|Dinitrophenol ||Lowering the mitochondrial membrane potential with the uncoupler dinitrophenol increases replicative lifespan . ||— ||— ||— ||— |
|Spermidine ||Administration of spermidine extends lifespan of yeast, flies and worms and human immune cells. In yeast spermidine treatment triggers deacetylation of H3 through inhibition of histone acetylatranserfases, suppresses oxidative stress and necrosis. Altered acetylation of the chromatin results in upregulation of various autophagy-related genes and triggers autophagy . ||— ||— ||— ||— |
|Mitochondrial back-signaling ||Induction of the mitochondrial back-signaling by deletion of AFO1 increases replicative lifespan . ||— ||+60 ||— ||+40 |
|— ||— ||— ||— ||— ||— |
|his-5 RNAi ||Knockdown of his-5 via RNAi started after the animal reached the late L4 stage increase or decreases lifespan by 2 and 3%, respectively . ||— ||— ||— ||— |
|kat-1 RNAi ||Knockdown of kat-1 via RNAi started after the animal reached the late L4 stage has no significant effect on mean lifespan . ||— ||— ||— ||— |
|Sirt1 overexpression ||Sirt1 overexpression mimicks the effect on reservatrol on mitochondrial function, but failed to extend lifespan . ||— ||— ||— ||— |
|Inhibition of TOR signaling ||Inhibition of TOR signaling increases lifespan [Bjedov et al., Harrison et al., 2009; Kapahi et al., 2010; Kenyon, 2010; Selman et al., 2009; Stanfel et al., 2009 in (Robida-Stubbs et al., 2012)]. ||— ||— ||— ||— |
|CG11015 RNAi ||Under rich nutritional conditions lifespan of CG11015 RNAi treated animals is indistinguishable from that of controls, while upon DR, lifespan extension is diminished in males and females . ||— ||— ||— ||— |
|Dgat1 knockout ||Deficiency in Dagat1 promotes leanless and extends mean, median and oldest 10% survival by 23, 26 and 9% without limiting food intake . ||— ||+23 ||+26 ||— |
|Overexpression of Cat and Sod1 ||Simultaneous overexpression of catalase and Sod1 results in a one-third (i.e. 30%) lifespan extension, a slower rate of mortality acceleration, and a delayed loss in physical performance, but neither has any effect on lifespan alone . ||— ||+30 ||— ||— |
|daf-28 mutation ||Semi-dominant mutation in daf-28 increases lifespan by 10-15% . The daf-28 mutant is dauer constitutive . ||— ||+10 to +15 ||— ||— |
|fog-3 mutation ||The fog-3(q470) allele has no effect on lifespan . In fog-3 mutant animals cells that would normally become sperm differentiate into oocytes . ||— ||— ||— ||— |
|FPS1S overexpression ||Plants overexpressing FPS1S exhibit a cell death/senescence-like phenotype and grw vigorously than wild-type . In plants with increased FPS activity, the expression of senescence activated gene SAG12 is prematurely induced. ||— ||— ||— ||— |
|SIR2RP1 overexpression ||Overexpression of SIR2RP1 (alias LmSIR2) results in a significant increase in survival of the vertebrate stage under normla axenic culture conditions, but has no effect on survival of the insect stage of the parasite. SIR2RP1 is mainly localized within the cytoplasm . ||— ||— ||— ||— |
|PLD alpha antisense ||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 .
Antisense suppression of PLD alpha does not affect natural plant growth and development . ||— ||— ||— ||— |
|rad-8 mutation ||Mutation of rad-8 increases lifespan by approximately 30% at 16 degree Celsius but not at 20 degree Celsius 
rad-8 mutants are hypersensitive to UV radiation, but not X-rays or MMS  ||— ||— ||— ||— |
|RAD51 deletion ||Rad51 mutations result in a 40% reduced mean replicative lifespan in strain PSY316 . RAD51 is required for gene conversion, but not for repair of an HO-induced double-stranded break . RAD51 deletion decreases formation of extrachromosomal rDNA circles . ||— ||-40 ||— ||— |
|RIF deletion ||Deletion of RIF1 decrease replicative lifespan by 40% . RIF1 deletion increases telomere silencing and length [8319907; 1577274], and therefore likely recruits SIR2 from rDNA to the telomeres which result in lifespan shortening. The sir4-42 allele suppresses the short lifespan of a RIF1 mutant . ||— ||-40 ||— ||— |
|SGS101 antisense RNAi ||Antisense RNA interference of SAG101 in transgenic plants delays the onset of leaf senescence for approximately 4 days . ||— ||— ||— ||— |
|SGS101 chemical induced overexpression ||Chemical induced overexpression of SAG101 causes precocious senescence in both attached and detached leaves of transgenic plants . ||— ||— ||— ||— |
|SIP2 deletion ||Deletion of the N-myristoylprotein SIP2 results in reduced resistance to nutrient deprivation and a 60% shorter lifespan accompanied by signs of accelerated aging such as loss of silencing from telomeres and mating loci, redistribution of Sir3 to the nucleolus, progressive sterility, nucleolar fragmentation and enlargement, and accumulation of extrachromosomal rDNA .
SIP2 deletion increases replicative lifespan by 20% in the alpha strain .
SIP1 null mutation causes increase in the intracellular ATP and NAD+ levels in both young cells (generation 0-1) and older cells (generation 4), but the increase is greater in older cells . ||— ||-60 to +20 ||— ||— |
|unc-49 mutation ||The unc-49(e382) allele has no significant effect on lifespan .
unc-49 mutants are uncoordinated . ||— ||— ||— ||— |
|WRKY6 deletion ||Deletion of the WRKY6 promoter results in defects in root and leaf cell senescence . ||— ||— ||— ||— |
|C33H5.18 RNAi ||RNA interference of C33H5.18 decreases median lifespan by 44% in wild type animals, 77% in a daf-2 background and 14% in daf-2/daf-16 double mutants . ||— ||— ||-44 ||— |