| FAR11 deletion | Deletion of FAR11 significantly reduces mean chronological lifespan under starvation/extreme DR relatively to wild-type [20657825]. | Yeast | — | — | — |
| PPG1 deletion | PPG1 deletion reduces significantly mean chronological lifespan under starvation/extreme DR [20657825]. | Yeast | — | — | — |
| BUL1 deletion | Deletion of BUL1 does non-significantly reduces mean chronological lifespan under starvation/extreme DR [20657825]. | Yeast | — | — | — |
| PAN2 deletion | Deletion mutant of PAN2 live approximately as long as wild-type under starvation/extreme DR [20657825]. | Yeast | — | — | — |
| shc-1 knockout | Loss of shc-1 function results in accelerated aging and enhanced senstivity ro heat, oxidative stress and heavy metals. | Worm | — | — | — |
| 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 | — | — | — |
| Heterzygous Rpd3 null mutation | Males heterozygous for a null mutation of Rpd3 have a lifespan extension of 41 - 47%. Females carrying a null mutation have only modest increase in maximum lifespan (but not median lifespan). Longevity increases to the same extent in wild-type under low-calorie diet and rpd3 mutants fed normal diet. DR fails to further increase lifespan of rpd3 mutants [12459580]. | Fly | +41 to +47 | — | — |
| Bmcp knockout | Bmcp knockout flies live longer on low-calorie diets, have a decreased fertility, and gain less weight on high-calorie diets. Bmcp (ucp5) knockout mutants live longer than wild-type on low-calorie diets, but no longer on starvation or high-calorie diets. Ectopic neuronal expression of Bmcp transgene rescues starvation sensitive phenotype of Bmcp knockout mutants [16387864]. | Fly | — | — | — |
| 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 | — | — | — |
| unc-51 mutation | unc-51(e369) mutation reduces mean but extends maximum lifespan. unc-51(e369) mutation reduces lifespan of eat-2(ad1116) mutants to that of wild-type [18219227]. | 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 | — | — | — |
| Cisd2 knockout | Cisd2 knockout shortens lifespan resulting in premature aging [19451219]. | Mouse | — | — | — |
| sgg transposition | Several insertions of P-based vectors in the structural part of sgg are associated with alterations of male and female lifespan [22661237]. | Fly | — | — | — |
| ife-2 mutation | Loss-of-function mutation in ife-2 reduces protein synthesis and increases maximum lifespan by about 20%. It does not extend the lifespan of daf-16(RNAi) animals. TOR/let-373 RNA interference further extends lifespan of ife-2 mutants. Reduction of protein synthesis increases ATP availability and stress resistance [17266679]. | Worm | — | — | +20 |
| BCY1 deletion | Disruption in BCY1 by mutation results decreases mean and maximum replicative lifespan by 37 and 16% and is associated with increased PKA activity [8195187]. | Yeast | -37 | — | -16 |
| BRE5 deletion | Deletion of BRE5 increases mean replicative lifespan by 30% [16293764] and mean chronological lifespan in diploid cells [21447998] | Yeast | +30 | — | — |
| CCR4 deletion | Deletion of CCR4 increases mean chronological lifespan by 20 - 41% (20, 33, 41) in diploid cells [21447998]. In W303R CCR4 deletion shortens replicative lifespan by approximately 80% and results in temperature sensitivity that is suppressed by SSD1-V. SSD1-V partially suppresses the short-lifespan of ccr4 mutant. CCR4 mutation is synthetically lethal in combination with deletion of MPT5 in the absence of SSD1-V [11805047]. | Yeast | -80 to +20 | — | — |
| HPR1 deletion | Deletion of HPR1 decreases replicative lifespan [11756539] | Yeast | — | — | — |
| 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 | — | — | — |
GenAge
GenDR
