| bec-1 RNAi | bec-1 is required for normal dauer morphogenesis and lifespan extension. Knockdown of bec-1 via RNA interference results in a shortened mean and maximum lifespan by 14 and 5% [12958363]. bec-1 RNAi does not significantly change the lifespan of wild-type, but completely suppresses the longevity phenotype of eat-2 mutation [17912023; 18282106] and prevents lifespan extension by daf-2(e1370) mutation [12958363]. bec-1 RNAi causes the formation of abnormal dauers in a daf-2(e1379) background [12958363]. | Worm | -14 | — | -5 |
| beta-transducin RNAi | beta-transducin RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| bra-1 mutation | bra-1(nk1) mutation reduces mean lifespan by 6-25% [17900898]. | Worm | -6 to -25 | — | — |
| rict-1 RNAi | C. elegans with mutations in the TORC2 complex gene rict-1 (Rictor) grow slowly and have small body size, and live slightly longer than wild-type when maintained on ârichâ food such as the RNAi feeding strain HT115 and at elevuated temperature (25 degree Celsius) [Soukas et al., 2009 in (Robida-Stubbs et al., 2012)]. rict-1 RNAi at 20 degree Celsius in the adulthood increases mean, median, 75th %ile and maximum lifespan by 12-42, 22-29, 13-32 and 28-54%, respectively, dependent on skn-1. daf-16 is not required for lifespan to be increased by rict-1 RNAi, or when TORC1 and TORC2 are blocked by ragc-1;rict-1 RNAi. rict-1 RNAi extends mean, median, 75th %ile and maximum lifespan in the intestine-specific RNA stains VPS288 by 12-18, 19, 13-18 and 16%, respectively [22560223]. | Worm | +12 to +42 | +22 to +42 | +28 to +54 |
| C14A4.11 RNAi | C14A4.11 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| C14A4.14 RNAi | C14A4.14 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| C16C10.2 RNAi | C16C10.2 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| C26B2.2 knockout | C26B2.2 knockout mutations extend lifespan [15253933]. | Worm | — | — | — |
| C47D12.2 RNAi | C47D12.2 RNAi in the adulthood extends mean and maximum lifespan by 6 and 9% [23144747]. | Worm | +5.5 | — | +8.7 |
| C47D12.8 RNAi | C47D12.8 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| C56C10.10 RNAi | C56C10.10 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| cchl-1 RNAi | cchl-1 RNAi extends mean and maximum lifespan by 55% and 57%, respectively. Lifespan extension by RNAi of cchl-1 is not suppressed by daf-16 [12447374].
cchl-1 RNAi animals have lower ATP content and oxygen consumption [12447374]. | Worm | +55 | — | +57 |
| cdc-25.3 knockout | cdc-25.3 knockout mutants also display increased thermotolerance and a 40% lifespan extension [16741121]. | Worm | +40 | — | — |
| cdk-1 RNAi | cdk-1 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| ceh-6 RNAi | ceh-6 RNAi in the adulthood extends the lifespan [New longevity regulators]. | Worm | — | — | — |
| cep-1 mutation | cep-1 mutants live up to 33% longer. which is dependent upon functional daf-16 [17895432].
| Worm | +33 | — | — |
| 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 | — | — |
| chn-1 RNAi | chn-1 RNAi in the adulthood extends mean and maximum lifespan by 7 and 9%, respectively [23144747]. | Worm | +7.1 | — | +8.7 |
| ckr-1 RNAi | ckr-1 RNAi significantly reduces lifespan of eat-2 but not that of age-1 nor clk-1 mutants [19783783]. | Worm | — | — | — |
| ckr-2 RNAi | ckr-2 RNAi significantly reduces the lifespan of eat-2 but not that of age-1 nor clk-1 mutants [19783783]. | Worm | — | — | — |
| 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 | — | — | — |
| ctl-1 mutation | ctl-1 loss of function shortens lifespan to 77% of wild-type animals. ctl-1 mutants accumulate fluorescent material faster than wild-type, indicating accelerated aging [12610632]. ctl-1 mutation prevents lifespan extension by daf-2 or clk-1. Mutation of ctl-1 reudces catalase activty by 50% [10335847].
All these results have been retracted. | Worm | — | — | — |
| cup-4 overexpression | cup-4 overexpession reduces oxidative stress resistance and shortens lifespan of wild-type under AL [19783783]. | Worm | — | — | — |
GenAge
GenDR
