| 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 | — | — |
| lars-2 mutation | A mutation that impairs mitochondrial function was associated with a longer lifespan. Mutation of lrs-2/lars-2(mg312) extends lifespan and is associated with impaired mitochondrial function. The recessive allele mg312 of lars-2 extends lifespan by 200% at 20 degree Celsius and 30% at 25 degree Celsius. Lifespan extension by mg312 was not dependent on daf-16(mgDf47). Homozygous lars-2(mg312) worms had multiple pleotropies like lower rates of growth, pumping and defecation as well as remain the size of early L4 worms and are sterile, with an arrested gonad that exhibited no germ-cell differentiation lars-2 is ubiquitously express, with prominent expression in body-wall muscle and neurons, with a mitochondrial subcellular localisation. Mitochondria of lars-2 are noticeably disorganized, swollen and sometimes fused. lars-2 animals have lower ATP content and oxygen consumption [12447374]. | Worm | +30 to +200 | — | — |
| 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 | — | — | — |
| 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 | — | — | — |
| 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 | — | — | — |
| 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 | — | — | — |
| 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-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-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-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 | — | — |
| 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 | — | — |
| 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 | — | — | — |
| 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 | — | — |
| 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 |
| 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 | — | — |
| 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 | — | — |
| unc-13 mutation | Mutation in unc-13 results in a 150% life-extension in males, but has no effect on hermaphrodite lifespan [10747056]. | Worm | +150 | — | — |
| unc-15 mutation | Mutation of unc-15 has no effect on lifespan [9789046].
Some alleles of un-15 display severe paralysis [4366476; 2051482]. | Worm | — | — | — |
| unc-2 mutation | Loss of function in unc-2 has no effect on lifespan [9789046].
unc-2 mutant is uncoordinated [4366476] and its rate of pharyngeal pumping is reduced [8325482]. | Worm | — | — | — |
| unc-20 mutation | Mutation in unc-20 has no effect on lifespan [9789046].
unc-20 mutant is uncoordinated [4366476]. | Worm | — | — | — |
| unc-25 mutation | Mutations in unc-25 have no effect on lifespan [9789046].
unc-25 mutants are defective for foraging, locomotion, and defecation [8332190] as well as uncoordinated [4366476]. | Worm | — | — | — |
| 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 | — | — |
| unc-29 mutation | Mutation in unc-29 has no effect on lifespan [9789046] and fails to extend male lifespan [10747056].
unc-29 mutants are uncoordinated [4366476]. | Worm | — | — | — |
| unc-30 mutation | Mutations in unc-30 have no significant effect on lifespan [9789046].
unc-30 mutants are uncoordinated [4366476]. | Worm | — | — | — |
| 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 | — | — |
GenAge
GenDR
