Interventions

  • name effect species mean median maximum
    SFA1 deletion Deletion of SFA1 alone has no effect on replicative lifespan. sfa1;yhb1 double mutant cancels out the ability of moderate DR to extend replicative lifespan, but not chronological lifespan. Yhb1 and Sfa1 may play redundant roles hb1 and Sfa1 may play redundant roles [21584246]. Yeast
    RPD3 deletion Deletion of the histone deacetylase gene RPD3 extends lifespan by 41%, independently of an intact Sir silencing complex (in the short lived YSK661 strain) [10512855]. Deletion of RPD3 extends replicative lifespan and there was no additive effect by neither 0.1% glucose nor amino acid restriction [12213553]. RPD3 deletion increases rDNA silencing in a partially SIR2-dependent manner [10082585]. Its effects on chromatin functional state were evidenced by enhanced silencing at the three known heterochromatic regions in the genome, the silent mating type (HM), subtelomeric, and rDNA loci, which occurred even in the absence of SIR3 [10512855]. Yeast +41
    YHB1 deletion Deleting YHB1 partially abolished DR-induced replicative lifespan extension, whereas deleting SFA1 alone had no effect. sfa1;yhb1 double mutant cancels out the ability of moderate DR to extend replicative lifespan, but not chronological lifespan. Yhb1 and Sfa1 may play redundant roles [21584246]. Yeast
    SIR3 deletion Deletion of SIR3 shortens replicative lifespan by approximately 20% [10521401]. SIR3 mutants exhibit a loss of silencing at the silent mating loci [6098447; 3297920] and telomerease [1913809] and have a slighlty elevuated level of rDNA marker loss [10521401]. The lifespan reduction of SIR3 deletion is suppressed by preventing mating type heterozygosity and is therefore probably due to the simultaneous expression of a and alpha mating-type information, which indirectly causes an increase in rDNA recombination and likely increases the production of extrachromosomal rDNA circles [10521401]. Deletion of SIR3 itself has little effect on lifespan, although it markedly accelerates the increase in cell generation time that occurs during aging [10512855]. Yeast -30
    SFA1 YHB1 double mutation sfa1;yhb1 double mutant cancels out the ability of moderate DR to extend replicative lifespan, but not chronological lifespan. Indicating that NO homeostasis during DR-induced replicative lifespan extension is crucial. Deleting YHB1 partially abolished DR-induced replicative lifespan extension, whereas deleting SFA1 alone had no effect. Yhb1 and Sfa1 may play redundant roles [21584246]. Yeast
    RPL31A deletion Deletion of RPL31A increases mean replicative lifespan by 45% [16293764]. Mean replicative lifespan increases by 35% in the alpha strain and 50% in a strain [19030232; 18423200]. Mean replicative lifespan of the RPL31A deletion mutant increases by 35% in the ORF collection and by 29% in the remade strain [22377630]. RPL31A deletion increases significantly replicative lifespan [17174052]. Deletion of RPL31A extends replicative lifespan and is not further extended by 0.05% glucose restriction [18423200]. Yeast +29 to +50
    RPL6A deletion Deletion of RPL6A decrease mean replicative lifespan by 25% in the alpha strain [18340043; 18423200], but increases mean replicative lifespan by 40% in the remade strain. Its deletion non-significantly increases mean replicative lifespan in the ORF collection [22377630]. Yeast -25 to +40
    RPL6B deletion Deletion of RPL6B significantly increases replicative lifespan [17174052]. Replicative lifespan increases by 15% in the alpha strain and 30-40% in a strain [19030232;18340043;18423200]. RPL6B deletion increases replicative lifespan by 30% [16293764]. Yeast +15 to +40
    RSR1 deletion Deletion of RSR1 (alias BUD1) shortens replicative lifespan [9789734]. Yeast
    RTG2 deletion RTG2 is required for replicative lifespan extension associated with the retrograde response, a pathway that signals the functional status of mitochondria to the nucleus to regulate the expression of several genes [11024000]. RTG2 is not required for replicative lifespan extension by DR [11024000]. RTG2 null mutants are not petite [8422683], but display various nutrient auxotrphies and alterations of carbohydrate metabolism [7727418]. Yeast
    RTG3 deletion RTG3 deletion mutation causes an increase in mean replicative in lifespan by 55% increase at 2% glucose, suggesting that expression of genes regulated by Rtg1-Rtg3 has a negative effect on longevity in 2% glucose (in YPK9). A null mutant has 123% increased mean lifespan at 0.1% glucose relative to a wild-type strain at 2% glucose, indicating that reduced glucose and an RTG3 mutation have an additive effect on lifespan (in YPK9) [11024000]. RTG3 null mutant cannot grow on acetate medium and requires glutamate or aspartate for growth [9032238]. Yeast +55
