| 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 |
| aco-2 RNAi | RNA interference of aco-2 leads to lifespan extension [15998808]. | 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 |
| age-1 RNAi | RNAi against age-1 extends lifespan by 30% [8700226; 8608934]. age-1 RNAi increases mean and maximum lifespan by 36-46% and 48-50% [12447374]. RNAi against age-1 increases mean lifespan by 83% [18828672]. age-1(mg44) zygotic null mutants have a mean (99%) and maximum (117%) lifespan extension [18828672]. | Worm | +36 to +99 | — | +48 to +117 |
| akt-1 RNAi | RNA interference of akt-1 leads to lifespan extension [15998808]. | Worm | — | — | — |
| 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 | — | — | — |
| C48E7.2 RNAi | RNA interference of C48E7.2 in adulthood results in a 26% increase in mean lifespan [17521386]. | Worm | +26 | — | — |
| cco-1 RNAi | RNA interference of cco-1 results in a 45-61% increase in mean lifespan (in fer-15; fem-1 and N2 background, respectively) [16103914]. RNAi against cco-1 increases mean and maximum lifespan by 73% and 90%, respectively [12471266]. cco-1 RNAi extends mean and maximum lifespan by 41 and 50%. RNAi of cco-1 during the larval stages is necessary and sufficient for increased lifespan, while only during the adulthood it fails to to extend lifespan. cco-1 RNAi results in reduced pharyngeal pumping, defecation, motility, and body size as well as reduced ATP levels (by 60-80%) and oxygen consumption. daf-16 mutation fails to prevent lifespan extenison by RNAi of cco-1 and mutation of daf-2 further extends the lifespan of cco-1 RNAi animals [12447374]. RNAi of cco-1 only during the adulthood increases mean and 75th %ile lifespan by 22-32 and 16-33%, respectively [22560223]. | Worm | +22 to +73 | — | +50 to +90 |
| 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 | — | — | — |
GenAge
GenDR
