, respectively, in presence of abundant food but not under (two different protocols of) DR. Overexpression in pharynx was largely sufficient for this lifespan extension [21562563]. Worm +19 +35
    Pcmt overexpression Overexpression of Pcmt extends lifespan by 32-39% at 29 degrees but not at 25 degrees [11742076]. The adult lifespan of animals overexpressing Pcmt is extended [18772467]. Mouse 0 to 39
    Akh knockdown Knockdown of the adipokinetic hormone (Akh) by RNAi (with an RU486-inducible and ubiquitously expressing Actin 5C-GS Gal4 strain) does not by itself affect lifespan, but significantly inhibits the DR-dependent increase in lifespan across a range of yeast concentrations in both females and males. While control females and males exhibit a 113%/22% increase in lifespan under DR, upon Akh inhibition there was a significant reduction in lifespan extension with DR (52%/5%). Global Akh knockdown reduces starvation resistance by 24% upon DR, but no significant change upon AL. Also Akh RNAi repressed the DR-dependent increase in cold-stress resistance. Fat body and neuronal-specific inhibition of Akh by using RU486-inducible S(1)106-GS-Gal4 and Elav-GS-Gal4 enhancer traps, respectively, does not reduce lifespan extension upon DR. But, muscle-specific inhibition of Akh using RU486-inducible muscle enhancer trap (Mhc-GS-Gal4) reduces the DR-dependent increase in lifespan. While control exhibit a 47.2% lifespan extension, animals with muscle-specific Akh inhibition fails to result in any increase upon DR (i.e. completely blocked the DR lifespan extension). Muscle-specific Akh inhibition diminishes the increase in triglyceride synthesis and breakdown present normally under DR. A significant reduction in lifespan extension also occurs with a noninducible muscle driver (Mhc-Gal4). Controls on DR exhibit significant higher levels of spontaneous activity compared to Akh RNAi-inhibited animals at all ages. Akh inhibition reduces the protective effect of DR on age-related decline in muscle function/activity [22768842]. Fly
    Sod mutation Sod mutant flies display infertility and a reduction in lifespan [2539600]. Fly
    rpt-6 RNAi RNAi against rpt-6 started after the animal reached the late L4 stage does not affect lifespan significantly [22103665]. Worm
    mdt-15 mutation mdt-15(tm2182) mutation does not affect lifespan on ad libitum, but further increases the lifespan when combined with DR (starting at the 4th day of adulthood) even more as wild-type [22132200]. Worm
    pdk-1 mutation Loss-of-function alleles in pdk-1 extend lifespan by 60% [10364160]. pdk-1(sa680) mutants are dauer constitutive (suppressed by daf-16) [10364160]. Worm +60
    amt-2 RNAi RNA interference of amt-2 increases mean lifespan by 20% [17608836]. Worm -20
    sun mutation sun mutations increases lifespan and resistance to oxidative stress [15133470] Fly
    clec-266 RNAi RNAi against clec-266 started after the animal reached the late L4 stage does not affect lifespan significantly [22103665]. Worm
    trx-1 mutation Mutants with a deletion in the trx-1 gene display a decrease in lifespan and are sensitive to oxidative stress [16324156]. trx-1 null mutant display reduced mean and maximum lifespan. trx-1 deletion completely suppresses the lifespan extension caused by eat-2 mutation, but only partially suppresses that by daf-2 or osm-5 mutations [16387300]. Worm
    pept-2 RNAi RNAi of pept-1 increases mean lifespan by 14% [12845331]. Worm +14
    CG4389 knockdown Muscle specific RNAi knockdown of CG489 which reduces its mRNA levels by 25-35%, significantly reduces the DR-dependent lifespan extension. CG4389 RNAi animals exhibit only 20% increase while controls display an lifespan increase by 123% upon DR [22768842]. Fly
    Surf1 knockdown Surf1 knockdown results in larval lethality. However, knockdown in the central nervous system (CNS) not only bypasses the larval lethality but it results in an increase in maximum lifespan of about 20-30% [16172499]. Fly +20 to +30
    dpy-23 RNAi RNAi against dpy-23 after the animal reached the late L4 stage does not affect lifespan significantly [22103665]. Worm
    trx-1 overexpression trx-1 overexpression extends lifespan in wild-type but not in eat-2 mutants. Ectopic expression of trx-1 in ASJ neurons (but not in the intestine) in trx-1 mutants rescues the lifespan-extension conferred by eat-2 mutation. trx-1 overexpression extends lifespan of wild-type but not in eat-2 mutants. trx-1 deletion almost completely suppresses lifespan extension induced by dietary deprivation (DD). DD upregulates trx-1 expression in ASJ neurons. DR activates trx-1 in ASJ neurons which in turn triggers a trx-1-dependent non-cell autonomous mechanism to extend adult lifespan [21334311]. Worm
    Interventions are an extension of GenAge and GenDR.