Interventions

  • name effect species mean median maximum
    ATG10 deletion ATG10 deletion cancels out replicative lifespan extension by DR [18690010]. Yeast
    ATG11 deletion ATG11 deletion extends replicative lifespan under AL and abrogates DR-lifespan extension [18690010]. Yeast
    ATG17 deletion ATG17 deletion decreases replicative lifespan under AL and blocks DR-lifespan extension. ATG17 mutant's replicative lifespan decreases by 70% on DR [18690010]. Yeast
    ATG2 deletion ATG2 deletion prevents chronological lifespan extension induced by amino-acid DR [20421943]. Yeast
    ATG7 deletion ATG7 deletion reduces chronological lifespan by 70% [19302372]. Yeast
    Atm knockout Atm-deficient mice are viable, retarded in growth, infertile (male produce no mature sperm and female no gametes), display neurological dysfunction, and exhibit severe defects in T cell maturation while going on to develop thymomas [8917548; 8689683]. The majority of mutant mice rapidly develop thymic lymphomas and die before 4 months of age [8843194]. Cells of Atm(-/-) mice exhibit slow growth also in culture and premature senescence, telomeres are extensively shortened in multiple tissues [8689683]. Mice mutant for Atm and Terc display progressive multi-organ system compromise and features of accelerated aging [12540856]. Mouse
    Aut1 RNAi Aut1 depletion by RNAi form the first day of imaginal stage shortens lifespan by 28% on average in Drosophila and causes morphological behavioural features of premature aging [18219227]. Fly -28
    bar-1 mutation BAR-1 may play a role in regulating daf-16 during dauer formation, particularly in conditions of oxidative stress as it directly interaction with DAF-16 and loss of bar-1 reduces activity of DAF-16 in dauer formation and lifespan. Deletion of bar-1 reduces mean (44%) and maximal (18%) lifespan, which is to a similar degree as seen to daf-16 mutants [15905404]. Worm -44 -18
    Bmcp knockout Bmcp knockout flies live longer on low-calorie diets, have a decreased fertility, and gain less weight on high-calorie diets. Bmcp (ucp5) knockout mutants live longer than wild-type on low-calorie diets, but no longer on starvation or high-calorie diets. Ectopic neuronal expression of Bmcp transgene rescues starvation sensitive phenotype of Bmcp knockout mutants [16387864]. Fly
    C26B2.2 knockout C26B2.2 knockout mutations extend lifespan [15253933]. Worm
    che-2 mutation che-2 recessive loss-of-function mutations extend lifespan up to 50% (in Bristol N2) [10617200]. che-2 mutants are chemotactic defective, slightly small, defective for osmotic avoidance, have ciliated neurons with abnormal stunted ultrastructure, and are dauer defective [2428682; 1732156]. Worm +50
    CHL1 deletion CHL1 deletion mutant exhibits a shortened mean and maximum lifespan by 36 and 29%, respectively, as well as hypersensitivity to heat stress. CHL1 may modulate transcriptional silencing in the presence of Sir proteins [16182251]. Yeast -36 -29
    SKN1 deletion Chronological lifespan increased by 60% for single skn1 and double ipt1-skn1 deletion [16527275]. Yeast +60
    Cisd2 knockout Cisd2 knockout shortens lifespan resulting in premature aging [19451219]. 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
    cyc1 mutation cyc1 mutants have a reduced growth rate, a reduced reactive oxygen species production, and are long-lived [17081785].
