Interventions

  • Species: + -
  • name effect species mean median maximum
    unc-10 mutation Mutation in unc-10 reduces maximum lifespan 35% [17592521]. Worm -35
    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
    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
    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
    unc-17 mutation Mutation of unc-17 extends lifespan on NGM agar covered with killed or live bacteria. unc-17(CB933) extends mean, 75%ile, and maximum lifespan by 31-79%, 68-89%, and 68-79%. Lifespan extension by unc-17 mutation is totally abolished by RNAi inactivation of daf-16, but not skn-1. eat-2 RNAi further enhances the extension of lifespan by mutations of unc-17 [22768380]. Mutation and RNAi of unc-17 suppresses pheromone-induced dauer formation [22768380]. Worm +31 to +79 +68 to +79
    cco-1 RNAi RNA interference of cco-1 results in a 45-61% increase in mean lifespan (in fer-15; fem-1 and N2 background, respectively) [16103914]. RNAi against cco-1 increases mean and maximum lifespan by 73% and 90%, respectively [12471266]. cco-1 RNAi extends mean and maximum lifespan by 41 and 50%. RNAi of cco-1 during the larval stages is necessary and sufficient for increased lifespan, while only during the adulthood it fails to to extend lifespan. cco-1 RNAi results in reduced pharyngeal pumping, defecation, motility, and body size as well as reduced ATP levels (by 60-80%) and oxygen consumption. daf-16 mutation fails to prevent lifespan extenison by RNAi of cco-1 and mutation of daf-2 further extends the lifespan of cco-1 RNAi animals [12447374]. RNAi of cco-1 only during the adulthood increases mean and 75th %ile lifespan by 22-32 and 16-33%, respectively [22560223]. Worm +22 to +73 +50 to +90
    phi-44 RNAi phi-44 RNAi leads to 46% mean and 50% maximum lifespan extension. Lifespan extension by phi-44 is not suppressed by daf-16. phi-44 RNAi animals have lower ATP content and oxygene consumption [12447374]. Worm +46 +50
    age-1 RNAi RNAi against age-1 extends lifespan by 30% [8700226; 8608934]. age-1 RNAi increases mean and maximum lifespan by 36-46% and 48-50% [12447374]. RNAi against age-1 increases mean lifespan by 83% [18828672]. age-1(mg44) zygotic null mutants have a mean (99%) and maximum (117%) lifespan extension [18828672]. Worm +36 to +99 +48 to +117
    F57A8.4 mutation Mutation of F57A8.4 extends lifespan on NGM agar covered with killed or live bacteria as well as in liquid culture medium. F57A8.4(tm4341) mutation extends the mean, 75%ile, and maximum lifespan by 18-38, 21-25, and 42-68%. Lifespan extension by gar-3 mutation is not abolished by RNAi inactivation of either daf-16 nor skn-1. eat-2 RNAi shortens the lifespan of F57A8.4 mutants [22768380]. Mutation of F57A8.4 suppresses pheromone-induced dauer formation [22768380]. Worm +18 to +38 +42 to +68
    hsb-1 mutation hsb-1(cg116) mutation at 20 degree Celsius extends mean, 75%ile, and maximum lifespan by 57-60%, 52-59%, and 37-69%. Worm +57 to +60 +37 to +69
    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
    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
    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
    eat-2 mutation eat-2 mutations result in partial starvation by disrupting the function of the pharynx and an approximately 50% extension of lifespan. eat-2 mutants life significant longer by up to 57% [9789046]. eat-2(ad1116) mutants have an extended mean, 75%ile and maximum lifespan by 30, 35, and 24% [22810224]. sDR further increases the long lifespan of eat-2 mutants [19239417]. eat-2 mutants live longer than wild-type at high food concentration but are short lived at lower concentrations (via bacterial dilution) [19229346]. eat-2(ad1113) mutation increases mean lifespan by 56% and is non-additive with SCNA overexpression [16782295]. Combining eat-2 mutation with bacterial deprivation DR does not result in an additive increase in lifespan [17081160;17096674]. Loss of function of eat-2 extends lifespan by 20-30%. Lifespan extension is proposed to be similar to DR. eat-2;daf-2 double mutant live longer than daf-2 single mutants [9789046]. Therefore, eat-2 mutants can synergize with daf-2 mutants, but not with clk-1 mutants, for lifespan extension. Lifespan extension conferred by eat-2 is not suppressed by daf-16 mutation [9789046]. Worm +30 to +57 +24
