| BUL1 deletion | Deletion of BUL1 does non-significantly reduces mean chronological lifespan under starvation/extreme DR [20657825]. | Yeast | — | — | — |
| 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 | — | — |
| CAT5 deletion | Deletion of CAT5 decreases chronological lifespan by up to 50% [17492370] and also decreases replicative lifespan by 30% in the alpha strain [18340043]. | Yeast | -30 to -50 | — | — |
| 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 |
| CCR4 deletion | Deletion of CCR4 increases mean chronological lifespan by 20 - 41% (20, 33, 41) in diploid cells [21447998]. In W303R CCR4 deletion shortens replicative lifespan by approximately 80% and results in temperature sensitivity that is suppressed by SSD1-V. SSD1-V partially suppresses the short-lifespan of ccr4 mutant. CCR4 mutation is synthetically lethal in combination with deletion of MPT5 in the absence of SSD1-V [11805047]. | Yeast | -80 to +20 | — | — |
| CCS1 deletion | Deletion of CCS1 reduces replicative lifespan by 50% [17460215]. | Yeast | -50 | — | — |
| Cdkn1a knockout | Deletion of Cdkna1 (alias p21) prolongs the lifespan of telomerase-deficient mice with dysfunctional telomeres and improves the repopulation capacity and self-renewal of hematopoietic stem cells [17143283].
The p21(-/-) strains like the Cdkn1a(tmi/Tyj) exhibits enormous regenerative capacities as it closes ear holes similar to MRL mice [20231440; 21722344]. | Mouse | — | — | — |
| 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 | — | — |
| CHL1 deletion | CHL1 deletion mutant exhibits a shortened mean and maximum lifespan by 36 and 29%, respectively, as well as hypersensitivity to heat stress. CHL1 may modulate transcriptional silencing in the presence of Sir proteins [16182251]. | Yeast | -36 | — | -29 |
| Cisd2 knockout | Cisd2 knockout shortens lifespan resulting in premature aging [19451219]. | Mouse | — | — | — |
| CIT2 deletion | Deletion of CIT2 has no effect on replicative lifespan [10224252]. | Yeast | — | — | — |
| CKA2 deletion | CKA2 deletion approximately doubles mean chronological lifespan under starvation/extreme DR in BY4741 also increases as well as as heat-shock resistance in SDC medium in the W303-1A and DBY746 genetic backgrounds [20657825]. | Yeast | — | — | — |
| CKB2 deletion | Lack of Ckb2 promotes a modest but significant chronological lifespan extension and marked increase in yeat resistance [20657825]. | Yeast | — | — | — |
| CLA4 deletion | Deletion of CLA4 decreases replicative lifespan by 60% in the alpha strain [18340043; 19030232]. | Yeast | -60 | — | — |
| 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 | — | — | — |
| COQ3 deletion | Deletion of COQ3 decreases chronological lifespan and renders cells respiratory deficient and sensitive to hydrogen peroxide [12586694]. | Yeast | — | — | — |
| Coq7 knockout | Mice heterozygous in Coq7 live about 15 to 30% longer than controls [16195414]. | Mouse | +15 to +30 | — | — |
| CPR7 deletion | Deletion of CPR7 has no effect on lifespan replicative lifespan, but increases chronological lifespan [11361336] | Yeast | — | — | — |
GenAge
GenDR
