Interventions

  • name effect species mean median maximum
    Petite Respiratory deficient petite cells in YPK9 strain have a replicative lifespan that is extended by 39%. This lifespan extension is strain-specific as Petite cells in W303 have lifespan identical to grande cells and petite cels in strains SP1-1 and A364A have a shorter lifespan than grande cells [10224252]. Respiratory defective petite cells display defective mitochondria and are unable to grow on glycerol. Yeast +39
    Diazaborine Treatment of wild-type cells with 15 microgram/ml diazaborine extends mean (24.7 -> 36.9) and maximum replicative lifespan [18423200]. Yeast
    PHB1 deletion Deletion of PHB1 results in a slight reduction in mean and maximum replicative lifespan and a defect in mitochondrial membrane potential. When both PHB1 and PHB2 genes are deleted, the mean replicative lifespan is reduced by one third (30%) that of the wild-type strain [9259555]. Deletion of PHB1 decreases replicative lifespan by 20% [12882345]. Phenotypic changes characteristic of aging cells (e.g. lengthening of cell cycle and specific morphological changes) suggests that PHB1;PHB2 double mutants undergo premature aging, not simply reduction of viability [9259555]. There is no reduction in stress resistance or bulk growth rate in PHB1 mutants. PHB1;PHB2 double mutant have a strong defect in mitochondrial potential, while PHB1 mutant have only a slight defect [9259555]. PHB1 deletion is synthetical lethal with mutation of outer mitochondrial membrane proteins, Mdm12, Mdm10, or Mmm1 [9632789]. Yeast -30
    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
    PHB2 deletion PHB2 deletion leads to a slight reduction in both mean and maximum replicative lifespan, and when both PHB1 and PHB2 genes are deleted, the mean replicative lifespan is reduced by 40% [9259555]. Deletion of PHB2 decreases replicative lifespan by 30% [12882345]. Phenotypic changes characteristic of aging cells (e.g. lengthening of cell cycle and specific morphological changes) suggests that PHB1;PHB2 double mutants undergo premature aging, not simply reduction of viability [9259555]. PHB2 mutants exhibit no reduction in stress resistance or bulk growth rate. PHB1;PHB2 double mutant have a strong defect in mitochondrial potential [9259555]. Prohibitin-dependent mutation pbd1 and pdb2 behave in a different manner and probaly affect different aspects of prohibitin function. pdb1 mutants slightly extended lifespan by 11%, whereas in contrast, the pdb2 mutation results in a shortening in both the mean- and the maximum-lifespan (by 28 and 17%, respectively). pdb1 mutation also reduces chronological lifespan. Reducing the expression of the PHB2 in the pbd mutants retards the rate of growth and affects replicative lifespan [16710639]. Yeast -30
    Gonadermasides D treatment Application of gonadermasides D significantly increases the replicative lifespan in the K6001 strain by regulating UTH1 [21512225]. Yeast
    Ganodermasides A treatment Application of Ganodermasides A extends the replicative lifespan in K6001 strain by regulating UTH1 expression [20093034]. Yeast
    Ganodermasides B treatment Application of Ganodermasides B extends the replicative lifespan in K6001 strain by regulating UTH1 expression [20093034]. Yeast
    PNC1 overexpression Cells with 5 copies of PNC1 have a 70% longer replicative lifespan which is cancelled out by SIR2 deletion. Overexpression of PNC1 suppresses the effect of exogenously added nicotinamide on Sir2-dependent silencing at HM loci, telomeres and rDNA loci [12736687; 14729974]. PNC1 overexpression suppresses the inhibitory effect of exogenously added NAM on silencing, lifespan, and Hst1-mediated transcriptional repression [14729974]. Increased expression of PNC1 is both necessary and sufficient for replicative lifespan extension by DR and low-intensity stress. Under non-stressing conditions (2% glucose, 30 degree Celsius), a strain with additional copies of PNC1 (5XPNC1) has 70% longer replicative lifespan than the wild-type and some cells live for more than 70 divisions. Neither DR nor heat stress further increase the lifespan of the 5XPNC1 strain [12736687]. Yeast +70
    PNC1 deletion Deletion of PNC1 shortens replicative lifespan approximately by 10% [12736687] and largely prevents replicative lifespan extension of 0.5% glucose restriction. 0.5% glucose restriction slightly extends median replicative lifespan (by 10 - 15%) but not maximum replicative lifespan in pnc1Delta [14724176]. PNC1 deletion decreases chronological lifespan [17110466]. Yeast -10
    POL1 deletion Mutation of POL1 results in a 20-60% reduction in mean lifespan (in SS111) [12024027] Yeast -20 to -60
    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
    HST1 deletion Deletion of HST1 blocks the residual replicative lifespan extension by hxk2 mutant in a sir2;fob1;hst2 triple mutant background [16051752]. However, DR can increases the replicative lifespan to a similar extent in sir2;fob1;hst1;hst2 quadruple mutant cells as in sir2;fob1 double mutant cells under 0.5, 0.05 and 0.005% glucose conditions and even by hxk2 deletion mutant [16741098; 17129213]. Yeast
    PUF4 deletion Deletion of PUF4 has no effect on replicative lifespan in either uth4-14c (C-terminal truncation) or UTH4 background. However, PUF4 is required for lifespan extension by the semi-dominant Sir4-42 allele in the uth4-14c background [9150138]. PUF4 is required for nucleolar relocalization of Sir3 in a Sir4-42 background [9150138]. puf4;mpt5 double deletion strain has increased telomere silencing reltive to the mpt5 single mutant [9651685]. Yeast
    PCK1 deletion Loss of Pck1 activity blocks chronological lifespan extension caused by water starvation. Knockout of PCK1 dramatically reduces chronological lifespan in both water (extreme DR) and glucose-containing medium. Deletion of SIR2 does not alter the lifespan of PCK1 deletion mutant, pck1-K514R, and pck1-K514Q mutants [19303850]. Yeast
    CTT1 mutation Mutational inactivation of CTT1 increases chronological lifespan [20696905]. Yeast
    BNA6 deletion Deletion of BNA6 (alias QPT1) has no effect on replicative lifespan and is not required for lifespan extension by DR, but is lethal with mutation of NPT1 [11000115]. Deletion of BNA6 decreases chronological lifespan [17110466]. Yeast
    PCK1 mutation pck-1-K514Q mutation which abrogates enzymatic activity of Pck1, just like SIR2 deletion, extends chronological lifespan in water. Deletion of SIR2 does not alter the lifespan of PCK1 deletion mutant, pck1-K514R, and pck1-K514Q mutants [19303850]. Yeast
    CTT1 deletion Deletion of CTT1 confers longer chronological lifespan [21076178]. Yeast
    ESA1 mutation esa1-531 mutant has an even shorter chronological lifespan than PKA1 deletion mutant in both 2% glucose (ad libitum) and water (extreme DR) at 30 degree Celsius, a semipermissive temperature. At the permissive temperature (25 degree Celsius) there is little difference [19303850]. 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
    RAD1 mutation Deletion of RAD1 has no effect on replicative lifespan [10207108]. Yeast
    GSH1 deletion Deletion of GSH1 confers deficiency in glutathione biosynthesis and further increases chronological lifespan under 0.5% glucose restriction, but does not extend chronological lifespan under 2% glucose [18840459]. Therefore, GSH1 has a positive interaction with DR [18840459]. 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
    RAD26 deletion Deletion of RAD26 has no effect on replicative lifespan in PSY316 [10207108]. Yeast
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    • 25 of 378 interventions
    Interventions are an extension of GenAge and GenDR.