| unc-15 mutation | Mutation of unc-15 has no effect on lifespan [9789046].
Some alleles of un-15 display severe paralysis [4366476; 2051482]. | Worm | — | — | — |
| unc-13 mutation | Mutation in unc-13 results in a 150% life-extension in males, but has no effect on hermaphrodite lifespan [10747056]. | Worm | +150 | — | — |
| unc-10 mutation | Mutation in unc-10 reduces maximum lifespan 35% [17592521]. | Worm | — | — | -35 |
| unc-1 mutation | Mutation in unc-1 has no effect on lifespan [9789046] | Worm | — | — | — |
| ubc-18 mutation | Loss of ubc-18 function by mutation reduces lifespan at 25 degree Celsius, but only slightly at 20 degree Celsius [19553937]. | Worm | — | — | — |
| tub-1 mutation | Mutation of tub-1 (alleles nr2004 and nr2044) leads to 20-25% life-extension dependent on daf-16 [16054097].
tub-1 mutation promotes increased fat accumulation [16054097]. | Worm | +20 to +25 | — | — |
| 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 | — | — | — |
| tdp-1 mutation | tdp-1(ok803) mutation increases mean and maximum lifespan at 20 degree Celsius but not at 25 degree Celsius. tdp-1(ok803) reduce the lifespan of daf-2(e1370) mutants, but does not does not reduces the lifespan of daf-16(mu86) mutants [Vaccaro et al. 2012]. | Worm | — | — | — |
| tax-4 mutation | Recessive loss-of-function allele in tax-4 can increase lifespan by up to 100%. Lifespan extension by tax-4 mutation is suppressed by daf-16 and gonad ablation [10617200].
tax-4 mutants are thermotaxis and chemotaxis defective [8893027; 8348618]. Mutants are slighlty dauer constitutive and form dauers at 27 degree Celsius [9486798]. | Worm | +100 | — | — |
| tax-2 mutation | Loss of function mutation in tax-2 has no effect on lifespan [10617200].
tax-2 mutants are defective in chemotaxis, thermotaxis, odorant defect and have some dye-filling defects [8893026] as well as are exhibit some defects in dauer formation [10064800]. | Worm | — | — | — |
| spe-26 mutation | spe-26 mutation in both hermaphrodites and mated males renders them defective in spermatogenesis and increases mean lifespan by about 65%. In hermaprodites spe-26(hc138ts) mutation increases mean and maximum lifespan by 46 and 29%, respectively. Mating does not reduce lifespan in male with spe-26 mutation. Animals with a different spe-26 allele, it118ts, have a similar increase in mean lifespan both in mated males and mated hermaphrodites. Mating even increases spe-26 mutant male lifespan, although the increase is slight (16% increase in mean and 13% increase in maximum lifspan. While compared to wild-type mated spe-26 males have an increase in mean and maximum lifespan of 81 and 63%, respectively, in comparison to wild-type [1448167]. spe-26 loss of function mutation extends lifespan [8807294]. | Worm | +46 to +81 | — | +29 to +63 |
| 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 | — | — |
| SNCA overexpression | Transgenic lines overexpressing either human wild-type or mutant (A53T) forms of the SNCA (alpha-synclein) gene under a pan-neuronal promoter live on average about 25% longer, even in weak (m577) and strong (e1370) daf-2 mutant backgrounds, and exhibited decreased pharyngeal pumping and egg-laying. Wild-type SNCA crossed into eat-2(ad1113) does not significantly effect lifespan compared to that of the background strain. Pumping rate in wild-type SCNA and A53T SCNA overexpression mutants were less than control already at day 1 of adulthood. The attenuation of lifespan exptesion by SNCA overexpression by growing on thick bacterial lawns, suggests that DR may explain some fo the effects on lifespan. SCNA overexpression increases average lifespan by 21.3% (wild-type) and 16.3% (A53T) [16782295]. | Worm | +26 to +34 | — | +19 to +31 |
