|nhr-62 Mutation ||Mutation in *nhr-62* suppresses the lifespan extension of eat-2(ad465) animals (p<0.001) [Heestand et al. 2013]. ||Worm ||— ||— ||— |
|mrpl-37 RNAi ||Knockdown of mrpl-37 increases lifespan by 41% . ||Worm ||+41 ||— ||— |
|mrpl-2 RNAi ||Knockdown of mrpl-2 increases lifespan by 54% . ||Worm ||+54 ||— ||— |
|mrpl-1 RNAi ||Knockdown of mrpl-1 increases lifespan by 57% . ||Worm ||+57 ||— ||— |
|ttl-9 RNAi ||Knockdown of ttl-9 throughout the entire life increases the lifespan by 3% . ||Worm ||+3 ||— ||— |
|nkcc-1 RNAi ||Knockdown of nkcc-1 throughout the entire life increases the lifespan by 23% . ||Worm ||+23 ||— ||— |
|mrps-5 RNAi ||Knockdown of mrps-5 throughout the entire life increases the lifespan by 60%. mrps-5 RNAi prevents aging-associated functional decline and alters mitochondrial function. Knocking down mrps-5 after early development no longer affects nematode lifespan. When RNAi of mrps-5 was performed during the larval stages only, lifespan increases by 48%, whereas RNAi started from the L4 stage has no effect. mrps-5 RNAi results in fragmented mitochondria. mrps-5 RNAi increases lifespan by 40% in widltype, 37% in daf-16(mu86), 40% in sir-2.1(ok434) 69% in aak-2(ok524) and 112% in mev-1(kn1). Knockdown of cco-1 does not extend the lifespan of mrps-5 RNAi . ||Worm ||+60 ||— ||— |
|frh-1 RNAi ||Complete absence of frataxin is lethal, while its partial deficiency extends animal lifespan in a p53 dependent manner. Frataxin knockdown via RNAi extends mean and maximum lifespan by 19 and 37%, respectively .
Substantial reduction of frataxin protein expression is required to extend lifespan, affect sensory neurons functionality, remodel lipid metabolism and trigger autophagy. Beclin and p53 genes are required to induce autophagy and concurrently reduce lipid storages and extend animal lifespan in response to frataxin suppression . ||Worm ||+18.75 ||— ||+37.037037037 |
|wrn-1 mutation ||A nonfunctional wrn-1 DNA helicase decreases the lifespan .
The expression of miR-124 in whole wrn-1 mutant worms is significantly reduced .
Supplementation of vitamin C normalizes the median lifespan of wnr-1 and mir-124 mutants . ||Worm ||— ||— ||— |
|wrn-1 RNAi ||RNAi kockdown of wrn-1 shortens the lifespan, increases sensitivity to DNA damage, and accelerates aging phenoypes . ||Worm ||— ||— ||— |
|mir-124 mutation ||Loss of mir-124 increases reactive oxygen species formation and accumulation of the aging marker lipofuscin, reduces whole body ATP levels and results in reduction in lifespan .
Supplementation of vitamin C normalizes the reduced median lifespan of mir-124 mutants . ||Worm ||— ||— ||— |
|mir-80 mir-227(nDf53); mir-81-82(nDf54) ||mir-80 mir-227(nDf53); mir-81-82(nDf54) mutation decreases the mean lifespan by 20% . ||Worm ||-20 ||— ||— |
|mir-64-66 mir-229(nDf63) mutation ||mir-64-66 mir-229(nDf63) mutation decreases the lifespan by 30% . ||Worm ||-30 ||— ||— |
|mir-61 mir-250(nDf59) mutation ||mir-61 mir-250(nDf59) mutation decreases the mean lifespan by 25% . ||Worm ||-25 ||— ||— |
|mir-58 mutation ||mir-58(n4640) mutation decreases the mean lifespan by 20% . ||Worm ||-20 ||— ||— |
|mir-14 mutation ||Mutating mir-14 decreases lifespan in both sexes. mir-14 reduces the mean and maximum lifespan of females by 55 and 36%, respectively, while those of males is reduced by 29 and 21%, respectively . ||Worm ||-29 to -55 ||— ||-21 to -29 |
|mir-239 mutation ||Mutating mir-239 increases mean and maximum lifespan by 12 and 36%, respectively. Lifespan extension by mir-239 loss-of-function requires daf-16 . ||Worm ||+11.8 ||— ||+36.0 |
|mir-246 mutation ||Mutating mir-246 decreases mean and maximum lifespan by 12% . ||Worm ||-11.7 ||— ||-12.0 |
|mir-238 mutation ||Mutating mir-238 decreases mean and maximum lifespan by 18 and 24% . mir-238(n4112) mutation decreases mean lifespan by 20% . ||Worm ||-17.6 to -20 ||— ||-24 |
|lin-14 RNAi ||Knockdown of lin-14 only during adulthood is sufficient to extend lifespan and suppresses the short lifespan phenotype of lin-4 mutants. ||Worm ||— ||— ||— |
|lin-4 mutation ||Loss-of-function mutation in lin-4 shortens lifespan and accelerated tissue ageing . ||Worm ||— ||— ||— |
|alg-1 RNAi ||Adult-specific knockdown of the C. elegans argonaute-like gene 1 *alg-1* results in shortened lifespan with a reduction in the mean and maximum lifespan by 9 - 16% and 14%, respectively . ||Worm ||-9.6 to -16.1 ||— ||-13.7 |
|lin-14 loss-of-function mutation ||A loss-of-function mutation in lin-14 extends lifespan by 31% . lin-14(n719) mutation extends mean and maximum lifespan of control animals by 20 and 67%, respectively .
The life-extending effects is dependent on daf-16 and hsf-1 . Inactivation of lin-14 does not increase the lifespan of pash-1 mutants .
||Worm ||+20 to +31 ||— ||+67 |
|mir-71 mutation ||Loss-of-function of mir-71 decreases lifespan . mir-71 mutants have a reduced lifespan with 40% decrease in mean lifespan. Loss of mir-71 function suppresses the long lifespan of glp-1(e2141) mutants , ||Worm ||-40 ||— ||— |
|pash-1 mutation ||pash-1 mutants have a decreased lifespan and display phenotypic and molecular signs of advantaged age earlier.
pash-1(mj100) temperature sensitive loss-of-function mutation decreases (at the permissive temperature) mean and maximum lifespan by 31 and 71%, respectively. At the restrictive temperature pash-1 mutants are slightly short-lived with a mean and maximum lifespan reduction by 13 and 54%. Lifespan of pash-1 mutants is reduced by a 24h upshift to 25 degree Celsius at the young adult stage with (36 and 78% reduction mean and maximum lifespan, respectively) .
The rescue of pash-1 expression all tissues restored almost normal lifespan. Rescue specifically in hypodermis, pharynx muscle, gut had no effect on lifespan. Rescue in body wall muscle marginal extended the lifespan, while rescue specifically in the neurons significantly restored mean but not maximum lifespan. Lifespan was also restored by combined rescue in hypodermis and muscle . ||Worm ||-31 ||— ||-71 |