| 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 |
| 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 | — | — |
| daf-6 mutation | Loss-of-function mutations in daf-6 extend lifespan by up to 50% [10617200]. daf-6 mutants are dauer defective, chemotaxis defective, osmotic aviodance (osm), male mate poorly, and, dye filling defective [2428682]. Mutants of daf-6 have defective sheath cells causing the amphid and phasmids pores to be closed. | 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 | — | — |
| Overexpression of constitutive nuclear SKN-1 | skn-1 transgenes that overexpress a constitutive nuclear form of SKN-1 in the intestine extend the mean lifespan by 5-21%, independently of DAF-16 [18358814]. | Worm | +5 to +21 | — | — |
| 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 |
| 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-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 |
| 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 | — | — |
| cdc-25.3 knockout | cdc-25.3 knockout mutants also display increased thermotolerance and a 40% lifespan extension [16741121]. | 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 | — | — |
| 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 | — | — |
| cep-1 mutation | cep-1 mutants live up to 33% longer. which is dependent upon functional daf-16 [17895432].
| Worm | +33 | — | — |
| 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 |
| 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 |
| 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 |
| unc-26 mutation | Mutations in unc-26 extend lifespan by 30-50%. Lifespan extension is proposed to be similar to DR [9789046].
unc-26 mutants are uncoordinated, slow and have defects in pharyngeal pumping [4366476; 8462849]. | Worm | +30 to +50 | — | — |
| HG246 mutation | Strain HG246 has a lifespan that is 30% longer than wild-type [10708258].
mutant HG246 strain is heat shock resistant, exhibit lower fertility, and males are slightly defective for mating [10708258]. | Worm | +30 | — | — |
GenAge
GenDR