    ins-35 mutation Mutation of ins-35 extends lifespan on NGM agar covered with killed or live bacteria as well as in liquid culture medium. ins-35(TM290) mutation extends mean, 75%ile, and maximum lifespan by 15-17, 14-23, and 23-24%. Lifespan extension by ins-35 mutation is totally abolished by daf-16 or skn-1 RNAi inactivation eat-2 RNAi further enhances the extension of lifespan by mutation in ins-35 [22768380]. Mutation of ins-35 enhances pheromone-induced dauer formation [22768380]. Worm +15 to +17 +23 to +24
    shk-1 mutation Mutation of shk-1 extends lifespan on NGM agar covered with killed or live bacteria as well as in liquid culture medium. shk-1(RB1392) mutation extends mean, 75%ile, and maximum lifespan by 19-22, 19-21, and 20-24%. Lifespan extension by unc-17 mutation is totally abolished by RNAi inactivation of either daf-16 or skn-1. eat-2 RNAi shortens the lifespan of shk-1 mutants [22768380]. Mutation of shk-1 enhances pheromone-induced dauer formation [22768380]. Worm +19 to 22 +20 to 24
    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
    glc-4 mutation Mutation of glc-4 extends lifespan on NGM agar covered with killed or live bacteria as well as in liquid culture medium. glc-4(JD31) increases the mean, 75%ile, and maximum lifespan by 13-23, 11-23, 19-34%. Lifespan extension by glc-4 mutation is totally abolished by RNAi inactivation of either daf-16 or skn-1. eat-2 RNAi further enhances the extension of lifespan by glc-4 mutation [22768380]. Mutation of glc-4 suppresses pheromone-induced dauer formation [22768380]. Worm +13 to +23 +18 to +34
    gar-3 mutation Mutation of gar-3 extends lifespan on NGM agar covered with killed or live bacteria as well as in liquid culture medium. gar-3(VC670) mutation extends mean, 75%ile, and maximum lifespan by 5-18, 4-7 and 15-56%. Lifespan extension by gar-3 mutation is not abolished by RNAi inactivation of daf-16, skn-1, or eat-2 [22768380]. Worm +5 to +18 +15 to +56
    age-1 mutation Recessive knockout mutants of age-1 have a 40-65% increase in mean lifespan and a 65-110% increase in maximum lifespan [8608934; 8700226]. age-1(mg44) zygotic null mutants have a mean (99%) and maximum (117%) lifespan extension [18828672]. Even in axenic culture lifespan of age-1 is extended up to 100%. age-1 mutation significantly extends lifespan under AL, but only slightly under sDR [16720740]. age-1 mutants are dauer constitutive [8056303] and display lower brood size as well as increased embryonic lethality [9504918]. Additionally, age-1 mutants have elevated levels of superoxidase dismutase and catalase activities [8389142]. Worm +99 +117
    cha-1 mutation Mutation of cha-1 extends lifespan on NGM agar covered with killed or live bacteria as well as in liquid culture medium. cha-1(TY1652) mutation extends mean, 75%ile, and maximum lifespan by 23, 29, and 38%. The cha-1(PR1152) allele extends mean, 75%ile, and maximum lifespan by 22-49, 18-25, and 11-21%. Lifespan extension by cha-1 mutation is not abolished by daf-16 RNAi inactivation. eat-2 RNAi shortens the lifespan of cha-1 mutants [22768380]. Worm +22 to +49 +11 to +21
    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
    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
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    • 25 of 103 interventions
    Interventions are an extension of GenAge and GenDR.