We need to know every factor which determines lifespan.

Lifespan factors often but not always originate from defined genetic elements. They are not just genes, by definition they can be anything for which a Classifications schema can be build for that is related to the regulation of lifespan, such entities may include Single-Nucleotide Polymorphism, transcript variants, proteins and their complexes, compounds (i.e. small molecules like metabolites and drugs), etc. A factor should be based on a defined molecular entity or genomic position and been classified. It shall be highly flexible and scalable Concept.

While individual lifespan factors within each species or precise defined molecular entities will be captured within the Lifespan App, Data Entries of the Data App may summarize for instance the relevance of each factor class (e.g. homologous group; chemical derivate of related structure and properties, etc.) as well as draw overall conclusions. o


  • Types: + -
    Gene (1)  
  • symbol name observation species
    VPH2 Vacuolar pH 2 Overexpression of VPH2 increases the levels of assembled V-ATPase at the vacuolar membrane, increases vacuolar acidity and suppresses age-induced mitochondrial dysfunction of aged cells (17 or 18 cell divisions) which requires the V-ATPase activity. VPH2 overexpression significantly increases mean, median and maximum replicative lifespan by 23, 25 and 34%, respectively [23172144]. Budding yeast
    AVT1 Amino acid Vacuolar Transport 1 Overexpressing or deleting AVT1 is sufficient to extend or shorten replicative lifespan, respectively [23172144]. Overexpression of AVT1 prevents mitochondrial dysfunction, prevents alterations in mitochondrial structure and ΔΨ of aged cells even through the vacuolar acidity is reduced in these cells. AVT1 overexpression extends the mean, median and maximum replicative lifespan by 28, 28, and 22%, respectively [23172144]. Deletion of AVT1 accelerates the development of age-induced mitochondrial dysfunction without effecting the kinetics of vacuolar acidity decline and prevents the suppression of mitochondrial dysfunction by VMA1 and VPH2 overexpression without affecting vacuolar acidity. AVT1 deletion decreases mean, median and maximum replicative lifespan by 21, 22, and 12%, respectively [23172144]. Budding yeast
    VMA1 Vacuolar Membrane Atpase 1 Overexpression of VMA1 increases vacuolar acidity and suppresses age-induced mitochondrial dysfunction of aged cells (17 or 18 cell divisions) which requires the V-ATPase activity. VMA1 overexpression significantly increases mean, median and maximum lifespan by 39 - 45%, 39 - 48% and 50 - 60%, respectively. DR (0.5% glucose restriction) does not further increase the lifespan of VMA1 overexpression strain [23172144]. Budding yeast
    OSH2 OxySterol binding protein Homolog 2 Deletion of OSH2 decreases mean chronological lifespan [20657825]. Budding yeast
    VAC14 VACuole morphology and inheritance mutant 14 VAC14 mutants have a single vacuole and shortened lifespan on normal media [16293764]. Budding yeast
    PEP4 carboxyPEPtidase Y-deficient 4 Overexpression of vacuolar aspartyl protease (PEP4) extends chronological lifespan by increasing cytosolic polyamine and S-adenosylmethionine (SAM) levels. Deletion of PEP4 results in both apoptotic and necrotic cell death during chronological aging [21593793]. PEP4 is not DR-essential [18690010]. Budding yeast
    TEC1 Transposon Enhancement Control 1 Tec1 is a positive regulator of chronological lifespan. Absence of TEC1 causes a significant shortened chronological lifespan, but does not block chronological lifespan extension by rapamycin. TEC(AxY) mutation also reduces chronological lifespan, although not so pronounced as strains lacking TEC1. Rapamycin-induced chronological lifespan extension is almost completely blocked by TEC(AxY) allele [21840851]. Budding yeast
    NTH2 Neutral TreHalase 2 Deletion of NTH2 shortens mean chronological lifespan by 39% (at 30 degree Celsus in BY4742) [22783207]. NTH2 mutant cells have elevated trehalose concentration before they enter the non-proliferative stationary growth phase which remained high during the stationary phase. NTH2 deletion cells have no altered ROS levels in pre-quiescent cells [22783207]. Budding yeast
    TPS1 Trehalose-6-Phosphate Synthase 1 Deletion of TPS1 decreases intracellular trehalose concentration and shortens the mean chronological lifespan by 74% (at 30 degree Celsus in BY4742) [22783207]. Budding yeast
    ESA1 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]. Budding yeast
