| spe-10 | defective SPErmatogenesis family member (spe-10) | Mutation of spe-10 results in a 20% increase in mean lifespan on solid media [2744235].
spe-10 mutants have a temperature sensitive defect in sperm development and their lifespan correlates with thermoterance and UV resistance [2744235]. | Nematode |
| SAG101 | senescence-associated protein 101 | Antisense RNA interference of SAG101 in transgenic plants delays the onset of leaf senescence for approximately 4 days, whereas chemical induced overexpression of SAG101 causes precocious senescence in both attached and detached leaves of transgenic plants [11971136]. | — |
| rad-8 | RADiation sensitivity abnormal/yeast RAD-related 8 | Mutation of rad-8 increases lifespan by approximately 30% at 16 degree Celsius but not at 20 degree Celsius [8169328]
rad-8 mutants are hypersensitive to UV radiation, but not X-rays or MMS [7152245] | Nematode |
| PLD alpha | — | Antisense suppression of PLD alpha retards abscisic acid- and ethylene-induced senescence. Leaves detached from PLD alpha-deficient transgenic plants when inbutated in abscisic acid and ethylene exhibit a slower rate of senescence that those from wild-type and transgenic controls. PLD alpha deficient strains are associated with retardation of senescence as evidenced by delayed leaf yellowing, lower ion leakage, greater photosynthetic activity, and higher content of cholorophyl and phospholipids [9437863].
Antisense suppression of PLD alpha does not affect natural plant growth and development [9437863]. | — |
| MORF4 | mortality factor 4 | Overexpression of MORF4 reverses the immortal phenotype of immortal cell lines in complementation group B [9891081]. Cellular senescence is dominant over immortality in fused hybrids of normal and immortal human cell in culture [6879195]. Fusion of immortal cell lines with each other led to the idenetification of four complementation groups for immortality [3413074]. MORF4 rescues the immortal phenotype [9891081]. | Human |
| LMNA | lamin A/C | Dominant mutation in LMNA (lamin A/C) gene cause Hutchinson-Gilford progeria syndrome (HGPS) which is rare and characterized by prematurly senile appearing skin and hair, with death from coronary artery disease often by age 10 [Gilford 1904; Hutchinson 1886; OMIM]. The median age of death in HGPS individuals is 13.4 years. A C to T transition at nucleotide 1824 is associated with HGPS [Sandra-Giovannoli et al., 2003; Eriksson et al., 2003]. The 1824C-T allele appears to act in a dominant negative manner by interfering with normal splicing, resulting in production of both the normal transcript and a transcript deleted for 150 bp at the 3' end [Sandre-Giovannoli et al, 2003]. Cultured skin fibroblasts from individuals with progeria exhibit an increased fraction of hat-labile proteins [1128606].
Gilford (1904). Ateleiosis and progeria: continuous youth and premature old age. Brit Med J 2, 914-918.
Hutchinson, J. (1886). Case of congenital absence of hair, with atrophic condition of the skin and its appendages, in a boy whose mother had been almost wholly bald from alopecia areata from the age of six. Lancet 1, 923.LMNA was found to be associated with longevity [22340368]. LMNA was found to be associated with longevity [22340368]. LMNA was found to be associated with longevity [22279548]. LMNA was found to be associated with longevity [24244950]. | Human |
| MAPT | microtubule-associated protein tau | Expression of wild-type human MAPT (tau) moderately shortened lifespan. Expression of a mutant form of human MAPT (Arg406 Trp), associated with an early onset familial form of demetia, results in a several shortened lifespan. MAPT is implicated in the pathogenesis of Alzeimer's disease and related disorders in humans. Transgenic flies exhibit key features of the human disorders: adult onset, progressive neurodegeneration, early death, enhanced toxicity of mutant tau, accumulation of abnormal tau, and relative anatomic selectivity. However, neurodegeneration occurred without the neurofibrillary formation that is observed in humans disease and some rodent taupathy models [11408621]. | Human |
| AFUA_1G13190 | copper-activated transcription factor GRISEA | In Grisea (AFUA_1G13190) loss of function mutants, senescence is delayed two-fold [8804410].
Grisea disruption extends mean and maximum lifespan by 195 and 210% [17173038].
