| Cdk5 mutation | Cdk5 loss-of-function mutations result in defective axon guidance, age-dependent behavioral deficits and reduced lifespan by about one third [17368005]. | Fly | — | — | — |
| cert mutation | CG7207 mutants exhibit a shortened lifespan accompanied by enhanced oxidative damage to cellular proteins and metabolic compromise, such as increasing glucose levels, reminiscent of premature aging [17592126]. | Fly | — | — | — |
| Constitutive miR-277 expression | Constitutive miR-277 expression shortens lifespan and synthetically lethal with reduced insulin signaling, indicating that metabolic control underlies this phenotype [23669073]. | Fly | — | — | — |
| D-chiro-inositol supplementation | D-chiro-inositol supplementation to the diet extends adult longevity in both male and female animals. 20 microMolar dose of D-chiro-inositol extends median lifespan by 16.7 (p < 0.001) for males and 13% (p < 0.001) for females. Lifespan extension by D-chrio-inositol is accompanied by protection against oxidative and starvation stresses, improvement in health span, and not reduction in fecundity. Nuclear localization of foxo increases in D-chiro-inositol-fed animals [22843669].
| Fly | — | +13 to +16.7 | — |
| Sir2 RNAi | Decreased expression of Sir2 and Sir2-like genes in all cells causes lethality during development. Suppression of the Sir2 in neurons decreases the median lifespan by 10-30%, while ubiquitous silencing of the Sir2-like genes shortens lifespan. The effects are server at 28°C that at 25°C [17159295]. | Fly | — | -10 to -30 | — |
| Sirt2 RNAi | Decreased expression of Sirt2 by RNA interference causes lethality during development. Silencing in neurons shortened mean lifespan by 20% [17159295]. | Fly | -20 | — | — |
| Sirt6 RNAi | Decreased expression of Sirt6 by RNA interference causes lethality during development. Sirt6 silencing in neurons shortens mean lifespan by 20% [17159295]. | Fly | -20 | — | — |
| 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 | — |
| 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 | — | — |
| DHEA treatment | DHEA treatment increases the lifespan of female fruit flies [Li et al., 2000]. | Fly | — | — | — |
| Dietary restriction by 1% yeast medium | Dietary restriction by be reducing yeast content in medium to 1% extends the lifespan [19968629]. | Fly | — | — | — |
| esg transposition | Disruption of esg by insertion of the P{GT1} vector 300 bp downstream of its structural part increases male and female lifespan [22661237]. | Fly | — | — | — |
| DLP mutation | DLP mutants have a 20% shorter mean lifespan and reduced female fertility [17933869]. | Fly | -20 | — | — |
| Prx5 mutation | dprx5(-/-) null mutants are comparatively more susceptible to oxidative stress, have higher incidence of apoptosis, and a shortened mean lifespan, but thee is no significant difference in maximum lifespan (10% survival) [21826223]. | Fly | — | — | — |
| dys RNAi | dys RNAi-mediated knockdown in the mesoderm shortens lifespan [18221418]. | Fly | — | — | — |
| elav mutation | elav mutation significantly decreases the lifespan. Median lifespan in males is 66% lower [20589912]. | Fly | — | — | — |
| Atg8a overexpression | Enhanced expression of Atg8a in older fly brains extends average adult lifespan by 56% and promotes resistance to oxidative stress [18059160]. | Fly | +56 | — | — |
| Dominant negative Tor | Expression of a dominant-negative form of Tor extends lifespan [15186745]. Ubiquitious overexpression of dTOR with the da-GAL4 driver of UAS-dTOR(FRB) which contains the 11kDA FKB12-rapamycin binding domain led to a mean and maximum lifespan increase of 15% (24%) and 29% at 29°C and of 50% (26%) and 13% at 25°C, respectively [15186745].
Overexpression of the dominant-negative form of Tor specifically in the fat and muscle tissues is sufficient to extend the mean and maximum lifespan by 24 and 19%, respectively [15186745].
Overexpression of UAS-dTOR(WT) or UAS-dTOR(TED) prevents eclosion to adulthood [15186745]. | Fly | +15 to +50 | +13 to +29 | — |
| p53 dominant negative overexpression | Expression of dominant-negative versions of p53 in adult neurons extends lifespan by 58% in females and by 32% in males and increases resistance to genotoxic stress and resistance to oxidative stress, but not to starvation or heat stress, while not affecting egg production or physical activity. Dominant negative Dmp53 expression cancels out lifespan extension effect of DR, low calorie-food (5% SY). Muscle or fat body specific expression of a dominant negative form of Dmp53 as well as globally lack of Dmp53 decreases lifespan [16303568].
Expression of dominant-negative (DN) form of p53 in adult neurons, but not in muscle or fat body cells, extends median lifespan by 19% and maximum lifespan by 8%. The lifespan of dietary-restricted flies is not further extended by simultaneously expressing DN-DMp53 in the nervous system, indicating that a decrease in Dmp53 activity may be part of the DR lifespan-extending effect. Selective expression of DN-Dmp53 in only the 14 insulin-producing cell (IPCs) in the brain extends lifespan to the same extent as expression in all neurons and this lifespan extension is not additive with DR [17686972].
| Fly | +32 to +58 | +19 | +8 |
| MAPT overexpression | 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]. | Fly | — | — | — |
| Lazarillo supplementation | Extracellular forms of Laz have autocrine and paracrine protecting effects for oxidative stress-challanged Drosophila S2 cells. Local effects of GPI-linked Laz inside and outside the nervous system promote survival upon different stress forms, and extend lifespan and healthspan of the flies in a cell-type dependent manner. Ectopic enhancement of Laz expression increases mean, median, and maximum lifespan. Laz overexpression (via the use of a ubiquitous da-GAL4 driver) increases median lifepan by 28.3% (p < 0.0005). Overexpression of Laz specifically in muscles and brain (via GAL4109(2)80 driver) increases median lifespan by 43.5%. Laz overxpression in dopaminergic and serotenergic neurons and epidermis increases median lifespan bt 31.4% (p < 0.0005) [22846641]. | Fly | — | +28.3 to +43.5 | — |
| L744832 treatment | Farnesyl inhibitor L744832 increases lifespan [22737247]. | Fly | — | — | — |
| Fat-body specific Akh knockdown | Fat-body specific Akh RNAi results in increased spontaneous activity and a small but significant increase in lifespan upon AL [22768842].
| Fly | — | — | — |
| mld heterozygous mutation | Female, but not male, heterozygous mutants display a 42% increase in mean lifespan at 29 degrees Celsius. DTS-3 +/- female adults exhibit a 50% reduced ecdysone titer and reduced fertility [12610309]. Female, but not male, heterozygoutes also exhibit a temperature-dependent increase in starvation resistance. | Fly | +42 | — | — |
| l(3)DTS3 mutation | Female, but not male, heterozygous mutants exhibit a 42% increase in mean lifespan [12610309]. | Fly | +42 | — | — |
GenAge
GenDR
