| 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 |
| YLR460C deletion | Deletion of YLR460C decreases replicative lifespan by 30% in the alpha strain [19030232]. | Worm | -30 | — | — |
| 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 |
| 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 |
| 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 |
| 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 | — | — |
| 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 | — | — |
| 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 | — | — |
| 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 |
| egl-4 mutation | Mutations in egl-4 extends lifespan by up to 55%. Lifespan extension by mutation of egl-4 is suppressed by daf-16. egl-4 mutation results in normal morphology and development, however egl-4 animals are almost twice as big as normal and have weak eff-laying defects [12571101]. | Worm | +55 | — | — |
| che-2 mutation | Loss-of-function in che-3 extends lifespan by 50-100% depending on the allele, but life-extension is suppressed by daf-16 (in Bristol N2) [10617200]. che-3 mutations have defective sensory neurons [2428682; 10508861] and are defective in dye filling [2428682; 7705621] as well as dauer defective [1732156]. | Worm | +50 to +100 | — | — |
| 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-19 mutation | Loss-of-function mutations in daf-19 increase lifespan up to 50% [10617200]. daf-19 mutants are dauer constitutive, dye-filling defective, and lack sensory cilia [7219552; 9475731]. | Worm | +50 | — | — |
| unc-76 mutation | unc-76(e911) allele extends male lifespan by about 50%, but has no effect on hermaphrodite lifespan [10747056].
unc-76 mutants are uncoordinated [4366476]. | Worm | +50 | — | — |
| 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 |
| 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 |
| 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 | — | — |
| 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 | — | — |
| osm-1 mutation | Loss-of-function mutation in osm-1 increases lifespan by up to 40% [10617200].
osm-1 mutants are defective in chemotaxis, dye filling and daufer formation, have short axonemes and ectopicassembly of ciliary structures and microtubules in many sensory neurons [2428682]. | Worm | +40 | — | — |
| osm-6 mutation | Loss-of-function mutation in osm-6 increases lifespan by up to 40% [10617200].
osm-6 mutants are dauer-defective, chemotaxis defective [730048; 8348618], dye-filling defective [9475731], have extremly shortened axonemes, ectopic assembly of ciliary structures and microtubules in many sensory neurons [Perkins et al. 1986] | Worm | +40 | — | — |
| 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 |
| pgl-1 mutation | pgl-1(bn101) mutant animals that are sterile have a approximately 35% longer lifespan. In contrast, fertile pgl-1(bn101) animals have a wild-type lifespan [11799246].
PGL-1 is required for fertility and proliferation of germ line cells [9741628]. | Worm | +35 | — | — |
| 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 |
GenAge
GenDR
