| CDC6 mutation | The CDC6-1 conditional allele results in an approximately 20% increase in mean replicative life span. This allele is defective for replicative initiation form the rDNA ARS at 27 degree Celsius, resulting in a reduced rate of extrachromosomal rDNA circle accumulation [9428525]. The cdc6-1 allele results in genomic instability at the permissive temperature [8552037]. | Yeast | +20 | — | — |
| HPR1 deletion | Deletion of HPR1 decreases replicative lifespan [11756539] | Yeast | — | — | — |
| Transient CDC7 inactivation | Transient inactivation of CDC7 results in a shortened replicative lifespan [2698814]. | Yeast | — | — | — |
| ced-3 mutation | The ced-3(n1286) allele has no effect on lifespan, although the transgenic animals are defective in apoptosis [12136014]. | Worm | — | — | — |
| 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 | — | — |
| 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-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 | — | — |
| CIT2 deletion | Deletion of CIT2 has no effect on replicative lifespan [10224252]. | Yeast | — | — | — |
| ERCC8 mutation | Individuals with a mutation in ERCC8 (alias CKN1) have a shortened lifespan, short stature, precociously senile appearance, retinal degeneration, optic atrophy, sensitivity to sunlight, and mental retardation [14156156]. Hypertension and renal disease are also common in ERCC8 mutants [514720]. | Human | — | — | — |
| clk-2 mutation | Mutations in clk-2 slow down development and extend lifespan by 12-25% (at 20 degree Celsius in Bristol N2). clk-2 mutation slows growth and rhythms similar to clk-1. Mutation in clk-2 is embryonic lethal at 25 degree Celsius and results in some lethality at all temperatures [8638122]. clk-2 encodes a protein involved in DNA repair and perhaps telomere maintenance [14-16 in (Lee et al., 2003)]. clk-2 mutation affects telomere length and might result in shorter [11696330] or longer telomeres [11747819]. clk-2 overexpression may shorten telomeres [11747819]. | Worm | — | — | — |
| 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 | — | — | — |
| COQ3 deletion | Deletion of COQ3 decreases chronological lifespan and renders cells respiratory deficient and sensitive to hydrogen peroxide [12586694]. | Yeast | — | — | — |
| COX1 deletion | Deletion of mobile group II intron (intron alpha) from COX1 doubles lifespan and prevents accumulation of senescence-associated DNA concatemer corresponding to this of the mitochondrial genome [10330149]. Deletion encompassing COX1's intron alpha and its upstream exon abolishes the senescence process entirely [2999848]. | | — | — | — |
| COX5 deletion | Disruption of the nuclear COX5 gene delays senescence, increase longevity between 7- and 15-fold (in 30 tested isolates) and the onset of senescence is not associated by accumulation of senescence-specific mtDNA molecules. COX5 deletion results in exclusive use of the alternative respiratory pathway and a decrease in production of reactive oxygen species and the prevention of the accumulation of several senescence-specific mitochondrial DNA molecules [10759557]. | | — | — | — |
| CPR7 deletion | Deletion of CPR7 has no effect on lifespan replicative lifespan, but increases chronological lifespan [11361336] | Yeast | — | — | — |
| CTF4 deletion | Deletion of CTF4 results in an approximately 75% reduced mean replicative lifespan [12024027]. | Yeast | — | — | — |
| CYT1 deletion | Deletion of CYT1 increases replicative lifespan by 15% in the alpha strain and decreases replicative lifespan by 20% in a strain. Deletion of CYT1 decreases replicative lifespan and cancels out replicative lifespan extension by HAP4 overexpression. Initially, it was shown that deletion of CYT1 also prevents lifespan extension by 0.5% glucose restriction [12124627], but later it was shown that either 0.5 or 0.05 % glucose restriction increases replicative lifespan of cyt1Delta cells [16311627]. | Yeast | — | — | — |
| 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 | — | — |
| Prop1 knockout | Knockouts of Prop1 are dwarf (hence called the Ames dwarf mice) but live approximately 1 year longer than controls. Mean lifespan of males and females is extended by 49 and 68%, respectively Ames dwarf mice are small due to retarded post-natal growth and have primary pituitary deficiency consisting of the absence of, or extreme reduction in, anterior pituitary cells which produces growth hormone, prolactin and thyroid-stimulating hormone, and consequently a deficiency in these hormones. Levels of IGF1 is also extreme low in Ames dwarf mice [8900272]. | Mouse | +49 to +68 | — | — |
| 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-15 mutation | Mutations in daf-15 (raptor) extends adult lifespan by 15-30% in a daf-16 dependent manner. daf-15 mutation are dauer defective [15253933]. | Worm | +15 to +30 | — | — |
| 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 | — | — | — |
| 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-28 mutation | Semi-dominant mutation in daf-28 increases lifespan by 10-15% [8807293]. The daf-28 mutant is dauer constitutive [8005442]. | — | +10 to +15 | — | — |
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