Interventions

  • name effect species mean median maximum
    ARO7 deletion Under starvation/extreme DR deletion of ARO7 increases mean chronological lifespan and confers higher resistance to heat-shock, but made cell more sensitive to acetic acid and leads to growth defects. In W303-1A background ARO7 deletion causes an even more severe growth defect and mutants are short-lived [20657825]. Yeast
    FAR3 deletion Deletion of FAR3 significantly reduces mean chronological lifespan under starvation/extreme DR relatively to wild-type [20657825]. Yeast
    FAR11 deletion Deletion of FAR11 significantly reduces mean chronological lifespan under starvation/extreme DR relatively to wild-type [20657825]. Yeast
    PPG1 deletion PPG1 deletion reduces significantly mean chronological lifespan under starvation/extreme DR [20657825]. Yeast
    BUL1 deletion Deletion of BUL1 does non-significantly reduces mean chronological lifespan under starvation/extreme DR [20657825]. Yeast
    PAN2 deletion Deletion mutant of PAN2 live approximately as long as wild-type under starvation/extreme DR [20657825]. Yeast
    shc-1 knockout Loss of shc-1 function results in accelerated aging and enhanced senstivity ro heat, oxidative stress and heavy metals. Worm
    Ilp2 mutation Ilp2 null mutants are significant longer-lived with a 8-13% longer median lifespan [20195512]. Fly +8 to +13
    foxo mutation foxo null mutants are highly and significantly shorter-lived than wild-type on all food dilutions apart from 0.1 SY and under starvation. foxo null mutants are not more sensitive to starvation than wild-type [18241326]. Fly
    Heterzygous Rpd3 null mutation Males heterozygous for a null mutation of Rpd3 have a lifespan extension of 41 - 47%. Females carrying a null mutation have only modest increase in maximum lifespan (but not median lifespan). Longevity increases to the same extent in wild-type under low-calorie diet and rpd3 mutants fed normal diet. DR fails to further increase lifespan of rpd3 mutants [12459580]. Fly +41 to +47
    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
    mdt-15 mutation mdt-15(tm2182) mutation does not affect lifespan on ad libitum, but further increases the lifespan when combined with DR (starting at the 4th day of adulthood) even more as wild-type [22132200]. Worm
    slcf-1 mutation slcf-1 mutation increases average lifespan by 40%. DR (by dilution of bacteria on solid medium or by bacterial deprivation) failes to extend slcf-1 mutant's long lifespan and lifespan is even reduced by lowering bacteria concentration (i.e. higher strength of DR) [21040400]. Worm +40
    nlp-7 mutation Lifespan of nlp-7 mutants increases only moderately by sDR [19783783]. Worm
    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
    unc-51 mutation unc-51(e369) mutation reduces mean but extends maximum lifespan. unc-51(e369) mutation reduces lifespan of eat-2(ad1116) mutants to that of wild-type [18219227]. Worm
    ctbp-1 mutation Genetic inactivation of ctbp-1 results in lifespan extension dependent on daf-16, but independent of sir-2.1. RNAi of lips-7(C09E8.2) suppresses lifespan extension by ctbp-1 inactivation [19164523]. Worm
    Cisd2 knockout Cisd2 knockout shortens lifespan resulting in premature aging [19451219]. Mouse
    aPKC transposition Insertion of a P-based vectors in the structural part of aPKC increase male and female lifespan [22661237]. Fly
    esg transposition Disruption of esg by insertion of the P{GT1} vector 300 bp downstream of its structural part increases male and female lifespan [22661237]. Fly
    BLM mutation BLM mutation cuases Bloom syndrom. Individuals with Bloom syndrome have a shortend life expectancy []. Death is primary due to cancer, particulary leukemia and lymphoma [German, 1992]. Bloom syndrome is not a premature aging disease. Bloom syndrome characteristics are grwoth deficiency, sun-snesitivity, telangiectatic hypo- and hyperpigmented skin, predisposition to malignancy, and chromosomal instability [5770175]. Human
    BRE5 deletion Deletion of BRE5 increases mean replicative lifespan by 30% [16293764] and mean chronological lifespan in diploid cells [21447998] Yeast +30
    Bub1b mutation Bub1b mutation decreases median lifespan by 60% (from 15 to 6 months). Bub1b mutant mice develop many phenotypes suggestive of accelerated aging, including: progressive bilateral cataracts, substantial loss of sub dermal adipose tissue, spinal kyphosis, muscle atrophy, and decreased wound healing. Moreover, there is a pronounced increase in senescent associated Beta-galactosidase expression in late generation Bub1b mutant mice, indicative of increased rate of cellular senscence. Homozyogous knockout of Bub1b results in lethality, while heterozygous animals exhibit no aging phenotypes [15208629]. Mouse -60
    Replacement of Cebpa by Cebpb Replacing the Cebpa gene by Cebpb increases mean lifespan by about 20% [15289464]. C/ebpalpha(beta/beta) animals consume more food but weight less than controls [10982846], and have a slightly elevated body temperature (0.3-0.5 degree Celsius) [15289464]. Mouse +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.