daz-1 mutation | Mutation of daz-1 has no effect on lifespan [11799246]. daz-1 mutants are sterile and have a gonad that contains small nuclei and no oocytes [10662646]. Although sperm production is normal, oocytes precursors arrest at meiotic prophase and undergo apoptosis | Worm | — | — | — |
eat-10 mutation | The eat-10(ad606) allele exhibits no significant extension of lifespan [9789046], but displays defects in pharyngeal feeding behaviour [8462849]. | Worm | — | — | — |
eat-18 mutation | Mutations in eat-18 extend lifespan by 15-60%. Lifespan extension is proposed to be similar to DR [9789046]. eat-1 mutants have defects in pharyngeal feeding behavior [8462849]. | Worm | +15 to +60 | — | — |
eat-13 mutation | The eat-13(ad522) allele extends lifespan by 30%. Extension of lifespan is proposed to be similar to DR [9789046]. eat-1 mutants have defects in pharyngeal feeding behavior [8462849]. | Worm | +30 | — | — |
eat-3 mutation | The eat-3(ad426) allele extends lifespan by 10%. Lifespan extension is proposed to be similar to DR [9789046]. eat-1 mutants have defects in haryngeal feeding behavior [8462849]. | Worm | +10 | — | — |
eat-5 mutation | The eat-5(ad464) allele has no significant effect on lifespan [9789046], although it displays defects in pharyngeal feeding behaviour [8462849]. | Worm | — | — | — |
eat-6 mutation | Mutations in eat-6 extend lifespan by 15-40%. Lifespan extension is proposed to be similiar to DR [9789046]. eat-1 mutants have defects in haryngeal feeding behavior [8462849]. | Worm | +15 to +40 | — | — |
eat-7 mutation | The eat-7(ad450) allele decreases lifespan by 35% [9789046] exhibits defects in pharyngeal feeding behavior [8462849]. | Worm | -35 | — | — |
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 | — | — |
fem-3 mutation | fem-3(e1996) mutants do not produce sperm or self-progeny, therefore develop as females, but have a normal lifespan (See also ref 10) [8247153]. | Worm | — | — | — |
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 | — | — |
fog-1 mutation | The fog-1(q180) allele has no effect on lifespan [11799246]. fog-1 mutants are sterile and make oocytes but not sperm [2341035]. | Worm | — | — | — |
fog-2 mutation | fog-2(q71) allele has no effect on lifespan [10747056]. fog-2 mutant display hermaphrodite specific germ line feminization [11076749]. | 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 | — | — |
mec-1 mutation | Loss of function mutations in mec-1 do not effect lifespan [2428682]. mec-1 mutants are touch insenstive, lethargic, and have displacement of some microtubule cells and amphidial neurons as well as defective fasciculation [2428682]. | 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 | — | — | — |
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 | — | — | — |