| 272N18 Treatment | 272N18 (3-(3-nitrophenyl)-11-phenyl-2,3,4,5,10,11-hexohydro-1H-dibenzo[b,e] [1,4]diazepin-1-one dihdrochloride) increases lifespan by 20%, bears a structural resemblance to certain human antidepressants that affect signalling by the neurotransmitter serotonin. | Worm | — | — | — |
| aak-2 constitutive active mutation | A constitutive active mutation of aak-2 is sufficient to cause increase stress resistance as well as to significantly extend lifespan. Both increased stress resistance and extended lifespan is reverted in daf-16 knockdown by RNAi [17900900]. | Worm | — | — | — |
| lin-14 gain-of-function mutation | A gain-of-function mutation in lin-14 decreases lifespan [16373574]. | Worm | — | — | — |
| lin-14 loss-of-function mutation | A loss-of-function mutation in lin-14 extends lifespan by 31% [16373574]. lin-14(n719) mutation extends mean and maximum lifespan of control animals by 20 and 67%, respectively [23097426].
The life-extending effects is dependent on daf-16 and hsf-1 [16373574]. Inactivation of lin-14 does not increase the lifespan of pash-1 mutants [23097426].
| Worm | +20 to +31 | — | +67 |
| isp-1 mutation | A missense mutation in isp-1 leads to low oxygen consumption, decreased sensitivity to reactive oxygen species, and increased mean (60%) and maximum (100%) lifespan. An isp-1;daf-2 double mutant has a lifespan that is longer than either single mutant, but the lifespan extension of the double mutant is not addative relative to each single mutant [11709184]. | Worm | +60 | — | +100 |
| hsf-1 mutation | A mutant allele of hsf-1 slightly decreases lifespan under AL, but cancels out the lifespan extension effect of bDR. hsf-1 RNAi also prevents lifespan extension by bDR. Glucose or glycerol does not shorten the lifespan of hsf-1 mutants. Glucose treatment completely suppresses the long lifespan caused by hsf-1 overexpression [19883616]. sDR extends the lifespan of hsf-1 mutant with a premature stop codon, that eliminates activation domain, and that of wild-type to a similar extent [19239417]. | Worm | — | — | — |
| nrh-49 mutation | A mutant allele, nhr(nr2041) results in a short lifespan. nhr-49 mutant animals accumulate fat, due to decreased expression of enzymes involved in fatty acid beta-oxidation [15719061]. | Worm | — | — | — |
| lars-2 mutation | A mutation that impairs mitochondrial function was associated with a longer lifespan. Mutation of lrs-2/lars-2(mg312) extends lifespan and is associated with impaired mitochondrial function. The recessive allele mg312 of lars-2 extends lifespan by 200% at 20 degree Celsius and 30% at 25 degree Celsius. Lifespan extension by mg312 was not dependent on daf-16(mgDf47). Homozygous lars-2(mg312) worms had multiple pleotropies like lower rates of growth, pumping and defecation as well as remain the size of early L4 worms and are sterile, with an arrested gonad that exhibited no germ-cell differentiation lars-2 is ubiquitously express, with prominent expression in body-wall muscle and neurons, with a mitochondrial subcellular localisation. Mitochondria of lars-2 are noticeably disorganized, swollen and sometimes fused. lars-2 animals have lower ATP content and oxygen consumption [12447374]. | Worm | +30 to +200 | — | — |
| wrn-1 mutation | A nonfunctional wrn-1 DNA helicase decreases the lifespan [23075628].
The expression of miR-124 in whole wrn-1 mutant worms is significantly reduced [23075628].
Supplementation of vitamin C normalizes the median lifespan of wnr-1 and mir-124 mutants [23075628]. | Worm | — | — | — |
| ATP2 Mutation | A temperature sensitive allele of ATP2 causes a clonal senescence phenotype resulting from the disruption of the age asymmetry between mother and daughter cells in that that daughter cells are born as old as they mother cells at 36 degree Celsius. This Mutation of valine to isoleucine at amino acid 90 does not affect growth on non-fermentable carbon source. This allele is associated with loss of mitochondrial membrane potential as well as failure to segregate functional mitochondria to daughter cells [12242224]. | Worm | — | — | — |
| aak-1 mutation | aak-1 does not appear to be required for the control of lifespan [15574588]. | 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 |
| abce-1 RNAi | abce-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| abi-1 RNAi | abi-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| Germ-cell precursor ablation | Ablation of the germ-cell precursor, Z2 and Z3 as well as the precursors of the somatic gonad, Z1 and Z4 does not affect lifespan [8247153]. | Worm | — | — | — |
| Phloridzin treatment | Administration of the apple polyphenol phloridzin at doses of 3, 10, and 30 microMolar siginificantly prolongs the replicative lifespan in K6001 strain (p < 0.01; p < 0.001). Phloridizin improves the viability of cells under oxidative stress (7 microMolar H2O2) in a dose-dependent manner and increases the significantly the expression of SOD1, SOD2, and SIR2 [21597195]. | Worm | — | — | — |
| alg-1 RNAi | Adult-specific knockdown of the C. elegans argonaute-like gene 1 *alg-1* results in shortened lifespan with a reduction in the mean and maximum lifespan by 9 - 16% and 14%, respectively [21810936]. | Worm | -9.6 to -16.1 | — | -13.7 |
| 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 | — | — | — |
| aph-2 RNAi | aph-2 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| apr-1 RNAi | apr-1 RNAi in the adulthood extends the lifespan [99999999]. | Worm | — | — | — |
| aps-1 RNAi | aps-1 RNAi in the adulthood extends mean lifespan by 8% without any apparent effect on maximum lifespan [23144747]. | Worm | +7.9 | — | 0 |
| asb-1 RNAi | asb-1 RNAi in the adulthood extends the mean lifespan by 7% without changing the maximum lifespan [23144747]. | Worm | +6.4 | — | 0 |
| B0280.9 RNAi | B0280.9 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| B0393.6 RNAi | B0393.6 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| 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 |
GenAge
GenDR
