Interventions

  • Species: + -
  • name effect species mean median maximum
    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
    pdk-1 mutation Loss-of-function alleles in pdk-1 extend lifespan by 60% [10364160]. pdk-1(sa680) mutants are dauer constitutive (suppressed by daf-16) [10364160]. Worm +60
    trx-1 mutation Mutants with a deletion in the trx-1 gene display a decrease in lifespan and are sensitive to oxidative stress [16324156]. trx-1 null mutant display reduced mean and maximum lifespan. trx-1 deletion completely suppresses the lifespan extension caused by eat-2 mutation, but only partially suppresses that by daf-2 or osm-5 mutations [16387300]. Worm
    pept-2 mutation Deletion of pept-1 (alias opt-2 or pep-2) results in retarded development, reduced body size and extended reproductive lifespan. It also further extends (60%) the life-extension caused by daf-2 mutations [15155758]. pept-2 mutants exhibit a decrease in fat content. 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
    pgl-1 mutation pgl-1(bn101) mutant animals that are sterile have a approximately 35% longer lifespan. In contrast, fertile pgl-1(bn101) animals have a wild-type lifespan [11799246]. PGL-1 is required for fertility and proliferation of germ line cells [9741628]. Worm +35
    asg-2 mutation Knockout mutations in asg-2 result in developmental arrest and increased lifespan [11410594]. Worm
    aak-2 mutation aak-2(ok524) knockout mutants have a 12% and 18% shorter mean and maximum lifespan, respectively as well as faster age-dependent accumulation of a lipofuscin-like fluorescent pigment in the intestine [15574588]. aak-2 mutation suppresses lifespan extension and delay of the decline in locomotor activity resulting from sDR [17900900]. aak-2 mutation cancels out the lifespan extension effect of sDR and PD, regardless of the concentration of bacteria or peptones. bDR significantly extends lifespan of aak-2 mutants, but to lesser extent than that of wild-type. eat-2 mutation extends the lifespan of aak-2 mutants to the same extent than that of wild-type. Resveratrol does not increase lifespan of aak-2 mutants [19239417]. daf-2(m577);aak-2(ok524) double mutant has a lifespan that is indistinguishable from those of aak-2(ok524) single mutant [15574588]. Worm -12 -18
    cup-4 mutation Lifespan of cup-4 mutants increases only moderately by sDR [19783783]. Worm
    nlp-7 mutation Lifespan of nlp-7 mutants increases only moderately by sDR [19783783]. Worm
    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
    C26B2.2 knockout C26B2.2 knockout mutations extend lifespan [15253933]. Worm
    ife-2 mutation Loss-of-function mutation in ife-2 reduces protein synthesis and increases maximum lifespan by about 20%. It does not extend the lifespan of daf-16(RNAi) animals. TOR/let-373 RNA interference further extends lifespan of ife-2 mutants. Reduction of protein synthesis increases ATP availability and stress resistance [17266679]. Worm +20
    cdc-25.3 knockout cdc-25.3 knockout mutants also display increased thermotolerance and a 40% lifespan extension [16741121]. Worm +40
    ced-3 mutation The ced-3(n1286) allele has no effect on lifespan, although the transgenic animals are defective in apoptosis [12136014]. Worm
    cep-1 mutation cep-1 mutants live up to 33% longer. which is dependent upon functional daf-16 [17895432]. Worm +33
    che-11 mutation Loss-of-function muation in che-11 increases lifespan up to 40% (in Bristol N2) [10617200]. che-11 mutants are dye filling defective, defective in osmotic avoidance and dauer formation, and have irregular amphid cilia [2428682]. Worm +40
    che-13 mutation Loss-of-function mutation in che-13 increases lifespan up to 40% (in Bristol N2) [10617200]. che-13 Mutants are dye filling defective, have severely shortened axonemes and ectopic assembly of ciliary structures and microtubules in many sensory neurons as well as are defective in osmotic avoidance and dauer defective [2428682]. Worm +40
    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
    nhr-62 Mutation Mutation in *nhr-62* suppresses the lifespan extension of eat-2(ad465) animals (p<0.001) [Heestand et al. 2013]. Worm
    che-2 mutation Loss-of-function in che-3 extends lifespan by 50-100% depending on the allele, but life-extension is suppressed by daf-16 (in Bristol N2) [10617200]. che-3 mutations have defective sensory neurons [2428682; 10508861] and are defective in dye filling [2428682; 7705621] as well as dauer defective [1732156]. Worm +50 to +100
    clk-3 mutation Mutations in clk-3 slow down development and extend adult lifespan (at 20 degree Celsius in Bristol N2). clk-3 mutation slows growth and rhythms similiar to clk-1a and profounds maternal and zygotic rescue [8638122]. Worm
    spe-10 mutation Mutation of spe-10 results in a 20% increase in mean lifespan on solid media [2744235]. spe-10 mutants have a temperature sensitive defect in sperm development and their lifespan correlates with thermoterance and UV resistance [2744235]. Worm +20
    hsp-12.6 mutation hsp-12.6 loss-of-function mutation significantly extends lifespan under AL and significantly suppresses intermittent fasting (IF)-induced increase in lifespan, to a similar extend to that of daf-16 mutation. The extent of IF-induced longevity in daf-16 hsp-12.6 double mutant is similar to that of single hsp-12.6 or daf-16 mutants. hsp-12.6 and daf-16 function in same signaling pathway [19079239]. Worm
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    • 25 of 160 interventions
    Interventions are an extension of GenAge and GenDR.