Grisea mutant has altered norphology and defects in formation of female gametangia [9380708]. | Podospora anserine |
| Gh1 | growth hormone 1 | Animals carrying a single copy of an anti-sense Gh1 transgene (tg/-) live on average 7-10% longer. However, animals carrying two copies of the transgene (tg/tg) have a slighlty shorter lifespan compared to -/- animals, indicating that an optimal dosage of Gh1 is nessary to achieve lifespan exentension and too little GH has a detrimental effect on longevity. tg/tg and tg/- animals are dwarfs and exhibit reduced levels of serum IGF1 [12057928]. | Norway rat |
| gcy-18 | Guanylyl CYclase 18 | RNAi of gcy-18 increases mean lifespan by 25%. gcy-18 expression is repressed by daf-2 RNAi, but induced by combined RNAi of daf-16 and daf-2 [12845331]. | Nematode |
| iftb-1 | eIFTwoBeta (eIF2beta translation initiation factor) | RNAi knockdown of iftb-1 at 25.5 degree Celsius continuously extends mean and maximum lifespan by 13 and 11%, while knockdown only during the adulthood extends mean and maximum lifespan by 16 and 6% [16720740]. RNA interference if iftb-1 in adulthood increases maximum lifespan by about 30% [17266679]. | Nematode |
| daf-10 | abnormal DAuer Formation 10 | 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]. | Nematode |
| CPR7 | Cyclosporin-sensitive Proline Rotamase 7 | Deletion of CPR7 has no effect on lifespan replicative lifespan, but increases chronological lifespan [11361336] | Budding yeast |
| COX5 | — | 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]. | Podospora anserine |
| insc | inscuteable | insc disruption through an insertion of the P{EPgy2} vector in ts structural part prolongs female lifespan. Heterozygous esg and insc double mutants interact in the course of lifespan determination. The decrease of esg transcription is associated with lifespan increase in mutant esg and insc flies [22661237]. | Fruit fly |
| esg | Escargot | Disruption of esg by insertion of the P{GT1} vector 300 bp downstream of its structural part increases male and female lifespan. Heterozygous esg and insc double mutants interact in the course of lifespan determination. The decrease of esg transcription is associated with lifespan increase in mutant esg and insc flies [22661237]. | Fruit fly |
| aPKC | atypical protein kinase C | Insertion of a P-based vectors in the structural part of aPKC increase male and female lifespan [22661237]. | Fruit fly |
| ctbp-1 | CTBP (CtBP) transcriptional co-repressor homolog | 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]. | Nematode |
| Dgat1 | Diacylglycerol O-acyltransferase 1 | Deficiency in Dagat1 promotes leanless and extends mean, median and oldest 10% survival by 23, 26 and 9% without limiting food intake [22291164]. | House mouse |
| CG5389 | — | RNAi of complex V subunit CG5389 results in increased mean longevity under standard laboratory food conditions (3% yeast) in males. RNAi started from the development results in a mild lifespan increase in both sexes (3-11% in females and 3-8% in males). Post-developmental RNAi and silencing limited to neurons has variable effects with reduction in lifespan of up to 9% [19747824]. Under rich media conditions CG5389 knockdown throughout development and adulthood increases mean lifespan by 26% and abolished the lifespan extension by DR (started in the adulthood) in males. Suppression of CG5389 only during the adulthood either via RNAi by tub-GS or via oligomycin (a specific inhibitor of complex V) feeding prevents an increase in longevity under DR (started in the adulthood) in males [19968629]. | Fruit fly |
| shc-1 | SHC (Src Homology domain C-terminal) adaptor homolog | Loss of shc-1 function results in accelerated aging and enhanced senstivity ro heat, oxidative stress and heavy metals. | Nematode |
| CKB2 | Casein Kinase Beta' subunit | Lack of Ckb2 promotes a modest but significant chronological lifespan extension and marked increase in yeat resistance [20657825]. | Budding yeast |
| Prkar2b | protein kinase, cAMP dependent regulatory, type II beta | Loss of function of Prkar2b results in mice that are lean and insulin sensitive. Both median and maximum lifespan is increased by 14%. Median lifespan is increasesd (from 884 to 1005) and 80% lifespan increased from 941 to 1073 days. There is no difference either in median or 80% lifespan in female genotypes [19536287]. | House mouse |
| tag-322 | Temporarily Assigned Gene name | tag-322 RNAi increases mean and maximum lifespan by 18 and 12%, respectively [19293945]. | Nematode |
| F13G3.10 | — | RNAi of F13G3.10 extends mean and maximum lifespan by 11 and 14%, respectively [19293945]. | Nematode |
