|nhr-62 ||Nuclear Hormone Receptor family ||NHR-62 is required for metabolic and physiologic responses associated with DR-induced longevity. *nhr-62* mediates the longevity response of *eat-2* mutants and blunts the longevity by bacterial food dilution [Heestand, et al. 2012].
Mutation in *nhr-62* suppresses the lifespan extension of eat-2(ad465) animals (p<0.001) [Heestand et al. 2013].
Wild-type (N2) worms with extrachromosomal array dhEx627 (carrying a wild-type nhr-62) exhibit a significant increase in lifespan compared to wild-type (p<0.001) [Heestand et al. 2013]. ||Nematode |
|mrpl-37 ||— ||Knockdown of mrpl-37 increases lifespan by 41% . ||Nematode |
|mrpl-2 ||— ||Knockdown of mrpl-2 increases lifespan by 54% . ||Nematode |
|mrpl-1 ||— ||Knockdown of mrpl-1 increases lifespan by 57% . ||Nematode |
|ttll-9 ||Tubulin Tyrosine Ligase Like ||Knockdown of ttll-9 throughout the entire life increases the lifespan by 3% . ||Nematode |
|nkcc-1 ||Na-K-Cl Cotransporter homolog ||Knockdown of nkcc-1 throughout the entire life increases the lifespan by 23% . ||Nematode |
|mrps-5 ||— ||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 . ||Nematode |
|frh-1 ||FRataxin (involved in human Friedrich's ataxia) Homolog ||Complete absence of frataxin,the mitochondrial protein defective in individuals with Friedreich ataxia 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. Frataxin expression modulates autophagy in the absence of p53 . ||Nematode |
|wrn-1 ||human WRN (Werner's syndrome) related ||RNAi kockdown of wrn-1 shortens the lifespan, increases sensitivity to DNA damage, and accelerates aging phenoypes .
A nonfunctional wrn-1 DNA helicase decreases the lifespan. The expression of miR-124 in whole wrn-1 mutant worms is significantly reduced. Supplementation with vitamin C normalizes the median lifespan of wnr-1 and mir-124 mutants . ||Nematode |
|mir-124 ||— ||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 .
The expression of the conserved mir-124 in whole wrn-1 mutants (which premature age) is significantly reduced . ||Nematode |
|mir-58 ||— ||mir-58(n4640) mutation decreases the mean lifespan by 20% . ||Nematode |
|mir-239 ||— ||Mutating mir-239 increases mean and maximum lifespan by 12 and 36%, respectively, whereas overexpressing mir-239 decreases mean and maximum lifespan by 13 and 17 - 33%, respectively . ||Nematode |
|mir-246 ||— ||Mutating mir-246 decreases mean and maximum lifespan by 12%, while its overexpression increases mean and maximum lifespan by 6 and 5 - 14%, respectively . ||Nematode |
|mir-238 ||— ||Mutating mir-238 decreases mean and maximum lifespan by 18 and 24% . mir-238(n4112) mutation decreases mean lifespan by 20% . ||Nematode |
|mir-71 ||— ||Loss and gain-of-function of mir-71 decreases and increases lifespan, respectively . mir-71 mutants have a reduced lifespan with 40% decrease in mean lifespan, while extra copies of mir-71 extend the lifespan with an increase in lifespan by 15 - 25% ,
Loss of mir-71 function suppresses the long lifespan of glp-1(e2141) mutants ,
During adulthood mir-71 is strongly expressed in the intestine, body wall muscles and neurons. mir-71 is upregulated in aging adults , ||Nematode |
|alg-1 ||Argonaute (plant)-Like Gene ||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 . ||Nematode |
|pash-1 ||PArtner of DroSHa (DRSH-1 interactor) ||Inactivation of DGCR8/pash-1 in nematode reduces lifespan apparently due to accelerated aging. This intervention abrogates (lin-14 mutation and jnk-1(OE)) and suppresses (eat-2 and glp-1 mutants) several lifespan extending interventions, but not that conferred insulin-like signalling inhibition (daf-2 mutant) .
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 . ||Nematode |
|sir-2.4 ||yeast SIR related 2.4 ||RNA interference against sir-2.4 or overexpression of SIR-2.4 do not change the mean or maximum lifespan. Neither sir-2.4 RNAi nor SIR-2.4 overexpression affects the increased lifespan of daf-2(e1370) mutants [Tishkoff et al. 2012]. ||Nematode |
|gei-4 ||GEX Interacting protein 4 ||gei-4 RNAi in the adulthood reduces mean and maximum lifespan by 27 and 38% . ||Nematode |
|let-23 ||LEThal 23 ||Postdevelopmental inactivation of let-23 by RNA interference extends the lifespan by 5.6% [New Longevity Regulators]. ||Nematode |
|phi-50 ||— ||RNA interference of phi-50 decreases mean lifespan by 29% and suppresses lifespan extension by isp-1 and eat-2 mutation but does not significantly affect lifespan extension by daf-2 . ||Nematode |
|nekl-2 ||NEK (NEver in mitosis Kinase) Like 2 ||RNA intereference of nekl-2 decreases lifespan by 24% and suppresses lifespan extension by eat-2 mutation . ||Nematode |
|wnk-1 ||mammalian WNK-type protein kinase homolog 1 ||RNA interference of wnk-1 decreases lifespan by 9% and suppresses lifespan extension by eat-2 mutation . ||Nematode |
|cpf-2 ||Cleavage and Polyadenylation Factor 2 ||RNA interference of cpf-2 decreases mean lifespan by 6% and suppresses lifespan extension by eat-2 mutation . ||Nematode |
|pas-3 ||Proteasome Alpha Subunit 3 ||RNA interference of pas-3 shortens mean lifespan by 7% and suppresses lifespan extension by isp-1 mutation . ||Nematode |