| cnk-1 RNAi | cnk-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| frh-1 RNAi | Complete absence of frataxin is lethal, while its partial deficiency extends animal lifespan in a p53 dependent manner. Frataxin knockdown via RNAi extends mean and maximum lifespan by 19 and 37%, respectively [23247094].
Substantial reduction of frataxin protein expression is required to extend lifespan, affect sensory neurons functionality, remodel lipid metabolism and trigger autophagy. Beclin and p53 genes are required to induce autophagy and concurrently reduce lipid storages and extend animal lifespan in response to frataxin suppression [23247094]. | Worm | +18.75 | — | +37.037037037 |
| csn-5 RNAi | csn-5 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| cup-4 RNAi | cup-4 RNAi reduces oxidative stress resistance and shortens lifespan of wild-type under AL. cup-4 RNAi significantly reduces the extended lifespan of eat-2 mutants, but failed to block lifespan extension of age-1 or clk-1 mutants [19783783]. | Worm | — | — | — |
| cup-5 RNAi | cup-5 RNAi significantly decreases lifespan of eat-2 specifically, whereas lifespan of age-1 or clk-1 mutants are not affected [19783783]. | Worm | — | — | — |
| cyd-1 RNAi | cyd-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| cye-1 RNAi | cye-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| cyn-7 RNAi | cyn-7 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| daf-15 RNAi | daf-15 RNAi only during the adulthood increases mean and 75th %ile lifespan by 7-21 and 8-20%, respectively, which was abolished by either skn-1 or daf-16 mutation (with and without FUdR). daf-15 knockdown dramatically increases stress-tolerance in an skn-1, but not daf-16-dependent manner. Autophagy (measured by LGG-1 puncta) was increased by daf-15 RNAi [22560223]. | Worm | +7 to +21 | — | — |
| cbp-1 RNAi | daf-16 RNAi and cbp-1 RNAi reduce average lifespan under AL to about the same extent. Inhibiting cbp-1 via RNAi by 50%, specifically in adult phase and completely blocks lifespan extension of DD, bDR as well as eat-2, glp-1 and clk-1 mutation, but only partially that of daf-2 mutation and not at all that of cold. cbp-1 RNAi completely blocks the lifespan increase by daf-2 mutation under bDR. cbp-1 RNAi blocks the delay of other age-related pathologies by bDR. cbp-1 RNAi prevents protective effects of bDR and accelerates ABeta42-related pathology. bDR significantly delays onset of paralysis even in presence of cbp-1 RNAi. cbp-1 RNAi specifically in adults completely blocks lifespan extension by three distinct protocols of DR (mutation of eat-2), partly by daf-2 mutation but not of cold and blocks the delay of other age-related pathologies by bDR. cbp-1 RNAi has no effect on lifespan in daf-16 hypomorphic mutants. Combining cbp-1 and daf-16 RNAi in wild-type produces similar lifespan as either alone. Resistance to oxidative stress is strikingly reduced by cbp-1 RNAi and cbp-1 RNAi attenuates the protection against oxidative stress by bDR. cbp-1 RNAi accelerates accumulation of autofluorescence, but has no effect on activity, egg laying, or pharyngeal pumping. cbp-1 RNAi does not block induction of daf-16 or hsf-1 by bDR, but does block the induction of DAF-16 target gene, sod-3, and HSF-1 target gene, sip-1 by bDR. cbp-1 RNAi blocks induction of sod-3 expression by daf-2 RNAi. cbp-1 RNAi does not block the increased Nile Red staining produced by daf-2 mutation, but enhanced Nile Red staining. cbp-1 RNAi blocks the effect of bDR on metabolic gene expression from glycolysis towards beta-oxidation. Drugs that enhance histone acetylation increase lifespan and reduce ABeta42-related pathologies, but these protective effects are completely blocked by cbp-1 RNAi. cbp-1 RNAi decreases H4 Lys 5 acetylation and blocks the extension of lifespan as well as delays the onset of paralysis by ABeta1-42 transgene under AL and bDR by sodium butyrate (NaB) and trichostatin (TSA). cbp-1 RNAi does produce dye-filling defects in all C. elegans amphid neurons (ASI, ADL, ASK, AWB, ASH, and ASJ) [19924292]. | Worm | — | — | — |
