Interventions

  • name effect species mean median maximum
    GUP1 deletion GUP1 deletion extends mean and maximum replicative lifespan by 32 and 30%, respectively, as well as chronological lifespan. DR-induced maximal replicative lifespan extension is not further increased by GUP1 deletion, while gup1 mutant displayed longer chronological lifespan under DR [21584246]. Yeast +32 +30
    Efemp1 knockout Efemp1 knockout mice exhibited an early onset of aging-associated phenotypes including a 20% shorted median lifespan and 30% shorter maximum lifespan, decreased body mass, lordokyphosis, reduced hair growth, and atrophy [17872905]. Mouse +20 +30
    HSP12 deletion HSP12 deletion slightly increases mean, medium, and maximum replicative lifespan by 24, 27, and 3% under AL, but totally abolishes the lifespan extending effect of moderate DR [Alan Morgan, personal communication; Herbert et al. in press]. HSP12 deletion has no effect on resistance to variety of stresses (including oxidative stress) [Alan Morgan, personal communication]. Yeast +24 +27 +3
    FIS1 deletion Deletion of FIS1 prolongs significantly mean and maximum lifespan by 13 and 29% as well as improves the fitness of old mother cells (in BY4741) [17173038]. Yeast +13 +29
    RAS1 deletion Deletion in RAS1 increases mean (23%) and maximum (29%) replicative lifespan (in SP1) [8034612]. RAS1 deletion increases replicative lifespan by 15% in the alpha strain [19030232]. However, deletion of RAS1 slightly shortens chronological lifespan (in SP1) [12586694]. Yeast +15 to +23 +29
    GPR1 deletion Deletion of GRP1 increases mean and maximum replicative lifespan by 41% and 26%, respectively. GRP1 deletion mutants have also longer chronological lifespan. Deletion of GPR1 extends replicative lifespan by reducing cAMP-PKA activity and provides a genetically model for DR [11000115]. Yeast +41 +26
    GPA2 deletion Deletion of GPA2 increases mean and maximum replicative lifespan by 40% and 26%, respectively. GPA2 deletion extends replicative lifespan by reducing cAMP-PKA activity and provides a genetic model for DR [11000115]. Yeast +40 +26
    Pou1f1 knockout Snell dwarf mutation (Pit1dw) due to knockout of Pou1f1 results in a dramatic lifespan extension. The mean, median and maximum lifespan is increased by 40-50% for Snell dwarf (Pit1dw/Pit1dw) DW/J females, and 25-50% for dwarf DWC3F1 males and females with a compound heterozygous Pit1dw/Pit1dw-J genotype. Although, Snell dwarf (Pit1dw/Pit1dw) DW/J males exhibit aspects of delayed senescence, their median lifespan is by about 25% shorter, probably due to the affects of housing conditions [11718806]. Mice homozygous for loss-of-function mutations at Pit1 locus have a mean and maximum lifespan extension over 40%. Mutant dwJ/dw animals exhibit delays in age-dependent collagen cross-linking and in six age-senstive indices of immune system status. Pituitary transplantation into dwarf mice does not reverse the lifespan extension effect. Male Snell dwarf mice become obese and exhibit proportionately high leptin levels in old age [11371619]. Mouse +25 to +50 +25 to +50 +25 to +50
    eat-2 mutation eat-2 mutations result in partial starvation by disrupting the function of the pharynx and an approximately 50% extension of lifespan. eat-2 mutants life significant longer by up to 57% [9789046]. eat-2(ad1116) mutants have an extended mean, 75%ile and maximum lifespan by 30, 35, and 24% [22810224]. sDR further increases the long lifespan of eat-2 mutants [19239417]. eat-2 mutants live longer than wild-type at high food concentration but are short lived at lower concentrations (via bacterial dilution) [19229346]. eat-2(ad1113) mutation increases mean lifespan by 56% and is non-additive with SCNA overexpression [16782295]. Combining eat-2 mutation with bacterial deprivation DR does not result in an additive increase in lifespan [17081160;17096674]. Loss of function of eat-2 extends lifespan by 20-30%. Lifespan extension is proposed to be similar to DR. eat-2;daf-2 double mutant live longer than daf-2 single mutants [9789046]. Therefore, eat-2 mutants can synergize with daf-2 mutants, but not with clk-1 mutants, for lifespan extension. Lifespan extension conferred by eat-2 is not suppressed by daf-16 mutation [9789046]. Worm +30 to +57 +24
