Interventions

  • Species: + -
  • name effect species mean median maximum
    wwp-1 mutation Loss of wwp-1 function by mutation reduces lifespan at 25 degree Celsius, but not 20 degree Celsius. Lifespan of wwp-1 mutants across entire food concentration range by bacterial dilution in liquid culture or on solid plates does not noticeable change. Reduced levels of wwp-1 completely suppress the extended longevity of eat-2 mutants [19553937]. Worm -9
    skn-1 mutation skn-1 mutation does not alter lifespan under AL, but cancels out the lifespan extension effect of lDR or food variation at all. Response to lDR in skn-1 mutant is restored by ectopic expression of skn-1 in ASI neurons and gut. Ectopic expression of skn-1b in ASI neurons rescued lDR longevity defects of skn-1. lDR worms exhibit elevated respiration, which is absent in skn-1 mutants. skn-1 is necessary for increased respiration and the increase in respiration is necessary for lDR longevity effect, because two different inhibitors of mitochondrial electron transport chain complex III, myxothiazol and antimycin, suppress lDR longevity without shortening lifespan under AL. IF significantly extends lifespan of skn-1 mutants [19079239]. sDR extends lifespan of a skn-1 loss-of-function mutant (which displays a premature stop codon in all three isoforms) and wild-type to a similar extent [19239417]. skn-1(zu67) mutation decreases mean, median, and maximum lifespan by 11-23, 13-28 and 12-23%, respectively, and totally cancels out lifespan extension by ragc-1 RNAi [22560223]. Worm -11 to -23 -13 to -28 -12 to -23
    glp-1 mutation glp-1(qu158) mutations result in defects in germ-line proliferation and extension of lifespan by about 30%, which requires daf-16 [11799246]. glp-1(bn18) mutation increases mean, median, 75th %ile and maximum lifespan by 27-37, 26-33, 24-29 and 35%, respectively [22560223]. glp-1(e2141) mutation increases mean (32%) and maximum (53%) lifespan [18828672]. Two alleles of glp-1 that cause overproliferation of gemrline cells, glp-1(oz112gf) and glp-1(q485), result in a shortened lifespan [11799246]. In glp-1 mutants, Z2 and Z3 generate only a few germ cells, which enter meiosis and differentiate as sperm [3677168]. Worm +27 to +37 +26 to +33 +35
    daf-11 mutation Lifespan of daf-11(m84) mutant is not significant different from wild type [8247153]. Worm
    daf-7 mutation daf-7 mutation does not significantly change lifespan [8247153]. Mutations in daf-7 cause up to 50% mean and maximum life-extension. This effect is dependent upon daf-3 and on daf-16 but independent of daf-2. daf-7(e1372) increases mean and maximum lifespan by 13-39% and 55%, respectively. daf-7(m62) increases mean and maximum lifespan by 20-29% and 29% [17900898]. Worm +13 to +39 +29 to +55
    bra-1 mutation bra-1(nk1) mutation reduces mean lifespan by 6-25% [17900898]. Worm -6 to -25
    daf-8 mutation daf-8 mutation in adults increases mean lifespan by 9-31% but it did not increase maximum lifespan [17900898]. Worm +9 to +31
    daf-14 mutation daf-14(m77) mutation increases mean lifespan by 21-44% and maximum lifespan by 29% [17900898]. Worm +21 to +44 +29
    daf-5 mutation daf-5(e1386) mutation reduces mean lifespan by 19% and maximum lifespan by 21% [17900898]. Worm -19 -21
    kri-1 mutation kri-1(ok1251) mutation does not shorten the lifespan significantly [22560223]. Worm
    rsks-1 mutation rsks-1 deletion mutants also live longer. TOR RNA interference further extends lifespan of rsks-1 mutants [17266679]. Worm
    rrf-1 mutation Although rrf-1(pk1417) mutants seem to have elevated DAF-16 activity (as sod-3 transcript level is increased) the mean and maximum lifespan or ability to withstand elevated temperature is not different from wild-type [22574120]. Worm
    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
    hcf-1 mutation hcf-1 inactivation by mutation cause a daf-16-dependent lifespan extension of up to 40% and heightened resistance to specific stimuli [18828672]. HCF-1 forms a complex with DAF-16. hcf-1 inactivation by mutation cause a daf-16-dependent lifespan extension of up to 40% and heightened resistance to specific stimuli. The hcf-1(ok559) mutation increases mean and maximum lifespan by 10-37 and 29%, while the strong hcf-1(pk924) mutation extends mean and maximum lifespan by 29-31 and 53-88%, respectively. In the absence of hcf-1 there is a greater enrichment of DAF-16 at its target gene promoters and more robust DAF-16-mediated regulation of selective transcriptional targets. hcf-1 mutation extends lifespan of glp-1(e2141) mutants which lack germline cells, [18828672]. Worm +10 to +37 +29 to +88
    shc-1 knockout Loss of shc-1 function results in accelerated aging and enhanced senstivity ro heat, oxidative stress and heavy metals. 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
    slcf-1 mutation slcf-1 mutation increases average lifespan by 40%. DR (by dilution of bacteria on solid medium or by bacterial deprivation) failes to extend slcf-1 mutant's long lifespan and lifespan is even reduced by lowering bacteria concentration (i.e. higher strength of DR) [21040400]. Worm +40
    nlp-7 mutation Lifespan of nlp-7 mutants increases only moderately by sDR [19783783]. Worm
    unc-51 mutation unc-51(e369) mutation reduces mean but extends maximum lifespan. unc-51(e369) mutation reduces lifespan of eat-2(ad1116) mutants to that of wild-type [18219227]. Worm
    ctbp-1 mutation Genetic inactivation of ctbp-1 results in lifespan extension dependent on daf-16, but independent of sir-2.1. RNAi of lips-7(C09E8.2) suppresses lifespan extension by ctbp-1 inactivation [19164523]. Worm
    ife-2 mutation Loss-of-function mutation in ife-2 reduces protein synthesis and increases maximum lifespan by about 20%. It does not extend the lifespan of daf-16(RNAi) animals. TOR/let-373 RNA interference further extends lifespan of ife-2 mutants. Reduction of protein synthesis increases ATP availability and stress resistance [17266679]. Worm +20
    ced-3 mutation The ced-3(n1286) allele has no effect on lifespan, although the transgenic animals are defective in apoptosis [12136014]. Worm
    che-11 mutation Loss-of-function muation in che-11 increases lifespan up to 40% (in Bristol N2) [10617200]. che-11 mutants are dye filling defective, defective in osmotic avoidance and dauer formation, and have irregular amphid cilia [2428682]. Worm +40
    che-13 mutation Loss-of-function mutation in che-13 increases lifespan up to 40% (in Bristol N2) [10617200]. che-13 Mutants are dye filling defective, have severely shortened axonemes and ectopic assembly of ciliary structures and microtubules in many sensory neurons as well as are defective in osmotic avoidance and dauer defective [2428682]. Worm +40
    che-2 mutation che-2 recessive loss-of-function mutations extend lifespan up to 50% (in Bristol N2) [10617200]. che-2 mutants are chemotactic defective, slightly small, defective for osmotic avoidance, have ciliated neurons with abnormal stunted ultrastructure, and are dauer defective [2428682; 1732156]. Worm +50
    • Page 1 of 6
    • 25 of 150 interventions
    Interventions are an extension of GenAge and GenDR.