    BRE5 deletion Deletion of BRE5 increases mean replicative lifespan by 30% [16293764] and mean chronological lifespan in diploid cells [21447998] Yeast +30
    ATG10 deletion ATG10 deletion cancels out replicative lifespan extension by DR [18690010]. Yeast
    SCP1 deletion Increasing actin dynamics by deletion of SCP1, encoding an actin bundling protein, increases replicative lifespan by 67% as well as chronological lifespan by 88% [15024029]. Yeast +67 to +88
    ATG11 deletion ATG11 deletion extends replicative lifespan under AL and abrogates DR-lifespan extension [18690010]. Yeast
    SCP1 overexpression Overexpression of SCP1 leads to elevuated ROS levels and reduces chronological lifespan [15024029]. Yeast
    ERG2 overexpression Overexpression of ERG2 with the promoter of ERG6 (Perg6-ERG2) extends replicative lifespan and this effect was overlapping with moderate DR, because DR can not extend the lifespan of this mutant [Tang et al., unpublished]. Yeast
    FKH1 FKH2 deletion Deletion of FKH1 or FKH2 has no effect on neither replicative, nor chronological lifespan [18225956]. Deletion of both FKH1 and FKH2 reduces mean chronological lifespan by 50% and abrogates lifespan extension and increased stress resistance conferred from water starvation (extreme DR). Modest increase in FKH1 or FKH2 expression results in a slight increased chronological and replicative lifespan as well as stress resistance [22438832]. Yeast
    SGS1 mutation Deletion of SGS1 causes premature aging including a shortened replicative lifespan by approximately 60%, sterility, fragmentation of the nucleolus and redistribution of the Sir3 silencing protein from telomeres to the nucleolus [Sinclair et al, 1997]. Mutation in SGS1 shortens replicative lifespan by 30% [11290710]. Introduction of mutant allele with a point mutation (SGS1 K(706)-->A) in the RecQ helicase domain that eliminates the DNA helicase activity of Sgs1 fails to rescue the premature aging of the sgs1Delta strain, demonstrating that Sgs1 DNA helicase activity is required for a normal lifespan [11861900]. Most cell death in sgs1 mutant cells is caused by a stochastic cell cycle arrest that is associated with a large-budded terminal morpholgy [McVey et al, 2001]. Overexpression of SIR2 or deletion of FOB1 extend lifespan of only those sgs1 cells that escape this arrest [11290710; 10230397]. sgs mutants have greater rate of telomere loss than wild-type cells in the abscence of telomerase [11179234]. Yeast -60
    ADE4 deletion ade4 mutation extends chronological lifespan, but not replicative lifespan, and is non-additive with 0.5% glucose or amino-acid DR on chronological lifespan extension. ADE4 deletion in atg16 mutants results only in a partial extension of the chronological lifespan by 0.5% glucose DR [20421943]. Yeast
    SGS1 overexpression Overexpression of SGS1 extends the maximum lifespan of cells lacking SRS2, but not the mean lifespan [11861900]. Yeast
    SWH1 deletion SWH1 (alias OSH1) deletion mutants have an extended replicative lifespan (p=0.02) and DR does not increase the long lifespan of SWH1 deletion mutants [Xia et al. unpublished]. Yeast
    SIM1 deletion Disruption of SIM1 shortens mean (87.5%), but not maximum, lifespan without causing any other gross changes in cell cycle parameter or growth characteristics [8810036]. Cells bearing deletions in CLB1-4 are unable to undergo mitosis and normally arrest in G2. SIM1 disruption in clb1-4 mutant backgrounds will allow a second round of DNA synthesis without mitosis [8574583]. sim1delta;uth1delta double mutants exhibit various defects, including binucleated cells, benomyl sensitivity, heat shock sensitivity, inability to store glycogen, sensitivity to starvation and failure of spores to germinate [10612745]. Yeast
    SRX1 deletion Extra copy of SRX1 counteracts age-related hyperoxidation of Tsa1 and extends replicative lifespan by 15 - 20% in a TSA1-dependent manner. Replicative lifespan extension in sir2;fob1 double mutant by DR is reduced by SRX1 deletion. Wild-type cells require SRX1 to fully extend lifespan. DR fails to further extend replicative lifespan of cells carrying an extra copy of SRX1. Mutation in CDC35 (adenylate cyclase), a genetic mimetic of DR, is dependent on SRX1 to extend replicative lifespan [21884982]. Yeast +15 to +20
    CCR4 deletion Deletion of CCR4 increases mean chronological lifespan by 20 - 41% (20, 33, 41) in diploid cells [21447998]. In W303R CCR4 deletion shortens replicative lifespan by approximately 80% and results in temperature sensitivity that is suppressed by SSD1-V. SSD1-V partially suppresses the short-lifespan of ccr4 mutant. CCR4 mutation is synthetically lethal in combination with deletion of MPT5 in the absence of SSD1-V [11805047]. Yeast -80 to +20
    Interventions are an extension of GenAge and GenDR.