| Sirt1 knockout | Sirt1 knock-out mouse embryonic fibroblasts (MEFs) have a significant greater replicative capacity in culture. p19ARF levels are significantly reduced in Sirt1 knock-out MEFs [16054100].
Sirt1-null mice do not exhibit lifespan extension upon Dietary Restriction [18335035]. | Mouse | — | — | — |
| Homozygous GH1 deletion | Mean lifespan in untreated, affected individuals homozyogus for a deletion at the GH1 locus is significantly shorter (P < 0.05) than in affected siblings or the general population. Individuals homozygous for GH1 deletion demonstrate hereditary dwarfism [12915652]. | Human | — | — | — |
| tert knockout | First-generation tert(-/-) zebrafish die prematurely with shorter telomeres. tert(-/-) fish develop degenerative phenotypes, including premature infertility, gastrointestinal atrophy, and sarcopenia. tert(-/-) mutants have impaired cell proliferation, accumulation of DNA damage markers, and a p53 response leading to early apoptosis, followed by accumulation of senescence cells. Apoptosis is primarily observed in the proliferative niche and germ cells. Cell proliferation, but not apoptosis, is rescued in tp53(-/-)tert(-/-) mutants, underscoring p53 as mediator of telomerase deficiency and consequent telomere instability [http://denigma.de/url/3p]. | Zebra | — | — | — |
| Ilp2 mutation | Ilp2 null mutants are significant longer-lived with a 8-13% longer median lifespan [20195512]. | Fly | — | +8 to +13 | — |
| foxo mutation | foxo null mutants are highly and significantly shorter-lived than wild-type on all food dilutions apart from 0.1 SY and under starvation. foxo null mutants are not more sensitive to starvation than wild-type [18241326]. | Fly | — | — | — |
| Ilp3 mutation | Ilp3 null mutants have a normal lifespan under AL and a normal DR response. Ilp2 Ilp3 Ilp5 triple null mutants fail to have a normal response to DR. Their response is right shifted, with mutants being shorter-lived compared to wild-type on low but longer-lived on high yeast concentrations [20195512]. | Fly | — | — | — |
| Ilp5 mutation | Abundance of Ilp5 mRNA is reduced under DR. Ilp5 null mutants have a normal lifespan under AL and a normal DR response. Ilp2 Ilp3 Ilp5 triple null mutants fail to have a normal response to DR. Their response is right shifted, with mutants being shorter-lived compared to wild-type on low but longer-lived on high yeast concentrations [20195512]. | Fly | — | — | — |
| Scgdelta deletion | Deletion of Scgdelta has detrimental effects on the flight muscles of adult animals and heart function. Median lifespan is reduced 15-30% [17855453]. | Fly | — | -15 to -30 | — |
| Ilp2/Ilp3/Ilp5 mutation | Ilp5 null mutants have a normal lifespan under AL and a normal DR response. Ilp2 Ilp3 Ilp5 triple null mutants fail to have a normal response to DR. Their response is right shifted, with mutants being shorter-lived compared to wild-type on low but longer-lived on high yeast concentrations [20195512]. | Fly | — | — | — |
| SNF4Agamma deletion | Deletion of SNF4Agamma from the first day of the imaginal stage shortens mean lifespan by 23% and causes morphological and behavioural features of premature aging [18219227]. | Fly | -23 | — | — |
| rsks-1 mutation | rsks-1 deletion mutants also live longer. TOR RNA interference further extends lifespan of rsks-1 mutants [17266679]. | Worm | — | — | — |
| shc-1 knockout | Loss of shc-1 function results in accelerated aging and enhanced senstivity ro heat, oxidative stress and heavy metals. | Worm | — | — | — |
| mdt-15 mutation | mdt-15(tm2182) mutation does not affect lifespan on ad libitum, but further increases the lifespan when combined with DR (starting at the 4th day of adulthood) even more as wild-type [22132200]. | Worm | — | — | — |
| slcf-1 mutation | slcf-1 mutation increases average lifespan by 40%. DR (by dilution of bacteria on solid medium or by bacterial deprivation) failes to extend slcf-1 mutant's long lifespan and lifespan is even reduced by lowering bacteria concentration (i.e. higher strength of DR) [21040400]. | Worm | +40 | — | — |
| nlp-7 mutation | Lifespan of nlp-7 mutants increases only moderately by sDR [19783783]. | Worm | — | — | — |
| ctbp-1 mutation | Genetic inactivation of ctbp-1 results in lifespan extension dependent on daf-16, but independent of sir-2.1. RNAi of lips-7(C09E8.2) suppresses lifespan extension by ctbp-1 inactivation [19164523]. | 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 | — | — |
| 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 | — | — | — |
| 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 | — | — |
| 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 | — | — | — |
| unc-76 mutation | unc-76(e911) allele extends male lifespan by about 50%, but has no effect on hermaphrodite lifespan [10747056].
unc-76 mutants are uncoordinated [4366476]. | Worm | +50 | — | — |
GenAge
GenDR
