| 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 |
| age-1 mutation | Recessive knockout mutants of age-1 have a 40-65% increase in mean lifespan and a 65-110% increase in maximum lifespan [8608934; 8700226]. age-1(mg44) zygotic null mutants have a mean (99%) and maximum (117%) lifespan extension [18828672]. Even in axenic culture lifespan of age-1 is extended up to 100%. age-1 mutation significantly extends lifespan under AL, but only slightly under sDR [16720740].
age-1 mutants are dauer constitutive [8056303] and display lower brood size as well as increased embryonic lethality [9504918]. Additionally, age-1 mutants have elevated levels of superoxidase dismutase and catalase activities [8389142]. | Worm | +99 | — | +117 |
| asg-2 mutation | Knockout mutations in asg-2 result in developmental arrest and increased lifespan [11410594]. | 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 |
| C26B2.2 knockout | C26B2.2 knockout mutations extend lifespan [15253933]. | Worm | — | — | — |
| cha-1 mutation | Mutation of cha-1 extends lifespan on NGM agar covered with killed or live bacteria as well as in liquid culture medium. cha-1(TY1652) mutation extends mean, 75%ile, and maximum lifespan by 23, 29, and 38%. The cha-1(PR1152) allele extends mean, 75%ile, and maximum lifespan by 22-49, 18-25, and 11-21%. Lifespan extension by cha-1 mutation is not abolished by daf-16 RNAi inactivation. eat-2 RNAi shortens the lifespan of cha-1 mutants [22768380]. | Worm | +22 to +49 | — | +11 to +21 |
| 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-1 mutation | Mutations in clk-1 slow down development and extend lifespan by 30%. Mutation of both clk-1 and daf-2 results in nearly 5-fold (500%) increase in lifespan [8638122]. Food restriction by eat-2 mutation does not further extend the long lifespan of clk-1 mutant [9789046]. DR and clk-1 mutations may extend lifespan by a similar process. DR by intermittent fasting (IF) significantly extends lifespan of clk-1 mutants, but to a lesser extent than that of wild-type [19079239]. clk-1 mutants do not respond to sDR-induced lifespan extension [19239417].
clk-1 encodes a enzyme participating in coenzyme Q synthesis [9020081; 11136229]. clk-1 mutants have a decreased pharyngeal pumping and may provoke volunteering DR [9789046]. Mutations in clk-1 are highly pleiotropic resulting in an average lengthing of embryonic development, post-embryonic development, and adult rhythmic behaviours such as defecation, swimming and pharyngeal pumping [7768437]. clk-1 mutant requires coeznyme Q [11136229]. | Worm | +30 | — | — |
| 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 | — | — | — |
| 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 | — | — | — |
| cup-4 mutation | Lifespan of cup-4 mutants increases only moderately by sDR [19783783]. | Worm | — | — | — |
| D1054.8 RNAi | RNA interference of D1054.8 results in lifespan extension [15998808]. | 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 | — | — | — |
| daf-16 mutation | daf-16(m26) mutation slightly, insignificantly decreases lifespan, but completely suppresses lifespan extension of daf-2(e1370) adults [8247153]. daf-16 is required for lifespan extension by mutation of daf-2 or age-1 [8247153]. Mutations in daf-16 suppressed life-extension caused by mutations in daf-2 [8247153]. Loss of function alleles of daf-16 shorten lifespan, but some alleles have lifespan equal to wild-type [8247153]. daf-16 mutation significantly reduces lifespan under AL (-20%), but does not prevent lifespan extension by sDR. In another experiment daf-16 mutation totally suppresses lifespan extension by sDR [16720740]. sDR does not stimulate DAF-16 translocation to the nucleus, but daf-16 mutation cancelled out the ability of sDR to extend lifespan and to delay the decline in locomotor activity [17900900]. DR by bacterial dilution extends lifespan