| 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 |
| bra-1 mutation | bra-1(nk1) mutation reduces mean lifespan by 6-25% [17900898]. | Worm | -6 to -25 | — | — |
| 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 |
| mir-71 mutation | Loss-of-function of mir-71 decreases lifespan [21129974]. mir-71 mutants have a reduced lifespan with 40% decrease in mean lifespan. Loss of mir-71 function suppresses the long lifespan of glp-1(e2141) mutants [22482727], | Worm | -40 | — | — |
| eat-7 mutation | The eat-7(ad450) allele decreases lifespan by 35% [9789046] exhibits defects in pharyngeal feeding behavior [8462849]. | Worm | -35 | — | — |
| 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 |
| mir-64-66 mir-229(nDf63) mutation | mir-64-66 mir-229(nDf63) mutation decreases the lifespan by 30% [22482727]. | Worm | -30 | — | — |
| YLR460C deletion | Deletion of YLR460C decreases replicative lifespan by 30% in the alpha strain [19030232]. | Worm | -30 | — | — |
| 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 |
| mir-61 mir-250(nDf59) mutation | mir-61 mir-250(nDf59) mutation decreases the mean lifespan by 25% [22482727]. | Worm | -25 | — | — |
| mir-58 mutation | mir-58(n4640) mutation decreases the mean lifespan by 20% [22482727]. | Worm | -20 | — | — |
| mir-80 mir-227(nDf53); mir-81-82(nDf54) | mir-80 mir-227(nDf53); mir-81-82(nDf54) mutation decreases the mean lifespan by 20% [22482727]. | Worm | -20 | — | — |
| daf-5 mutation | daf-5(e1386) mutation reduces mean lifespan by 19% and maximum lifespan by 21% [17900898]. | Worm | -19 | — | -21 |
| 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 |
| 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 |
| fer-15 mutation | Mutation of fer-15 results in a slight (10%) reduction in mean lifespan. Dietary restriction of coenzyme Q extends the lifespan of fer-15 animals. fer-15(b26ts) animals are temperature sensitive and sterile [11778046]. | Worm | -10 | — | — |
| 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 |
| 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 | — | — |
| unc-31 mutation | Mutation in unc-31 increases hermaphrodite lifespan by approximately 70% and male lifespan by 150% [10377425; 11063684; 10747056]. unc-31 also cause constitutive dauer formation. Both phenotypes, enhanced longevity and constitutive dauer formation are suppressed by mutations in daf-16 [10377425].
unc-31 mutants are uncoordinated [4366476] and exhibit dauer constitutive phenotype [10377425], are lethargic, feed constitutively, are defective in egg-laying, and produce dauer larvae that fail to recover [8462849]. | Worm | +70 to +150 | — | — |
| unc-64 mutation | Mutations in unc-64 result in constitutive dauer formation and increase lifespan, which is suppressed by mutations in daf-16 [10377425]. unc-64 mutation increases mean and maximum lifespan [16280150]. unc-64 mutation increased lifespan of hermaphrodites by approximately 70% and those of males by 150% [10377425; 4366476; 10747056].
unc-64 mutants are uncoordinated [4366476]. | Worm | +70 to +150 | — | — |
| 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 | — | — |
| daf-10 mutation | Loss of function mutation in daf-10 increases lifespan by 60% (in Bristol N2) [10617200]. daf-10 mutants are dauer defective, dye filling defective, octopamine deficient and have abnormal chemotaxis and osmotic avoidance. Mutants in daf-10 display abnormal sensory anatomy, especially amophidial neurons and sheath cells, and cephalic neurons. daf-10 mutant males do not mate [2428682]. | Worm | +60 | — | — |
GenAge
GenDR
