| 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 |
| pash-1 mutation | pash-1 mutants have a decreased lifespan and display phenotypic and molecular signs of advantaged age earlier.
pash-1(mj100) temperature sensitive loss-of-function mutation decreases (at the permissive temperature) mean and maximum lifespan by 31 and 71%, respectively. At the restrictive temperature pash-1 mutants are slightly short-lived with a mean and maximum lifespan reduction by 13 and 54%. Lifespan of pash-1 mutants is reduced by a 24h upshift to 25 degree Celsius at the young adult stage with (36 and 78% reduction mean and maximum lifespan, respectively) [23097426].
The rescue of pash-1 expression all tissues restored almost normal lifespan. Rescue specifically in hypodermis, pharynx muscle, gut had no effect on lifespan. Rescue in body wall muscle marginal extended the lifespan, while rescue specifically in the neurons significantly restored mean but not maximum lifespan. Lifespan was also restored by combined rescue in hypodermis and muscle [23097426]. | Worm | -31 | — | -71 |
| 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 |
| mir-238 mutation | Mutating mir-238 decreases mean and maximum lifespan by 18 and 24% [21129974]. mir-238(n4112) mutation decreases mean lifespan by 20% [22482727]. | Worm | -17.6 to -20 | — | -24 |
| mir-14 mutation | Mutating mir-14 decreases lifespan in both sexes. mir-14 reduces the mean and maximum lifespan of females by 55 and 36%, respectively, while those of males is reduced by 29 and 21%, respectively [12725740]. | Worm | -29 to -55 | — | -21 to -29 |
| daf-5 mutation | daf-5(e1386) mutation reduces mean lifespan by 19% and maximum lifespan by 21% [17900898]. | Worm | -19 | — | -21 |
| 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 |
| mir-246 mutation | Mutating mir-246 decreases mean and maximum lifespan by 12% [21129974]. | Worm | -11.7 | — | -12.0 |
| 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 |
| 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 |
| 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 |
| 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 |
| 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 |
| mir-239 mutation | Mutating mir-239 increases mean and maximum lifespan by 12 and 36%, respectively. Lifespan extension by mir-239 loss-of-function requires daf-16 [21129974]. | Worm | +11.8 | — | +36.0 |
| 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 |
| spe-26 mutation | spe-26 mutation in both hermaphrodites and mated males renders them defective in spermatogenesis and increases mean lifespan by about 65%. In hermaprodites spe-26(hc138ts) mutation increases mean and maximum lifespan by 46 and 29%, respectively. Mating does not reduce lifespan in male with spe-26 mutation. Animals with a different spe-26 allele, it118ts, have a similar increase in mean lifespan both in mated males and mated hermaphrodites. Mating even increases spe-26 mutant male lifespan, although the increase is slight (16% increase in mean and 13% increase in maximum lifspan. While compared to wild-type mated spe-26 males have an increase in mean and maximum lifespan of 81 and 63%, respectively, in comparison to wild-type [1448167]. spe-26 loss of function mutation extends lifespan [8807294]. | Worm | +46 to +81 | — | +29 to +63 |
| 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-14 mutation | daf-14(m77) mutation increases mean lifespan by 21-44% and maximum lifespan by 29% [17900898]. | Worm | +21 to +44 | — | +29 |
| 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-9 mutation | Mutations in daf-9 increase lifespan up to 52% [11740945]. Mutation of daf-9 extends mean and maximum lifespan at 15 degree Celsius by 15-75% and 28-96%, respectively [11782415]. Lifespan extension conferred by mutation of daf-9 is suppressed by mutation of daf-12, but not by mutation of daf-16. daf-3 mutation results in a wild-type lfiespan, but greatly extends the long-lived daf-9 mutant lifespan. daf-9 mutants are dauer-constitutive [3350212], exhibit gonadal cell migration defect [11782415], and a post-dauer molting defect. | Worm | +15 to +75 | — | +28 to +96 |
| 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 |
GenAge
GenDR
