atp-3;cep-1

There is no network for this step.

Fullscreen mode

Hide graph

Legend

Genetic mutants with atp-3, cep-1 alterations

Names of genes are ordered alphabetically. For the order of interventions, please see the specific paper.

Temperature °C
20
Lifespan (days)
25.7
Lifespan change (compared to wild type)
61.64%
Phenotype
Specifically, undiluted atp-3 RNAi decreased the lifespan of the wild-type strain below that of control RNAi-treated animals, while in the cep-1(gk138) mutant strain lifespan was increased with the same RNAi treatment.
Lifespan comparisons
Double mutant atp-3(RNAi);cep-1(gk138) has a lifespan of 25.7 days, while single mutant atp-3(RNAi) has a lifespan of 8.4 days, single mutant cep-1(gk138) has a lifespan of 17.6 days and wild type has a lifespan of 15.9 days.
Type of interaction
See methods
Enhancer, opposite lifespan effects
Citation
View abstract
Ventura N et al., 2009, p53/CEP-1 increases or decreases lifespan, depending on level of mitochondrial bioenergetic stress. Aging Cell. 8(4):380-93 19416129 Click here to select all mutants from this PubMed ID in the graph
Abstract
Mitochondrial pathologies underlie a number of life-shortening diseases in humans. In the nematode Caenorhabditis elegans, severely reduced expression of mitochondrial proteins involved in electron transport chain-mediated energy production also leads to pathological phenotypes, including arrested development and/or shorter life; in sharp contrast, mild suppression of these same proteins extends lifespan. In this study, we show that the C. elegans p53 ortholog cep-1 mediates these opposite effects. We found that cep-1 is required to extend longevity in response to mild suppression of several bioenergetically relevant mitochondrial proteins, including frataxin - the protein defective in patients with Friedreich's Ataxia. Importantly, we show that cep-1 also mediates both the developmental arrest and life shortening induced by severe mitochondrial stress. These findings support an evolutionarily conserved function for p53 in modulating organismal responses to mitochondrial dysfunction and suggest that metabolic checkpoint responses may play a role in longevity control and in human mitochondrial-associated diseases.

Names of genes are ordered alphabetically. For the order of interventions, please see the specific paper.

Temperature °C
20
Lifespan (days)
12.3
Lifespan change (compared to wild type)
-27.65%
Lifespan comparisons
Double mutant atp-3(RNAi);cep-1(lg12501) has a lifespan of 12.3 days, while single mutant atp-3(RNAi) has a lifespan of 7.0 days, single mutant cep-1(lg12501) has a lifespan of 19.1 days and wild type has a lifespan of 17.0 days.
Type of interaction
See methods
Opposite lifespan effects of single mutants
Citation
View abstract
Ventura N et al., 2009, p53/CEP-1 increases or decreases lifespan, depending on level of mitochondrial bioenergetic stress. Aging Cell. 8(4):380-93 19416129 Click here to select all mutants from this PubMed ID in the graph
Abstract
Mitochondrial pathologies underlie a number of life-shortening diseases in humans. In the nematode Caenorhabditis elegans, severely reduced expression of mitochondrial proteins involved in electron transport chain-mediated energy production also leads to pathological phenotypes, including arrested development and/or shorter life; in sharp contrast, mild suppression of these same proteins extends lifespan. In this study, we show that the C. elegans p53 ortholog cep-1 mediates these opposite effects. We found that cep-1 is required to extend longevity in response to mild suppression of several bioenergetically relevant mitochondrial proteins, including frataxin - the protein defective in patients with Friedreich's Ataxia. Importantly, we show that cep-1 also mediates both the developmental arrest and life shortening induced by severe mitochondrial stress. These findings support an evolutionarily conserved function for p53 in modulating organismal responses to mitochondrial dysfunction and suggest that metabolic checkpoint responses may play a role in longevity control and in human mitochondrial-associated diseases.

Search genes: atp-3 cep-1

Entrez ID
Symbol
GenAge
Wormbase ID

172195
atp-3
View on GenAge (atp-3)
WBGene00000230

ATP synthase subunit

Locus: CELE_F27C1.7

Wormbase description: atp-3 encodes the C. elegans homolog of the ATP5O subunit of mitochondrial ATP synthase (complex V); as part of the ATP synthase complex, ATP-3 controls respiration and regulates growth rate and body size, aging, and rates of behaviors such as pharyngeal pumping, defecation, and locomotion; loss of atp-3 function during larval development indicates that respiratory rates established during development persist into adulthood.

Entrez ID
Symbol
GenAge
Wormbase ID

172616
cep-1
View on GenAge (cep-1)
WBGene00000467

Transcription factor cep-1

Locus: CELE_F52B5.5

Wormbase description: cep-1 encodes an ortholog of the human tumor suppressor p53 (OMIM:191170, mutated in Li-Fraumeni syndrome) that promotes DNA damage-induced apoptosis and is required for normal meiotic segregation in the germ line, and affects sensitivity to hypoxia-induced lethality and longevity in response to starvation; CEP-1 is expressed ubiquitously in embryos and in the nucleoli of a subset of pharyngeal cells.

Orthologs of atp-3;cep-1 in SynergyAge

Show in SynergyAge
Species	Gene

Not in SynergyAge
Species	Gene

Orthologs of atp-3 in SynergyAge

Show in SynergyAge
Species	Gene

Not in SynergyAge
Species	Gene
Drosophila melanogaster	ATPsynO
Mus musculus	Atp5o

Orthologs of cep-1 in SynergyAge

Show in SynergyAge
Species	Gene