Interventions

  • Species: + -
  • name effect species mean median maximum
    lin-14 loss-of-function mutation A loss-of-function mutation in lin-14 extends lifespan by 31% [16373574]. lin-14(n719) mutation extends mean and maximum lifespan of control animals by 20 and 67%, respectively [23097426]. The life-extending effects is dependent on daf-16 and hsf-1 [16373574]. Inactivation of lin-14 does not increase the lifespan of pash-1 mutants [23097426]. Worm +20 to +31 +67
    isp-1 mutation A missense mutation in isp-1 leads to low oxygen consumption, decreased sensitivity to reactive oxygen species, and increased mean (60%) and maximum (100%) lifespan. An isp-1;daf-2 double mutant has a lifespan that is longer than either single mutant, but the lifespan extension of the double mutant is not addative relative to each single mutant [11709184]. Worm +60 +100
    hsf-1 mutation A mutant allele of hsf-1 slightly decreases lifespan under AL, but cancels out the lifespan extension effect of bDR. hsf-1 RNAi also prevents lifespan extension by bDR. Glucose or glycerol does not shorten the lifespan of hsf-1 mutants. Glucose treatment completely suppresses the long lifespan caused by hsf-1 overexpression [19883616]. sDR extends the lifespan of hsf-1 mutant with a premature stop codon, that eliminates activation domain, and that of wild-type to a similar extent [19239417]. Worm
    nrh-49 mutation A mutant allele, nhr(nr2041) results in a short lifespan. nhr-49 mutant animals accumulate fat, due to decreased expression of enzymes involved in fatty acid beta-oxidation [15719061]. Worm
    wrn-1 mutation A nonfunctional wrn-1 DNA helicase decreases the lifespan [23075628]. The expression of miR-124 in whole wrn-1 mutant worms is significantly reduced [23075628]. Supplementation of vitamin C normalizes the median lifespan of wnr-1 and mir-124 mutants [23075628]. Worm
    aak-1 mutation aak-1 does not appear to be required for the control of lifespan [15574588]. Worm
    aak-2 mutation aak-2(ok524) knockout mutants have a 12% and 18% shorter mean and maximum lifespan, respectively as well as faster age-dependent accumulation of a lipofuscin-like fluorescent pigment in the intestine [15574588]. aak-2 mutation suppresses lifespan extension and delay of the decline in locomotor activity resulting from sDR [17900900]. aak-2 mutation cancels out the lifespan extension effect of sDR and PD, regardless of the concentration of bacteria or peptones. bDR significantly extends lifespan of aak-2 mutants, but to lesser extent than that of wild-type. eat-2 mutation extends the lifespan of aak-2 mutants to the same extent than that of wild-type. Resveratrol does not increase lifespan of aak-2 mutants [19239417]. daf-2(m577);aak-2(ok524) double mutant has a lifespan that is indistinguishable from those of aak-2(ok524) single mutant [15574588]. Worm -12 -18
    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
    bra-1 mutation bra-1(nk1) mutation reduces mean lifespan by 6-25% [17900898]. Worm -6 to -25
    C26B2.2 knockout C26B2.2 knockout mutations extend lifespan [15253933]. Worm
    cdc-25.3 knockout cdc-25.3 knockout mutants also display increased thermotolerance and a 40% lifespan extension [16741121]. Worm +40
    cep-1 mutation cep-1 mutants live up to 33% longer. which is dependent upon functional daf-16 [17895432]. Worm +33
    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
    daf-1 mutation daf-1(mk40) mutation increases mean lifespan by 18-46% and maximum lifespan by 29% [17900898]. The daf-1(m40) allele has no effect on lifespan and fails to prevent lifespan extension by sir-2.1 overexpression, but it results in a temperautre-sensitive, dauer-constitutive phenotype in larvae [11242085]. Worm +18 to +46 +29
    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-16 mutation daf-16(m26) mutation slightly, insignificantly decreases lifespan, but completely suppresses lifespan extension of daf-2(e1370) adults [8247153]. daf-16 is required for lifespan extension by mutation of daf-2 or age-1 [8247153]. Mutations in daf-16 suppressed life-extension caused by mutations in daf-2 [8247153]. Loss of function alleles of daf-16 shorten lifespan, but some alleles have lifespan equal to wild-type [8247153]. daf-16 mutation significantly reduces lifespan under AL (-20%), but does not prevent lifespan extension by sDR. In another experiment daf-16 mutation totally suppresses lifespan extension by sDR [16720740]. sDR does not stimulate DAF-16 translocation to the nucleus, but daf-16 mutation cancelled out the ability of sDR to extend lifespan and to delay the decline in locomotor activity [17900900]. DR by bacterial dilution extends lifespan of daf-16 mutants [17538612]. daf-16 mutation decreases lifespan under AL, but fails to prevent bDR to further extend lifespan [18331616]. IF-induced lifespan-extension by either 24h/48h/72h per 4 days is significantly diminished in null mutants of daf-16. All these regimens extend lifespan of daf-16 to a lesser extent than wild-type. daf-16 partially mediates IF-induced longevity [19079239]. Glucose or glycerol does not shorten lifespan of daf-16 mutants [19883616]. daf-16 mutation cancels out the lifespan extension effect of sDR and PD, regardless of the concentration of bacteria or peptones. bDR significantly extends lifespan of daf-16 mutants, but to a lesser extent than that of wild-type. eat-2 mutation extends the lifespan of daf-16 mutants to the same extent than that of wild-type. Resveratrol extends lifespan of daf-16 mutants [19239417]. daf-16 RNAi completely blocks lifespan extension by daf-2 mutation, but only partially