Interventions

  • name effect species mean median maximum
    rrf-1 mutation Although rrf-1(pk1417) mutants seem to have elevated DAF-16 activity (as sod-3 transcript level is increased) the mean and maximum lifespan or ability to withstand elevated temperature is not different from wild-type [22574120]. Worm
    SSN2 deletion Although SSN2 was identified as a potential long-lived mutant strain in a bar-code screen, deletion of SSN2 does not significantly affect chronological lifespan under starvation/extreme DR [20657825]. Yeast
    Heterozygous Gh1 anti-sense transgene Animals carrying a single copy of an anti-sense Gh1 transgene (tg/-) live on average 7-10% longer. tg/- animals are dwarfs and exhibit reduced levels of serum IGF1 [12057928]. Rat +7 to +10
    Homozygous Gh1 anti-sense transgene Animals carrying two copies of a Gh1 anti-sense transgene (tg/tg) have a slighlty shorter lifespan (by 5-10%) compared to -/- animals. tg/tg animals are dwarfs and exhibit reduced levels of serum IGF1 [12057928]. Rat -5 to -10
    Hsp22 transposition Animals that do not express Hsp22 (due to a transposition into its transcriptional starting site) have a 40% decrease in lifespan, exhibit a 30% decrease in locomotor activity and are sensitive to mild stress [20036725]. Fly -40
    PLD alpha antisense Antisense suppression of PLD alpha retards abscisic acid- and ethylene-induced senescence. Leaves detached from PLD alpha-deficient transgenic plants when inbutated in abscisic acid and ethylene exhibit a slower rate of senescence that those from wild-type and transgenic controls. PLD alpha deficient strains are associated with retardation of senescence as evidenced by delayed leaf yellowing, lower ion leakage, greater photosynthetic activity, and higher content of cholorophyl and phospholipids [9437863]. Antisense suppression of PLD alpha does not affect natural plant growth and development [9437863].
    ATG1 deletion ATG1 deletion reduces chronological lifespan by 70% [19302372]. Deletion of ATG1 reduces replicative lifespan by 20% in the alpha strain [18340043]. Yeast -20 to -70
    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
    Bam mutation Bam mutants have an extended lifespan due to germ cell loss. Lifespan of females is on average up to 50% higher and that of males on average s up to 27.8% higher [18434551]. Fly +27.8 to +50
    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
    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
    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
    bra-1 mutation bra-1(nk1) mutation reduces mean lifespan by 6-25% [17900898]. Worm -6 to -25
    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
    bwa mutation bwa (alias Dacer) inactivation increases Drosophila pre-adult development time and anti-oxidative stress capacity. Mean lifespan is increased by 16% in females, by 21% in males and by 19% in total. Maximum lifespan of females, males is also extended by 20 and 12%, respectively [20112046]. Fly +16 to +21 +12 to +20
    C26B2.2 knockout C26B2.2 knockout mutations extend lifespan [15253933]. Worm
    dnc mutation cAMP phosphodiesterase-deficient dunce mutants have an extended maximum lifespan by about 70% [17369827]. Fly +70
    cdc-25.3 knockout cdc-25.3 knockout mutants also display increased thermotolerance and a 40% lifespan extension [16741121]. Worm +40
    Cdk5 mutation Cdk5 loss-of-function mutations result in defective axon guidance, age-dependent behavioral deficits and reduced lifespan by about one third [17368005]. Fly
    cep-1 mutation cep-1 mutants live up to 33% longer. which is dependent upon functional daf-16 [17895432]. Worm +33
    Interventions are an extension of GenAge and GenDR.