|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 . ||— ||— ||— ||— |
|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 ||— |
|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 . ||— ||— ||— ||— |
|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 ||— ||— |
|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 ||— |
|YUH1 deletion ||Deletion of YUH1 decreases replicative lifespan decreased 30% in the alpha strain . ||— ||-30 ||— ||— |
|ERCC1 and ERCC4 deficieny ||ERCC1-ERCC4-deficient mice exhibit signs of premature aging . ||— ||— ||— ||— |
|Fxn disruption ||Disruption results in reduced lifespan, increased oxidative stress, impaired respiration, and the development of hepatic tumors . ||— ||— ||— ||— |
|kermit disruption ||The disruption of kermit (alias dGIPC) function results in premature loss of locomotor activity and reduced mean lifespan . ||— ||— ||— ||— |
|git3 deletion ||git3 encodes a G protein-coupled receptor for glucose. git3 deletion increases chronological lifespan in conditions where glucose consumption is not affected. The anti-aging effect of DR and git3 deletion mutation is accompanied by increased respiration and lower ROS production . || ||— ||— ||— |
|sty1 deletion ||Deleting sty1 cancels out chronological lifespan extension and enhanced heat stress resistance by DR . || ||— ||— ||— |
|atf1 deletion ||Deleting atf1 cancels out DR-mediated chronological lifespan extension and enhanced heat stress resistance. || ||— ||— ||— |
|pka1 deletion ||pka1 knockouts exhibits a three-fold increase in chronological lifespan with up to 187% longer maximum lifespan . Deleting ser/thr cAMP-activated protein kinase pka1 extends chronological lifespan under normal condition, but there is no additive effect with DR . || ||+300 ||— ||+187 |
|SCH9 Deletion ||SCH9 deletion increases chronological lifespan by up to threefold. Stress-resistance transcription factors Msn2/Msn4 and protein kinase Rim15 are required for this life-extension. Deletion of the mitochondrial antioxidant enzyme superoxide dismutase gene SOD2 prevents the increased chronological lifespan caused by SCH9 deletion . Mutations that decrease the activity of the Ras/Cyr1/PKA pathway also extend longevity and increase stress resistance by activating transcription factors Msn2/Msn4 and Sod2 . SCH9 deletion mutants exhibit more than 3-fold extension of chronological lifespan. By day 9 of medium depletion all the wild-type cells were dead while 50% sch9 mutants survived . Deletion of SCH9 also increases resistance to heat shock and oxidative stress , and increases replicative lifespan by 18% (in DBY746) . SCH9 deletion increases the replicative lifespan by 40% in the alpha strain  and increases mean chronological lifespan by 97 - 246% (97, 133, 154, 226, 246) in diploid cells . Mutation or deletion of SCH9 increases resistance to oxidants and extends chronological lifespan [11292860; 16286010]. The extended lifespan of SCH9 deletion mutants is not further extended by low glucose DR and is independent of Sir2 . Deletion of RIM15 or GIS1 reverses chronological lifespan extension associated with sch9Delta. Water restriction further increases chronological lifespan of sch9Delta . Deletion of SCH9 results in a longer chronological lifespan . ||Yeast ||+18 to +300 ||— ||— |
|TOR1 Deletion ||TOR1 deletion extends mean and maximum replicative lifespan by 21 and 25%  as well as chronological lifespan . This lifespan extension is independent of SIR2 and additive with deletion of FOB1 . Deletion of TOR1 fails to increase the replicative lifespan of a sir2 mutant . Deletion of TOR1 substantially extends chronological lifespan, increasing median survival almost 3-fold (wild-type 4.5 days, tor1 null 12 days), i.e. by 167%. By 21 days in culture, the vast majority of wild-type cells had died (>99.9%), whereas many tor1 null cells remained viable. Deletion of TOR1 also extends the chronological lifespan of the relatively short-lived BY4742 strain, one of the two haploid genetic backgrounds of the widely used Yeast Knockout Collection available from Open Biosystems. Deletion of TOR1 fails to extend chronological lifespan in Petite strains that are unable to respire . TOR1 deletion increases replicative lifespan by 30% in the alpha strain and 20% in a strain . TOR1 deletion mutant have and increased mean and maximum replicative lifespan by 21% and 6%, respectively . Deletion of TOR1 extends replicative lifespan as well as chronological lifespan  and glucose restriction fails to further extend the long replicative lifespan of tor1Delta [16293764; 16418483; 18225956]. Water starvation (extreme DR) further extends chronological lifespan of tor1 mutants . ||Yeast ||+21 to +30 ||+167 ||+6 to +25 |