| daf-2 mutation | daf-2 mutants live more than twice as long as controls. daf-2(sa189) mutation extends mean and maximum lifespan by 133 and 129%, respectively, when shifted to 20 degree Celsius. The daf-2(e1370) mutation extends mean and maximum lifespan by 32 and 119%, respectively, when shifted to 25 degree Celsius and by 110 and 145%, respectively, at 20 degree Celsius. daf-2(sa189) mutation extends mean lifespan by 67% as well as maximum lifespan [8247153]. This lifespan extension requires the activity of daf-16 [8247153]. The lifespan extension of daf-2(e1370) mutants is cancelled out by daf-16(m26) mutation. daf-2 mutants still exhibit a long lifespan after ablation of the gonad and germ cells. [8247153]. daf-2(e1370) increases mean (95-118%) and maximum (165%) lifespan [18828672]. daf-2 mutation extends lifespan of wild-type and eat-2 mutants [9789046]. Long lifespan of daf-2 insulin receptor mutation is further extended by sDR. However, daf-2 mutation is not a null mutation, therefore it is still possible that part of sDR-induced increase in lifespan might depend on insulin receptor pathway [17900900]. DR by bacterial dilution extends lifespan of daf-2 mutants [17538612]. IF does not markedly extend lifespan of daf-2 mutants [19079239]. 2% glucose reduce fractions of animals that become dauers at 22.5 degree Celsius in daf-2 mutants. Glucose almost completely suppresses lifespan extension of daf-2 ligand binding domain and tyrosine kinase mutants back to wild-type levels [19883616]. daf-2 mutation increases average lifespan by 157%. Under AL daf-2 mutation increases lifespan by 30%. bDR increases lifespan by 65%. daf-2 mutation further increases lifespan under bDR by 40%. Resistance to oxidative stress is reduced daf-2 mutation [19924292]. daf-2(m577) mutation increases mean and maximum lifespan by 33 and 29%, respectively, while daf-2(e1370) mutation increases mean and maximum lifespan by 101 and 181%, respectively [16782295]. DR from eat-2(ad465) mutation has an addative effect on lifespan of daf-2(e1370) adults, but not on lifespan of daf-2(e1368) adults [18043747]. Mutation in daf-2 in combination with mutation of daf-12 results in nearly 300% increase in lifespan [7789761]. daf-2 mutants are dauer constitutive [7219552] and exhibit reduced brood size [9504918; 9725835]. daf-2 mutants synergize with germ line ablation for lifespan extension [10360574] and also exhibit synergy with clk-1 mutation for lifespan prolongation [8638122]. All the phenotypes of daf-2 mutants are suppressed by mutation of daf-16 [8247153; 8601482; 7789761; 9725835; 9504918]. Mutation of daf-2 increases expression of sod-3 [10428762]. daf-2(e1370) increases mean lifespan by 146% [23097426].
| Worm | +32 to +146 | — | +119 to +165 |
| dcn-1 RNAi | dcn-1 RNAi in the adulthood extends the lifespan [23144747]. | Worm | — | — | — |
| dcn-1 RNAi | dcn-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| dcp-66 RNAi | dcp-66 RNAi shortens the mean lifespan by 29% and suppresses lifespan extension by isp-1 mutation, but does not significantly affect lifespan extension neither by eat-2 nor daf-2 mutation [22829775]. | Worm | -29 | — | — |
| dct-11 RNAi | dct-11 stimulates the growth of gld-1 tumors. RNA interference of dct-11 increases mean lifespan up to 19% in a gld-1 mutant background and reduces mean lifespan by 10% in a wild-type background [17934462]. | Worm | -10 | — | — |
| dct-12 RNAi | dct-12 appears to stimulate the growth of gld-1 tumours. RNA interference of dct-12 increases mean lifespan by 14% in wild-type animals, 16% in daf-16 mutants and 12% in gld-1 mutants [17934462]. | Worm | +14 | — | — |
| dct-13 RNAi | dct-13 appears to stimulate the growth of gld-1 tumours. RNA interference of dct-13 increases mean lifespan by 23% and maximum lifespan by 20% in wild-type animals. It also increases mean lifespan by 21% in daf-16 mutants and 13% in gld-1 mutants [17934462]. | Worm | +23 | — | +20 |
| dct-14 RNAi | dct-14 appears to stimulate the growth of gld-1 tumours. RNA interference increases mean lifespan by 19% in wild-type animals, 21% in daf-16 mutants and 13% in gld-1 mutants [17934462]. | Worm | +19 | — | — |
| dct-15 RNAi | dct-15 appears to stimulate the growth of gld-1 tumours. RNA interference of dct-15 increases mean lifespan up to 10% in wild-type animals and 9% in gld-1 mutants [17934462]. | Worm | +10 | — | — |
| dct-18 RNAi | dct-18 stimulates the growth of gld-1 tumors. RNA interference of dc-18 increases mean lifespan up to 12% in a gld-1 mutant background and reduces mean lifespan by 8% in wild-type worms [17934462]. | Worm | — | — | — |
| scl-1 RNAi | Downregulation of scl-1 by RNAi reduces slightly but reproducibly lifespan as well as stress resistance, similar to the effect of mutation in daf-16. scl-1 RNAi prevents lifespan extension associated with mutation of daf-2 or age-1 [12620193].
RNAi of scl-1 causes hat shock and UV sensitivity [12620193]. | Worm | — | — | — |
| dpy-22 RNAi | dpy-22 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| dpy-27 RNAi | dpy-27 RNAi in the adulthood shortens mean and maximum lifespan by 24 and 25%, respectively [23144747]. | Worm | -23.5 | — | -25.0 |
| drs-1 RNAi | drs-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| dve-1 RNAi | dve-1 RNAi attenuates lifespan extension by bDR, but only partially that of daf-2 mutation. dve-1 RNAi attenuates protection against oxidative stress by bDR [19924292]. | Worm | — | — | — |
GenAge
GenDR
