| wwp-1 RNAi | RNA interference of wwp-1 decreases median lifespan by 9% in wild-type animals and 24% in daf-2 mutants [18006689]. Loss of wwp-1 function by RNAi reduces lifespan at 25 degree Celsius, but not 20 degree Celsius. Reduced levels of wwp-1 completely suppress the extended longevity of eat-2 mutants. wwp-1 RNAi does not suppress the extended lifespan of isp-1 mutants and has only minor suppressive effects on lifespan of another mitochondrial mutant, clk-1, and in cyc-1 RNAi treated worms. RNAi depletion of wwp-1 has no effect on long lifespan of daf-2 mutants [19553937].
| Worm | — | -9 | — |
| wwp-1 mutation | Loss of wwp-1 function by mutation reduces lifespan at 25 degree Celsius, but not 20 degree Celsius. Lifespan of wwp-1 mutants across entire food concentration range by bacterial dilution in liquid culture or on solid plates does not noticeable change. Reduced levels of wwp-1 completely suppress the extended longevity of eat-2 mutants [19553937].
| Worm | — | -9 | — |
| glp-1 mutation | glp-1(qu158) mutations result in defects in germ-line proliferation and extension of lifespan by about 30%, which requires daf-16 [11799246]. glp-1(bn18) mutation increases mean, median, 75th %ile and maximum lifespan by 27-37, 26-33, 24-29 and 35%, respectively [22560223]. glp-1(e2141) mutation increases mean (32%) and maximum (53%) lifespan [18828672]. Two alleles of glp-1 that cause overproliferation of gemrline cells, glp-1(oz112gf) and glp-1(q485), result in a shortened lifespan [11799246]. In glp-1 mutants, Z2 and Z3 generate only a few germ cells, which enter meiosis and differentiate as sperm [3677168]. | Worm | +27 to +37 | +26 to +33 | +35 |
| 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 | — | — | — |
| 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 |
| hcf-1 mutation | hcf-1 inactivation by mutation cause a daf-16-dependent lifespan extension of up to 40% and heightened resistance to specific stimuli [18828672].
HCF-1 forms a complex with DAF-16. hcf-1 inactivation by mutation cause a daf-16-dependent lifespan extension of up to 40% and heightened resistance to specific stimuli. The hcf-1(ok559) mutation increases mean and maximum lifespan by 10-37 and 29%, while the strong hcf-1(pk924) mutation extends mean and maximum lifespan by 29-31 and 53-88%, respectively. In the absence of hcf-1 there is a greater enrichment of DAF-16 at its target gene promoters and more robust DAF-16-mediated regulation of selective transcriptional targets. hcf-1 mutation extends lifespan of glp-1(e2141) mutants which lack germline cells, [18828672]. | Worm | +10 to +37 | — | +29 to +88 |
| shc-1 knockout | Loss of shc-1 function results in accelerated aging and enhanced senstivity ro heat, oxidative stress and heavy metals. | Worm | — | — | — |
| 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 | — | — | — |
| 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 | — | — |
| 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 | — | — | — |
| 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 |
| 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 | — | — |
| 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-2 mutation | Mutations in clk-2 slow down development and extend lifespan by 12-25% (at 20 degree Celsius in Bristol N2). clk-2 mutation slows growth and rhythms similar to clk-1. Mutation in clk-2 is embryonic lethal at 25 degree Celsius and results in some lethality at all temperatures [8638122]. clk-2 encodes a protein involved in DNA repair and perhaps telomere maintenance [14-16 in (Lee et al., 2003)]. clk-2 mutation affects telomere length and might result in shorter [11696330] or longer telomeres [11747819]. clk-2 overexpression may shorten telomeres [11747819]. | Worm | — | — | — |
| 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 | — | — | — |
| daf-1 mutation | daf-1(mk40) mutation increases mean lifespan by 18-46% and maximum lifespan by 29% [17900898]. The daf-1(m40) allele has no effect on lifespan and fails to prevent lifespan extension by sir-2.1 overexpression, but it results in a temperautre-sensitive, dauer-constitutive phenotype in larvae [11242085]. | Worm | +18 to +46 | — | +29 |
| daf-10 mutation | Loss of function mutation in daf-10 increases lifespan by 60% (in Bristol N2) [10617200]. daf-10 mutants are dauer defective, dye filling defective, octopamine deficient and have abnormal chemotaxis and osmotic avoidance. Mutants in daf-10 display abnormal sensory anatomy, especially amophidial neurons and sheath cells, and cephalic neurons. daf-10 mutant males do not mate [2428682]. | Worm | +60 | — | — |
| daf-12 mutation | Mutations in daf-2 and daf-12, but not mutations in daf-12 alone, nearly quadruples lifespan [7789761]. Recessive loss of function mutation in daf-12 shortens lifespan. daf-12 activity is required for lifespan extension after germ line ablation [10360574]. daf-12 mutation suppresses the lifespan extension by mutation in daf-28 [8807293]. daf-12 mutants are dauer defective and heterochronic [7219552]. Some daf-12 alleles exhibit synthetic lethality with mutation of age-1 [8807293] or daf-12 [1732156]. | Worm | — | — | — |
| hsb-1 mutation | hsb-1(cg116) mutation at 20 degree Celsius extends mean, 75%ile, and maximum lifespan by 57-60%, 52-59%, and 37-69%.
| Worm | +57 to +60 | — | +37 to +69 |
| daf-18 mutation | daf-18 is required for complete dauer formation. daf-18 mutation partially suppresses the lifespan extension of age-1 and daf-2 mutants. daf-18 mutants are defective for dauer formation and form some dauer-like larvae when starved [7789761; 8601482]. | Worm | — | — | — |
GenAge
GenDR