    daf-1 mutation daf-1(mk40) mutation increases mean lifespan by 18-46% and maximum lifespan by 29% [17900898]. The daf-1(m40) allele has no effect on lifespan and fails to prevent lifespan extension by sir-2.1 overexpression, but it results in a temperautre-sensitive, dauer-constitutive phenotype in larvae [11242085]. Worm +18 to +46 +29
    daf-16 mutation daf-16(m26) mutation slightly, insignificantly decreases lifespan, but completely suppresses lifespan extension of daf-2(e1370) adults [8247153]. daf-16 is required for lifespan extension by mutation of daf-2 or age-1 [8247153]. Mutations in daf-16 suppressed life-extension caused by mutations in daf-2 [8247153]. Loss of function alleles of daf-16 shorten lifespan, but some alleles have lifespan equal to wild-type [8247153]. daf-16 mutation significantly reduces lifespan under AL (-20%), but does not prevent lifespan extension by sDR. In another experiment daf-16 mutation totally suppresses lifespan extension by sDR [16720740]. sDR does not stimulate DAF-16 translocation to the nucleus, but daf-16 mutation cancelled out the ability of sDR to extend lifespan and to delay the decline in locomotor activity [17900900]. DR by bacterial dilution extends lifespan of daf-16 mutants [17538612]. daf-16 mutation decreases lifespan under AL, but fails to prevent bDR to further extend lifespan [18331616]. IF-induced lifespan-extension by either 24h/48h/72h per 4 days is significantly diminished in null mutants of daf-16. All these regimens extend lifespan of daf-16 to a lesser extent than wild-type. daf-16 partially mediates IF-induced longevity [19079239]. Glucose or glycerol does not shorten lifespan of daf-16 mutants [19883616]. daf-16 mutation cancels out the lifespan extension effect of sDR and PD, regardless of the concentration of bacteria or peptones. bDR significantly extends lifespan of daf-16 mutants, but to a lesser extent than that of wild-type. eat-2 mutation extends the lifespan of daf-16 mutants to the same extent than that of wild-type. Resveratrol extends lifespan of daf-16 mutants [19239417]. daf-16 RNAi completely blocks lifespan extension by daf-2 mutation, but only partially by bDR. daf-16 RNAi attenuates protection against oxidative stress by bDR. daf-16 expression is induced by bDR [19924292]. Knockdown of daf-16 decreases mean and maximum lifespan by 50% and 54%, respectively [22509016]. DAF-16 reduces expression of rsks-1 and daf-15 [15253933; 22560223]. daf-16(mu86) mutation decreases mean (44%) and maximum (18%) lifespan [15905404]. daf-16(mgDf47) decreases mean (18-37%) and maximum (29%) lifespan [18828672]. daf-16 mutants are dauer defective [7219552] and completely suppress all the phenotypes of daf-2 and age-1 mutations, including lifespan extension, dauer arrest, reduced fertility, and viability defects [8247153; 7789761; 9504918; 7789761]. Mutations in daf-16 also suppress lifespan extension of animals that have a germ line ablation [10360574]. Sex-specific lifespan potential requires daf-16 [10747056]. daf-16 mutation suppresses enhanced UV resistance as well as increase longevity of daf-2, daf-23, spe-26, and clk-1 mutants. Mutation in daf-16 does not alter the reduced fertility in spe-26. daf-16 mutants are more fertile than wild-type [8807294]. Worm -18 to -37 -29
    daf-18 mutation daf-18 is required for complete dauer formation. daf-18 mutation partially suppresses the lifespan extension of age-1 and daf-2 mutants. daf-18 mutants are defective for dauer formation and form some dauer-like larvae when starved [7789761; 8601482]. Worm
    DAP2 deletion DAP2 deletion decreases mean and maximum replicative lifespan under AL by 19 and 36%, respectively, and cancels out the lifespan extending effect of moderate DR [22912585]. Yeast -19 -36
    Dgat1 knockout Deficiency in Dagat1 promotes leanless and extends mean, median and oldest 10% survival by 23, 26 and 9% without limiting food intake [22291164]. +23 +26
    atf1 deletion Deleting atf1 cancels out DR-mediated chronological lifespan extension and enhanced heat stress resistance[20075862].
    BMH1 deletion Deleting BMH1 extends chronological lifespan by 25% and is associated with activated stress response, decreased ROS levels and increased heat-shock-element-driven transcription activity. BMH1 deletion was non-additive with the genetic DR mimetic cdc25 and tor1. Water starvation (a form of extreme DR) extends chronological lifespan of BMH1 mutant even more as it does in wild-type [19805817]. Yeast +25
    LAT1 deletion Deleting LAT1 abolishes replicative lifespan extension induced by 0.5% and 0.05% glucose restriction [17200108]. Yeast
    SNF4 deletion Deleting SNF4 extends replicative lifespan by 10-20% in S288C strain [10921902]. Yeast +10 t +20
    Interventions are an extension of GenAge and GenDR.