• name effect species mean median maximum
    Diazaborine Treatment of wild-type cells with 15 microgram/ml diazaborine extends mean (24.7 -> 36.9) and maximum replicative lifespan [18423200]. Yeast
    Deletion of mitochondrial DNA Activation of the retrograde response by deletion of mitchondrial DNA (rho0) extends mean and maximum replicative lifespan by 24 - 51% and 15 - 65%, respectively [10224252]. Lifespan extension associated with impaired mitochondria depends on a retrograde intracellular signalling involving at leas three transcription factors, which adjust nuclear gene expression an induce shift of metabolism from Krebs cycle to the glyoxylate cycle [Refs 41,42 i Lee et al., 2002]. Yeast +24 to +51 +15 to +65
    Hesperidin treatment Hesperidin derived from the Citrus genus extends replicative lifespan at doses of 5 and 10 microMolar. Hesperdin inihibts ROS and UTH1 gene expression, but increases Sir2 and SOD gene expression. UTH1 and SKN7 are involved in lifespan extension mediated by hesperidin [22484922]. Yeast
    CTT1 mutation Mutational inactivation of CTT1 increases chronological lifespan [20696905]. Yeast
    CTT1 deletion Deletion of CTT1 confers longer chronological lifespan [21076178]. Yeast
    CTT1 overexpression Overexpression of cytosolic catalase T CTT1 alone slightly shortens stationary phase survival in strain DBY746. Overexpression CTT1 in combination with SOD1 increases stationary phase survival by about 10% [12586694]. Yeast
    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 [11292860]. 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 [12855292]. 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 [17710147]. Deletion of SCH9 also increases resistance to heat shock and oxidative stress [11292860], and increases replicative lifespan by 18% (in DBY746) [12586694]. SCH9 deletion increases the replicative lifespan by 40% in the alpha strain [18340043] and increases mean chronological lifespan by 97 - 246% (97, 133, 154, 226, 246) in diploid cells [21447998]. 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 [16293764]. Deletion of RIM15 or GIS1 reverses chronological lifespan extension associated with sch9Delta. Water restriction further increases chronological lifespan of sch9Delta [18225956]. Deletion of SCH9 results in a longer chronological lifespan [21076178]. Yeast +18 to +300
    TOR1 Deletion TOR1 deletion extends mean and maximum replicative lifespan by 21 and 25% [16293764] as well as chronological lifespan [21076178]. This lifespan extension is independent of SIR2 and additive with deletion of FOB1 [16293764]. Deletion of TOR1 fails to increase the replicative lifespan of a sir2 mutant [20947565]. 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 [17403371]. TOR1 deletion increases replicative lifespan by 30% in the alpha strain and 20% in a strain [19030232]. TOR1 deletion mutant have and increased mean and maximum replicative lifespan by 21% and 6%, respectively [21931558]. Deletion of TOR1 extends replicative lifespan as well as chronological lifespan [21076178] 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 [18225956]. Yeast +21 to +30 +167 +6 to +25
    RAS2 deletion RAS2 deletion causes a 23% decrease in mean and a 30% decrease in maximum lifespan [8034612]. Deletion of RAS2 leads to a longer chronological lifespan [21076178]. Deletion of the RAS2 gene, which functions upstream of CYR1, doubles the mean chronological lifespan by a mechanism that requires Msn2/4 and Sod2 [12586694]. DR further extends chronological lifespan of ras2Delta [18225956]. Yeast -23 -30
    Buffering pH to 6.0 Buffering the pH to 6.0 extends chronological lifespan [21076178]. Yeast
    GSH Treatment GSH treatment increases chronological lifespan [21076178]. Yeast
    CTA1 Deletion Deletion of CTA1 increases chronological lifespan [21076178]. Yeast
    PDE2 Deletion Deletion of PDE2 decreases mean replicative lifespan by 26% [11000115] and also results in a shorter chronological lifespan [21076178]. PDE2 null mutant are sensitive to oxidative stress [10394911]. Yeast -26
    SNF1 deletion Deletion of SNF1 increases replicative lifespan by 50% in the alpha strain [19030232], but decreases chronological lifespan [21076178]. Yeast +50
    RIM15 deletion RIM15 deletion results in 50% reduction of maximal chronological lifespan [11292860] and consistently decreases chronological lifespan under AL [21076178]. Rim15 is required for chronological lifespan extension caused by deficiency in RAS2, TOR1, or SCH9, as well as by 0.5% glucose restriction, but not by water starvation [18225956]. Yeast
    SIC1 Deletion SIC1 deletion decreases chronological lifespan [21076178]. Yeast
    SOD2 deletion SOD2 deletion decreases replicative lifespan by 72% [17460215]. SOD2 deletion decreases chronological lifespan [21076178]. Deletion of SOD2 decreases chronological lifespan in wild-type and abolishes chronological lifespan extension in sch9Delta mutants as well as decreases chronological lifespan in cyr1:mTn mutants [12586694]. SOD2 deletion mutants are hypersensitive to oxygen and grow poorly in ethanol [10222047]. Yeast -72
    High Glucose High glucose concentration decreases chronological lifespan [21076178]. Yeast
    N-acetylcysteine Treatment Treatment with N-acetylcysteine decreases chronological lifespan [21076178]. Yeast
    ATP2 Deletion ATP2 deletion decreases replicative lifespan by 50% in the alpha strain [18340043]. Yeast
    HXK2 deletion Deletion of HXK2 extends mean and maximum replicative lifespan by about 53% and 33%, respectively. Limiting glucose availability by mutating HXK2 significantly extends replicative lifespan and provides a genetically model of DR [11000115]. HXK2 deletion increases oxygene consumption. Changes in gene expression HXK2 mutation are quite similar to those of dietary-restricted cells. In fact, HXK2 mutants have a transcriptional profile that significantly resembles DR cells and cell overexpressing HAP4 [12124627]. Yeast +53 +33
    VPS21 deletion Lack of VPS21 reduces lifespan under starvation conditions to a level similiar to that of wild-type cells incubated in synthetic complete medium and therefore blocked the lifespan-extending effect of DR [20657825]. Yeast
    ATG7 deletion ATG7 deletion reduces chronological lifespan by 70% [19302372]. Yeast
    VPS8 deletion Lack of VPS8 reduces lifespan under starvation conditions to a level similiar to that of wild-type cells incubated in synthetic complete medium and therefore blocked the lifespan-extending effect of DR [20657825]. Yeast
    VPS25 deletion Under starvation conditions VPS25 deletion mutants have a dramatically reduced lifespan [20953148]. Yeast
    • Page 1 of 16
    • 25 of 378 interventions
    Interventions are an extension of GenAge and GenDR.