by bDR. daf-16 RNAi attenuates protection against oxidative stress by bDR. daf-16 expression is induced by bDR [19924292]. Knockdown of daf-16 decreases mean and maximum lifespan by 50% and 54%, respectively [22509016]. DAF-16 reduces expression of rsks-1 and daf-15 [15253933; 22560223]. daf-16(mu86) mutation decreases mean (44%) and maximum (18%) lifespan [15905404]. daf-16(mgDf47) decreases mean (18-37%) and maximum (29%) lifespan [18828672]. daf-16 mutants are dauer defective [7219552] and completely suppress all the phenotypes of daf-2 and age-1 mutations, including lifespan extension, dauer arrest, reduced fertility, and viability defects [8247153; 7789761; 9504918; 7789761]. Mutations in daf-16 also suppress lifespan extension of animals that have a germ line ablation [10360574]. Sex-specific lifespan potential requires daf-16 [10747056]. daf-16 mutation suppresses enhanced UV resistance as well as increase longevity of daf-2, daf-23, spe-26, and clk-1 mutants. Mutation in daf-16 does not alter the reduced fertility in spe-26. daf-16 mutants are more fertile than wild-type [8807294]. Worm -18 to -37 -29
    daf-18 mutation daf-18 is required for complete dauer formation. daf-18 mutation partially suppresses the lifespan extension of age-1 and daf-2 mutants. daf-18 mutants are defective for dauer formation and form some dauer-like larvae when starved [7789761; 8601482]. Worm
    daf-2 mutation daf-2 mutants live more than twice as long as controls. daf-2(sa189) mutation extends mean and maximum lifespan by 133 and 129%, respectively, when shifted to 20 degree Celsius. The daf-2(e1370) mutation extends mean and maximum lifespan by 32 and 119%, respectively, when shifted to 25 degree Celsius and by 110 and 145%, respectively, at 20 degree Celsius. daf-2(sa189) mutation extends mean lifespan by 67% as well as maximum lifespan [8247153]. This lifespan extension requires the activity of daf-16 [8247153]. The lifespan extension of daf-2(e1370) mutants is cancelled out by daf-16(m26) mutation. daf-2 mutants still exhibit a long lifespan after ablation of the gonad and germ cells. [8247153]. daf-2(e1370) increases mean (95-118%) and maximum (165%) lifespan [18828672]. daf-2 mutation extends lifespan of wild-type and eat-2 mutants [9789046]. Long lifespan of daf-2 insulin receptor mutation is further extended by sDR. However, daf-2 mutation is not a null mutation, therefore it is still possible that part of sDR-induced increase in lifespan might depend on insulin receptor pathway [17900900]. DR by bacterial dilution extends lifespan of daf-2 mutants [17538612]. IF does not markedly extend lifespan of daf-2 mutants [19079239]. 2% glucose reduce fractions of animals that become dauers at 22.5 degree Celsius in daf-2 mutants. Glucose almost completely suppresses lifespan extension of daf-2 ligand binding domain and tyrosine kinase mutants back to wild-type levels [19883616]. daf-2 mutation increases average lifespan by 157%. Under AL daf-2 mutation increases lifespan by 30%. bDR increases lifespan by 65%. daf-2 mutation further increases lifespan under bDR by 40%. Resistance to oxidative stress is reduced daf-2 mutation [19924292]. daf-2(m577) mutation increases mean and maximum lifespan by 33 and 29%, respectively, while daf-2(e1370) mutation increases mean and maximum lifespan by 101 and 181%, respectively [16782295]. DR from eat-2(ad465) mutation has an addative effect on lifespan of daf-2(e1370) adults, but not on lifespan of daf-2(e1368) adults [18043747]. Mutation in daf-2 in combination with mutation of daf-12 results in nearly 300% increase in lifespan [7789761]. daf-2 mutants are dauer constitutive [7219552] and exhibit reduced brood size [9504918; 9725835]. daf-2 mutants synergize with germ line ablation for lifespan extension [10360574] and also exhibit synergy with clk-1 mutation for lifespan prolongation [8638122]. All the phenotypes of daf-2 mutants are suppressed by mutation of daf-16 [8247153; 8601482; 7789761; 9725835; 9504918]. Mutation of daf-2 increases expression of sod-3 [10428762]. daf-2(e1370) increases mean lifespan by 146% [23097426]. Worm +32 to +146 +119 to +165
    daf-3 mutation daf-3(mgDf90) mutation decreases mean lifespan by 0-16% and maximum lifespan by up to 9-21%. daf-3(mgDf90) decreases mean lifespan even by 19% [17900898]. Mutation of daf-3 results in a wild-type lifespan, but greatly extends the lifespan of the long-lived daf-9 mutant [11782415]. daf-3 mutations are dauer defective. Worm 0 to -19 -9 to -21
    daf-4 mutation daf-4(e1374) mutation increases mean and maximum lifespan by 40-120% and 76-83%. daf-4(m63) allele has no effect on lifespan and fails to prevent lifespan extension by sir-2.1 [11242085]. mutation of daf-4 results in a temperature-sensitive, dauer-constitutive phenotype in larvae. sir-2.1 overexpression in the daf-4(m63) background results in an increase in the severity of the dauer-constitutive phenotype [11242085]. Worm +40 to +120 +76 to +83
    daf-5 mutation daf-5(e1386) mutation reduces mean lifespan by 19% and maximum lifespan by 21% [17900898]. Worm -19 -21
    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
    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
    pept-2 mutation Deletion of pept-1 (alias opt-2 or pep-2) results in retarded development, reduced body size and extended reproductive lifespan. It also further extends (60%) the life-extension caused by daf-2 mutations [15155758]. pept-2 mutants exhibit a decrease in fat content. Worm
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    • 25 of 150 interventions
    Interventions are an extension of GenAge and GenDR.