Interventions

  • name effect species mean median maximum
    Plasmodien infection With plasmodien infected mosquitous have a reduced fertility but life much longer [http://www.wissenschaft.de/wissenschaft/news/315905.html; http://rspb.royalsocietypublishing.org/content/early/2012/07/30/rspb.2012.1394].
    SAG12 overexpression Introduction of a SAG12 via bacterial gene transfer (pSAG12:ipt) increases longevity. The gene results in enhanced production of the hormone Cytokinin which affects growth and development as well as stimulates cell division and thereby extends the lifespan. pSAG::ipt transgenic plants exhibit delayed leaf senescence, increased branching and reduced internodal length. The leaves and flowers of the pSAG12:ipt plants are reduced in size and display a more intense coloration [http://www.wissenschaft.de/wissenschaft/news/316062.html; http://www.biomedcentral.com/1471-2229/12/156/abstract; Garcia-Sogo et al. 2012].
    YUH1 deletion Deletion of YUH1 decreases replicative lifespan decreased 30% in the alpha strain [18340043]. -30
    Carboxyfullerene SOD mimetic treatment Administration of a small-molecule synthetic enzyme superoxide dismutase mimetic to wild-type (i.e. non-transgenicm non-senescence accelerated) mice starting at middle age significantly extends lifespan and reduces age-associated oxidative stress and mitochondrial radical production. Treatment also improves performance on Morris water maze learning and memory task and therefore rescues age-related cognitive impairment [17079053].
    ERCC1 and ERCC4 deficieny ERCC1-ERCC4-deficient mice exhibit signs of premature aging [17183314].
    Fxn disruption Disruption results in reduced lifespan, increased oxidative stress, impaired respiration, and the development of hepatic tumors [16278235].
    Hsp22 doxycyline-regulated overexpression Doxycyline-regulated overexpression of Hsp22 makes animals more sensitive to heat and oxidative stress as well as reduces the mean lifespan by up to 21%, particularly at higher culture temperature [15491684]. -21
    kermit disruption The disruption of kermit (alias dGIPC) function results in premature loss of locomotor activity and reduced mean lifespan [21029723].
    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 [19266076].
    git3 constitutive activative mutation Constitutive activation of the G-alpha subunit acting downstream of Git3 accelerates aging and inhibits the effect of DR [19266076].
    gpa2 constitutive active mutation Constitutive active mutation of gpa2 (alias git8) decreases chronological lifespan under AL (2% glucose) and almost completely cancels out the lifespan extending effect of DR (0.2% glucose) [19266076].
    sty1 deletion Deleting sty1 cancels out chronological lifespan extension and enhanced heat stress resistance by DR [20075862].
    atf1 deletion Deleting atf1 cancels out DR-mediated chronological lifespan extension and enhanced heat stress resistance[20075862].
    atf1 overexpression Overexpressing atf1 is not sufficient to promote chronological lifespan extension in cells lacking sty1 [20075862].
    wis1 constitutive active mutation Constitutive active mutation of wis1 extends chronological lifespan and there is no further beneficial effect of DR [20075862].
    pka1 deletion pka1 knockouts exhibits a three-fold increase in chronological lifespan with up to 187% longer maximum lifespan [16822282]. Deleting ser/thr cAMP-activated protein kinase pka1 extends chronological lifespan under normal condition, but there is no additive effect with DR [20075862]. +300 +187
    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
    Interventions are an extension of GenAge and GenDR.