| aak-1 mutation | aak-1 does not appear to be required for the control of lifespan [15574588]. | 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 | — | — | — |
| 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 |
| Activating let-60 mutation | The let-60(n1046gf) activating mutation greatly reduces lifespan of wild-type, weakly suppresses constitutive dauer diapause in daf-2 and age-1 mutants and extends lifespan induced by mutation of daf-2 [16164423]. | Worm | — | — | — |
| 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 | — | — | — |
| 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 | — | — | — |
| 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 |
| bra-1 mutation | bra-1(nk1) mutation reduces mean lifespan by 6-25% [17900898]. | Worm | -6 to -25 | — | — |
| C26B2.2 knockout | C26B2.2 knockout mutations extend lifespan [15253933]. | Worm | — | — | — |
| cdc-25.3 knockout | cdc-25.3 knockout mutants also display increased thermotolerance and a 40% lifespan extension [16741121]. | Worm | +40 | — | — |
| ced-3 mutation | The ced-3(n1286) allele has no effect on lifespan, although the transgenic animals are defective in apoptosis [12136014]. | Worm | — | — | — |
| cep-1 mutation | cep-1 mutants live up to 33% longer. which is dependent upon functional daf-16 [17895432].
| Worm | +33 | — | — |
| 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 | — | — | — |
| Coq7 overexpression | Transgenic overexpression of mouse Coq7 reverts the extended lifespan of clk-1 mutants [11511092]. | 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 | — | — | — |
GenAge
GenDR