of daf-16 mutants [17538612]. daf-16 mutation decreases lifespan under AL, but fails to prevent bDR to further extend lifespan [18331616]. IF-induced lifespan-extension by either 24h/48h/72h per 4 days is significantly diminished in null mutants of daf-16. All these regimens extend lifespan of daf-16 to a lesser extent than wild-type. daf-16 partially mediates IF-induced longevity [19079239]. Glucose or glycerol does not shorten lifespan of daf-16 mutants [19883616]. daf-16 mutation cancels out the lifespan extension effect of sDR and PD, regardless of the concentration of bacteria or peptones. bDR significantly extends lifespan of daf-16 mutants, but to a lesser extent than that of wild-type. eat-2 mutation extends the lifespan of daf-16 mutants to the same extent than that of wild-type. Resveratrol extends lifespan of daf-16 mutants [19239417]. daf-16 RNAi completely blocks lifespan extension by daf-2 mutation, but only partially by bDR. daf-16 RNAi attenuates protection against oxidative stress by bDR. daf-16 expression is induced by bDR [19924292]. Knockdown of daf-16 decreases mean and maximum lifespan by 50% and 54%, respectively [22509016]. DAF-16 reduces expression of rsks-1 and daf-15 [15253933; 22560223]. daf-16(mu86) mutation decreases mean (44%) and maximum (18%) lifespan [15905404]. daf-16(mgDf47) decreases mean (18-37%) and maximum (29%) lifespan [18828672]. daf-16 mutants are dauer defective [7219552] and completely suppress all the phenotypes of daf-2 and age-1 mutations, including lifespan extension, dauer arrest, reduced fertility, and viability defects [8247153; 7789761; 9504918; 7789761]. Mutations in daf-16 also suppress lifespan extension of animals that have a germ line ablation [10360574]. Sex-specific lifespan potential requires daf-16 [10747056].
daf-16 mutation suppresses enhanced UV resistance as well as increase longevity of daf-2, daf-23, spe-26, and clk-1 mutants. Mutation in daf-16 does not alter the reduced fertility in spe-26. daf-16 mutants are more fertile than wild-type [8807294]. | Worm | -18 to -37 | — | -29 |
| 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 | — | — | — |
| daf-19 mutation | Loss-of-function mutations in daf-19 increase lifespan up to 50% [10617200]. daf-19 mutants are dauer constitutive, dye-filling defective, and lack sensory cilia [7219552; 9475731]. | Worm | +50 | — | — |
| eat-2 mutation | eat-2 mutations result in partial starvation by disrupting the function of the pharynx and an approximately 50% extension of lifespan. eat-2 mutants life significant longer by up to 57% [9789046]. eat-2(ad1116) mutants have an extended mean, 75%ile and maximum lifespan by 30, 35, and 24% [22810224]. sDR further increases the long lifespan of eat-2 mutants [19239417]. eat-2 mutants live longer than wild-type at high food concentration but are short lived at lower concentrations (via bacterial dilution) [19229346]. eat-2(ad1113) mutation increases mean lifespan by 56% and is non-additive with SCNA overexpression [16782295]. Combining eat-2 mutation with bacterial deprivation DR does not result in an additive increase in lifespan [17081160;17096674]. Loss of function of eat-2 extends lifespan by 20-30%. Lifespan extension is proposed to be similar to DR. eat-2;daf-2 double mutant live longer than daf-2 single mutants [9789046]. Therefore, eat-2 mutants can synergize with daf-2 mutants, but not with clk-1 mutants, for lifespan extension. Lifespan extension conferred by eat-2 is not suppressed by daf-16 mutation [9789046].
| Worm | +30 to +57 | — | +24 |
| egl-4 mutation | Mutations in egl-4 extends lifespan by up to 55%. Lifespan extension by mutation of egl-4 is suppressed by daf-16. egl-4 mutation results in normal morphology and development, however egl-4 animals are almost twice as big as normal and have weak eff-laying defects [12571101]. | Worm | +55 | — | — |
GenAge
GenDR