    IMD2 deletion Deletion of IMD2 did non-significantly decrease mean replicative lifespan by 1% and non-significantly increased maximum replicative lifespan by 21% [20550517]. Yeast -1 +21
    IPK1 deletion Deletion of IPK1 increases mean replicative lifespan by 41 - 40% in the alpha strain [16293764; 19030232]. IPK1 deletion extends mean and maximum replicative lifespan by 24 and 19%, respectively, and was non-synergistic with moderate DR [21584246]. Yeast +24 to +40 +19
    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
    SML1 deletion Deletion of SML1 increases non-significantly mean replicative lifespan by 3% and non-significantly maximum lifespan by 16% [20550517]. Yeast +3 +16
    IDH2 deletion Deletion of IDH2 increases the mean replicative lifespan by about 30% [16293764]. IDH2 deletion extends mean replicative lifespan by 20% in the alpha strain and in a strain [19030232; 18340043]. IDH2 deletion extends mean, median and maximum lifespan by 15, 19 and 15% [23167605]. Yeast +15.4 to +30 +19.2 +15.4
    Heterozyogous fat-specific Insr knockout (FIRKO) Deletion of Insr specifically in adipose tissue results in a 15-18% increase in mean, median and maximum lifespan. Fat-specific insulin-receptor knockout (FIRKO) reduces fat mass and protects against age-related obesity and its subsequent metabolic abnormality, without an decrease in food intake. Both male and female FIRKO mice have an increase in mean lifespan of around 134 days (18%), with parallel increases in median and maximum lifespan. FIRKO mice consume the same amount of food on per animal basis as control littermates, but have 15-25% lower body-mass and 50-70% reduced fat mass [12543978]. Disruption of Insr in all tissues reults in neonatal lethality [8612577]. Mouse +15 to +18 +15 to +18 +15 to +18
    DNM1 deletion Deletion of DNM1 extends significantly mean and maximum lifespan by 49 and 111% in FY10 strain and by 15 and 12% in BY4741 strain [17173038]. Yeast +15 to +49 +12 to +111
    Whole-body Sirt1 deletion in the adulthood Whole-body deletion of Sirt1 in the adulthood results in mice which are seemingly normal in every way. When mice were given low doses of resveratrol after Sirt1 was disabled, there were no discernible improvement in mitochondrial function or any paramenter, while mice with normal Sirt1 function given reservatrol showed dramatic increases in energy, mitochondrial biogenesis and function, AMPK activation and increased NAD+ levels in skeletal muscle. When mice lacking Sirt1 were given low doses of reserveratrol, AMPK was unaffected. When doses were significantly increased in these mice, AMPK was activated in a SIRT1-indepent manner, but still no benefit to mitochondrial function resulted [22560220]. Mouse
    rsks-1 mutation rsks-1 deletion mutants also live longer. TOR RNA interference further extends lifespan of rsks-1 mutants [17266679]. Worm
    ATG7 deletion ATG7 deletion reduces chronological lifespan by 70% [19302372]. Yeast
    VPS27 deletion Under starvation conditions VPS27 deletion mutants have a dramatically reduced lifespan [20953148]. Yeast
    SAM1 deletion Deletion of SAM1 increases replicative lifespan by 20% in the alpha strain and 15% in the a strain [18340043]. Yeast +15 to +20
    INP53 deletion Deletion of INP53 increases mean replicative lifespan by 31% [16293764]. INP53 deletion increases replicative lifespan by 31% in the alpha strain and by 10% in the a strain [18340043]. Yeast +31
    ATG18 deletion The replicative lifespan of ATG18 deletion mutant is not shorter than that of wild-type under DR [18690010]. Yeast
    HNRNPD deletion HNRNPD deletion leads to accelerated aging as evidenced by strinking telomere erosion, markedly increased DNA damage repsosne at telomere ends, pronounced cellular senescence and rapid premature aging that increases with successive generations [Pont et al., 2012]. Mouse
    CKA2 deletion CKA2 deletion approximately doubles mean chronological lifespan under starvation/extreme DR in BY4741 also increases as well as as heat-shock resistance in SDC medium in the W303-1A and DBY746 genetic backgrounds [20657825]. Yeast
    Interventions are an extension of GenAge and GenDR.