| 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 | — | — | — |
| 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-1 mutation | daf-1(mk40) mutation increases mean lifespan by 18-46% and maximum lifespan by 29% [17900898]. The daf-1(m40) allele has no effect on lifespan and fails to prevent lifespan extension by sir-2.1 overexpression, but it results in a temperautre-sensitive, dauer-constitutive phenotype in larvae [11242085]. | Worm | +18 to +46 | — | +29 |
| 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 | — | — | — |
| 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-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 | — | — |
| 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 | — | — |
| cco-1 RNAi | RNA interference of cco-1 results in a 45-61% increase in mean lifespan (in fer-15; fem-1 and N2 background, respectively) [16103914]. RNAi against cco-1 increases mean and maximum lifespan by 73% and 90%, respectively [12471266]. cco-1 RNAi extends mean and maximum lifespan by 41 and 50%. RNAi of cco-1 during the larval stages is necessary and sufficient for increased lifespan, while only during the adulthood it fails to to extend lifespan. cco-1 RNAi results in reduced pharyngeal pumping, defecation, motility, and body size as well as reduced ATP levels (by 60-80%) and oxygen consumption. daf-16 mutation fails to prevent lifespan extenison by RNAi of cco-1 and mutation of daf-2 further extends the lifespan of cco-1 RNAi animals [12447374]. RNAi of cco-1 only during the adulthood increases mean and 75th %ile lifespan by 22-32 and 16-33%, respectively [22560223]. | Worm | +22 to +73 | — | +50 to +90 |
| FOB1 deletion | Mutation in FOB1 extends replicative lifespan by 30-50% [10230397]. FOB1 mutation increases replicative lifespan by 25% in the alpha strain and by 10% in a strain [19030232]. FOB1 mutant exhibit an about 20% mean replicative lifespan increase [15722108]. Deletion of FOB1 causes extension in the short life span of the sir2 mutant by around 50% [10521401]. Mutation of the FOB1 gene slows the generation of rDNA circles and thus extends life span by approximately 30% in W303 and 50% in K2307 [10230397]. Even in cells lacking both Sir2 and Fob1, nicotinamide prevents the lifespan extension by DR [16311627]. | Yeast | — | — | — |
| GAL83 deletion | Deletion of GAL83 has no effect on replicative lifespan in S228C [10921902] and general GAL83 mutants have no obvious phenotype [10990457]. | Yeast | — | — | — |
| Ghr knockout | Ghr knockouts (the so called Laron mice) are dwarfs with significantly extended lifespan by 40-50% [12933651]. Ghr-/- mice are significantly longer lived as Ghr+/+ or Ghr+/- mice (by 40-50%) in both females and males [10875265; 19370397]. 30% DR fails to affect overall survival, average or median long-lifespan of Growth hormone receptor knockout (GHRKO) mice and increased maximal lifespan only in females. Insulin sensitivity in GHRKO mutants is greater than in wild-type and is not further increased by DR [16682650]. Intermittent fasting also fails to extend the long lifespan of GHRKO mice [19747233].
Lifespan of mice with a deletion in the Ghr gene live almost 5 years [21123740]. In C57BL/6J this mutation increases life expectancy by 16 to 26% depending on gender [12933651] and in mice of mixed genetic background the increases amounted to 36-55% [9371826]. Serum levels of GH are elevated in mutant mice [9371826] and mutants are smaller than wild-type. IGF-1 and IGFBP-3 levels are also reduced in Ghr mutant mice [10875265]. The age-associated decline in memory retention is delayed in Ghr mutants [11336996]. | Mouse | +16 to +55 | — | — |
| Ghrhr knockout | Homozygosity for the Ghrhr(lit) knockout mutation (called little mouse) lowers plasma growth hormone levels, impairs growth and increases lonegevity about 20% [11371619]. Lit homozygous animals are smaller than normal mice [1270792] and their pituitary is defective in growth hormone and prolactin [978118]. | Mouse | +20 | — | — |
| GPD1 deletion | GPD1 deletion shortens replicative lifespan by 25% and prevents lifespan extension by high osmolarity [12391171]. | Yeast | +25 | — | — |
| 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 | — | — |
| HAP5 deletion | Deletion of HAP5 shortens replicative lifespan by approximately 40%. This is not a premature aging phenotype as "old" HAP5 cells do not become premature sterile or exhibit other biomarkers of yeast aging [9271578]. HAP5 null mutants are unable to grow on a non-fermentable carbon source [7828851]. | Yeast | -40 | — | — |
| HDA1 deletion | Deletion of HDA1 has no effect on longevity under AL, but acts synergistically with 0.1% glucose restriction to increase replicative lifespan [12213553]. Deletion of HDA1 leads to a slightly increased chronological lifespan [19801973]. Deletion of HDA1 has no effect on the wild-type lifespan in the short-lifespan of YSK771 strain, but suppresses the short-lifespan of SIR3 mutants [10512855]. Null mutation results in increased telomeric silencing and increased histone acetylation [8962081]. | Yeast | — | — | — |
| YKU70 deletion | Deletion fo YKU70 shortens lifespan, but does not accelerate the normal aging process [10521401]. YKU70 null mutants are defective for non-homologous end-joining [8754818] and for telomeric silencing [9635192]. | Yeast | — | — | — |
| YKU80 deletion | Deletion of YKU80 shortens replicative lifespan, but does not accelerate the normal aging process [10521401]. YKU80 null mutant is defective for non-homologous end-joining [8754818] and for telomere silincing [9501103; 9635192] | Yeast | — | — | — |
GenAge
GenDR