    ACH1 Acetyl CoA Hydrolase 1 ACH1 deletion cells accumulate a high amount of extracellular acetic acid and display a reduced mean and maximum chronological lifespan. Maximum lifespan is reduced by 32%. Lifespan shortening is completely abrogated by alleviating the acid stress either by a DR regimen that prevents acetic acid production or by transferring chronologically aging mutant cells to water. Deletion of ACH1 is accompanied by reactive oxygen species accumulation, severe mitochondrial damage, and an early insurgence of apoptosis [22754872]. Budding yeast
    NDT80 Non-DiTyrosine 80 Transient overexpression of NDT80 rejuvenates old cells [21700873]. Budding yeast
    IME1 Inducer of MEiosis 1 Transient overexpression of IME1 resets the replicative lifespan of old cells back to that of young cells [21700873]. Budding yeast
    SWI4 SWItching deficient 4 Deletion of SWI4 shortens replicative lifespan by approximately 90% [11805047]. SSD1-V partially suppresses the short lifespan of a swi4 mutant. Mutation of swi4 results in slow growth and temperature sensitivity, both of which are suppressed by SSD1-V [11805047]. Budding yeast
    SUN4 Disruption of SUN4 shortens mean (87.5% of normal), but not maximum, replicative lifespan in BKY1-14c [Austriaco, N.R. (1996) “UTH1 and the Genetic Control of Aging in the Yeast, Saccharomyces cerevisiae.” Ph.D. Thesis, Massachusetts Institute of Technology; 8810036] SUN4 mutation causes failure of daughter cells to completely detach and results in a multi-budded morphology [10683261]. Budding yeast
    SIM1 Start Independent of Mitosis 1 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]. Budding yeast
    RSR1 RaS-Related 1 Deletion of RSR1 (alias BUD1) shortens replicative lifespan [9789734]. Budding yeast
    POL1 POLymerase 1 Mutation of POL1 results in a 20-60% reduction in mean lifespan (in SS111) [12024027] Budding yeast
    NNT1 Nicotinamide N-methylTransferase 1 Deletion of NNT1 decreases mean and maximum lifespan by 9 and 19%. 0.5% glucose DR extends the mean and maximum lifespan of NNT1 deletion mutants by 35 and 40%. Overexpression of NNT1 by 5-fold extends mean and maximum replicative lifespan by 18 and 23%, which is approximately of the same magnitude as the lifespan extension obtained from DR. DR in NNT1 overexpression mutant fails to significantly affect the lifespan and only results in extended mean lifespan by 12% and reduced maximum lifespan by 11%. NNT1 overexpression increases rDNA silincing, whereas deletion decreases rDNA silencing. Overexpression of human nicotinamide N-methyltransferase also increases rDNA silencing [12736687]. Budding yeast
    NCA3 Nuclear Control of ATPase 3 Disruption in NCA3 shortens mean (87% of normal), nut not maximum replicative lifespan without causing any other gross changes in cell cycle parameters of growth characteristics [8810036]. In combination with an NCA2 disruption, NCA3 disruption causes a cryosensitive phenotype on non-fermentable carbon sources due to a defect in the F1-F0 ATP synthetase due to misbalancing of alternate spliceforms of mitochondrial mRNA encoding subunits 6 and 8 of the synthase [7586026]. Budding yeast
    HSC80 Deletion of HSC82 has no effect on replicative lifespan, but shortens chronological lifespan [11361336]. Budding yeast
    HOG1 High Osmolarity Glycerol response 1 Deletion of HOG1 shortens replicative lifespan by 25% and prevents lifespan extension by high osmolarity [12391171]. HOG1 is required for many of the transcriptional responses to high osmolarity, including increased glycerol biosynthesis and MSN2/4-dependent stress response [10722658]. HOG1 deletion slightly decreases chronological lifespan and partially suppresses the premature aging phenotype and short lifespan of ISC1 deletion [22445853]. Budding yeast
    HAP5 Heme Activator Protein 5 Deletion of HAP5 shortens replicative lifespan by approximately 40%. This is not a premature aging phenotype as "old" HAP5 cells do not become premature sterile or exhibit other biomarkers of yeast aging [9271578]. HAP5 null mutants are unable to grow on a non-fermentable carbon source [7828851]. Budding yeast
    GPD1 Glycerol-3-Phosphate Dehydrogenase 1 GPD1 deletion shortens replicative lifespan by 25% and prevents lifespan extension by high osmolarity [12391171]. Transcripational regulation of GPD1 by osmotic stress requires HOG1 [8196651]. Budding yeast
    COQ3 COenzyme Q 3 Deletion of COQ3 decreases chronological lifespan and renders cells respiratory deficient and sensitive to hydrogen peroxide [12586694]. Budding yeast
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    • 25 of 154 factors
    Factors are an extension of GenAge and GenDR.

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