| tub-1 mutation | Mutation of tub-1 (alleles nr2004 and nr2044) leads to 20-25% life-extension dependent on daf-16 [16054097].
tub-1 mutation promotes increased fat accumulation [16054097]. | Worm | +20 to +25 | — | — |
| tax-4 mutation | Recessive loss-of-function allele in tax-4 can increase lifespan by up to 100%. Lifespan extension by tax-4 mutation is suppressed by daf-16 and gonad ablation [10617200].
tax-4 mutants are thermotaxis and chemotaxis defective [8893027; 8348618]. Mutants are slighlty dauer constitutive and form dauers at 27 degree Celsius [9486798]. | Worm | +100 | — | — |
| 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 | — | — |
| pept-2 mutation | Deletion of pept-1 (alias opt-2 or pep-2) results in retarded development, reduced body size and extended reproductive lifespan. It also further extends (60%) the life-extension caused by daf-2 mutations [15155758].
pept-2 mutants exhibit a decrease in fat content. | Worm | — | — | — |
| 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 | — | — |
| 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 | — | — |
| osm-5 mutation | Loss-of-function mutation in osm-5 can increase lifespan by 100-150% [10617200].
osm-5 mutants are dauer-defective (suppressed by daf-2) [1732156] and chemotaxis defective [8348618], as well as day filling defective [Starich et al. 1995]. | Worm | +100 to +150 | — | — |
| osm-3 mutation | Recessive osm-3 loss-of-function alleles can extend lifespan by 100%, which is suppressed by gonad ablation but not germ line ablation [10617200].
osm-3 mutants do not form dauers in response to starvation and have defective cilia [1732156] as well as are defective in chemosensory response and chemotaxis [7714894]. | Worm | +100 | — | — |
| 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 | — | — |
| nrh-49 mutation | A mutant allele, nhr(nr2041) results in a short lifespan. nhr-49 mutant animals accumulate fat, due to decreased expression of enzymes involved in fatty acid beta-oxidation [15719061]. | Worm | — | — | — |
| mev-1 mutation | Loss of function in mev-1 shortens lifespan to 66% of wild-type (i.e. by 34%) and accelerates accumulation of aging-associated biomarkers such as protein carboynls and fluorescent materials. mev-1 mutants are hypersensitive to raised oxygen concentrations and their lifespan decreases dramatically as oxygen concentrations increase [9716135]. Mutation of mev-1 results in paraquat sensitivity, slow grows, and low fecundity. mev-1 mutants have a 50% reduction in superoxide dismutase activt relatively to wild-type [2233820]. | Worm | — | — | — |
| mes-1 mutation | mes-1(bn7) mutant animals that lack germ cells live about 60% longer than fertile mes-1(bn7) controls. This lifespan extension requires daf-16 [11799246]. Homozygous mes-1 mutant progeny from homozygous mutant mothers are sterile [1783292]. | Worm | — | — | — |
| mec-8 mutation | Recessive loss of function allele in mec-8 extends lifespan [10617200]. mec-8 mutations are mechanosensory defective and have defective dye filling of sensory neurons [8625846]. | Worm | — | — | — |
| hsf-1 mutation | A mutant allele of hsf-1 slightly decreases lifespan under AL, but cancels out the lifespan extension effect of bDR. hsf-1 RNAi also prevents lifespan extension by bDR. Glucose or glycerol does not shorten the lifespan of hsf-1 mutants. Glucose treatment completely suppresses the long lifespan caused by hsf-1 overexpression [19883616]. sDR extends the lifespan of hsf-1 mutant with a premature stop codon, that eliminates activation domain, and that of wild-type to a similar extent [19239417]. | Worm | — | — | — |
| gro-1 mutation | Mutation in gro-1 extends lifespan extension by 29% and slows growth. Post-embryonic growth rate is greatly reduced in gro-1 mutants. gro-1 mutant exhibit increased resistance to heat-shock and tends to avoid bacterial lawn [Mutation in gro-1 extends lifespan extension by 29% and slows growth. Post-embryonic growth rate is greatly reduced in gro-1 mutants. gro-1 mutant exhibit increased resistance to heat-shock and tends to avoid bacterial lawn [8638122]. | Worm | +29 | — | — |
| 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 | — | — |
| 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-18 mutation | daf-18 is required for complete dauer formation. daf-18 mutation partially suppresses the lifespan extension of age-1 and daf-2 mutants. daf-18 mutants are defective for dauer formation and form some dauer-like larvae when starved [7789761; 8601482]. | Worm | — | — | — |
| 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 |
| daf-12 mutation | Mutations in daf-2 and daf-12, but not mutations in daf-12 alone, nearly quadruples lifespan [7789761]. Recessive loss of function mutation in daf-12 shortens lifespan. daf-12 activity is required for lifespan extension after germ line ablation [10360574]. daf-12 mutation suppresses the lifespan extension by mutation in daf-28 [8807293]. daf-12 mutants are dauer defective and heterochronic [7219552]. Some daf-12 alleles exhibit synthetic lethality with mutation of age-1 [8807293] or daf-12 [1732156]. | Worm | — | — | — |
| 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 | — | — |
| clk-3 mutation | Mutations in clk-3 slow down development and extend adult lifespan (at 20 degree Celsius in Bristol N2). clk-3 mutation slows growth and rhythms similiar to clk-1a and profounds maternal and zygotic rescue [8638122]. | Worm | — | — | — |
| 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 | — | — |
| 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 | — | — |
GenAge
GenDR