| smk-1 mutation | Loss of smk-1 by temperature sensitive allele suppresses the extended lifespan under optimal bDR, but not the response to DR itself [17476212]. | Worm | — | — | — |
| smk-1 mutation | Loss of smk-1 by temperature sensitive allele suppresses the extended lifespan under optimal bDR, but not the response to DR itself [17476212]. | 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 | — | — |
| skn-1 mutation | skn-1 mutation does not alter lifespan under AL, but cancels out the lifespan extension effect of lDR or food variation at all. Response to lDR in skn-1 mutant is restored by ectopic expression of skn-1 in ASI neurons and gut. Ectopic expression of skn-1b in ASI neurons rescued lDR longevity defects of skn-1. lDR worms exhibit elevated respiration, which is absent in skn-1 mutants. skn-1 is necessary for increased respiration and the increase in respiration is necessary for lDR longevity effect, because two different inhibitors of mitochondrial electron transport chain complex III, myxothiazol and antimycin, suppress lDR longevity without shortening lifespan under AL. IF significantly extends lifespan of skn-1 mutants [19079239]. sDR extends lifespan of a skn-1 loss-of-function mutant (which displays a premature stop codon in all three isoforms) and wild-type to a similar extent [19239417]. skn-1(zu67) mutation decreases mean, median, and maximum lifespan by 11-23, 13-28 and 12-23%, respectively, and totally cancels out lifespan extension by ragc-1 RNAi [22560223]. | Worm | -11 to -23 | -13 to -28 | -12 to -23 |
| sir-2.1 deletion | sir-2.1 deletion slightly reduces lifespan of wild-type [16860373]. sir-2.1 suppresses longevity of unc-13 and eat-2, but not daf-2 or unc-64 mutants [16860373]. sir-2.1 is therefore partially required for lifespan extension from mutation of eat-2 [16860373], but is completely independent for lifespan extension from DR using a reduced feeding protocol [Kaeberlein et al. in press]. sDR increases lifespan of wild-type and sir-2.1 mutants to the same extent [19239417]. | Worm | — | — | — |
| shk-1 mutation | Mutation of shk-1 extends lifespan on NGM agar covered with killed or live bacteria as well as in liquid culture medium. shk-1(RB1392) mutation extends mean, 75%ile, and maximum lifespan by 19-22, 19-21, and 20-24%. Lifespan extension by unc-17 mutation is totally abolished by RNAi inactivation of either daf-16 or skn-1. eat-2 RNAi shortens the lifespan of shk-1 mutants [22768380].
Mutation of shk-1 enhances pheromone-induced dauer formation [22768380]. | Worm | +19 to 22 | — | +20 to 24 |
| shc-1 knockout | Loss of shc-1 function results in accelerated aging and enhanced senstivity ro heat, oxidative stress and heavy metals. | Worm | — | — | — |
| rsks-1 mutation | rsks-1 deletion mutants also live longer. TOR RNA interference further extends lifespan of rsks-1 mutants [17266679]. | Worm | — | — | — |
| 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 | — | — | — |
| pyk-1 mutation | pyk-1(ok1754) mutation extends the lifespan and this effect is non-additive with the lifespan extension mediated by DDS treatment [20974969]. | Worm | — | — | — |
| PIB1 deletion | Deletion of PIB1 increases replicative lifespan by 25% in the alpha strain [16293764; 19030232]. | Worm | +25 | — | — |
| pha-4 mutation | Mutants of pha-4 do not respond to bacterial DR. Therefore, loss of pha-4 completely blocks the response to varying food concentration. Reduction of pha-4 does not suppress the long lifespan of daf-2 mutants or animals with defective electron transport chain [17476212]. IF significantly extends lifespan of pha-4 [19079239]. sDR extends lifespan of mutants with a temperature sensitive allele of pha-4, but not daf-16 RNAi [19239417].
| Worm | — | — | — |
GenAge
GenDR
