ArticlePLoS genetics2009
A regulated response to impaired respiration slows behavioral rates and increases lifespan in Caenorhabditis elegans.
Article in PLoS genetics, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 91 papers, 1 of them a synthesis that pooled it.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
91 citing papers in PubMed, 1 synthesis or guideline pooled it, 162 citations in OpenAlex.
- Pooled it
- Article
- Multiple Molecular Pathways to Longevity: Opposing Gene Expression Programs Define Distinct Aging Strategies.bioRxiv : the preprint server for biology · 2026Article
- Gene- and Isoform-Level Responses to Extreme Acidic pH Stress in an Emerging Marine Invertebrate Model OrganismAntioxidants (Basel, Switzerland) · 2026Article
- Respirometry-Based Screening of Marine Natural Products Identifies Leptochelin A as a Novel Modulator of Mitochondrial Function.Oxidative medicine and cellular longevity · 2026Article
- Reduced Usage ofPhenomics (Cham, Switzerland) · 2025Article
- Mutations of the Electron Transport Chain Affect Lifespan and ROS Levels inAntioxidants (Basel, Switzerland) · 2025Review
- Genome-wide analysis of hepatic DNA methylation reveals impact of epigenetic aging on xenobiotic metabolism and transport genes in an aged mouse model.GeroScience · 2024Article
- Dimethylsulfoniopropionate (DMSP) Increases Longevity and Mitochondrial Function inEnvironment & health (Washington, D.C.) · 2024Article
- RNA Sequencing of Pooled Samples Effectively Identifies Differentially Expressed Genes.Biology · 2023Article
- Stimulation of RAS-dependent ROS signaling extends longevity by modulating a developmental program of global gene expression.Science advances · 2022Article
- Dietary-derived vitamin B12 protects Caenorhabditis elegans from thiol-reducing agents.BMC biology · 2022Article
- Naked mole-rat and Damaraland mole-rat exhibit lower respiration in mitochondria, cellular and organismal levels.Biochimica et biophysica acta. Bioenergetics · 2022Article
- Dysregulation of iron homeostasis and methamphetamine reward behaviors in Clk1-deficient mice.Acta pharmacologica Sinica · 2022Article
- C. elegans monitor energy status via the AMPK pathway to trigger innate immune responses against bacterial pathogens.Communications biology · 2022Article
- Neuroligin-mediated neurodevelopmental defects are induced by mitochondrial dysfunction and prevented by lutein in C. elegans.Nature communications · 2022Article
- LONP-1 and ATFS-1 sustain deleterious heteroplasmy by promoting mtDNA replication in dysfunctional mitochondria.Nature cell biology · 2022Article
- MON-2, a Golgi protein, mediates autophagy-dependent longevity inScience advances · 2021Article
- Animal Models of Coenzyme Q Deficiency: Mechanistic and Translational Learnings.Antioxidants (Basel, Switzerland) · 2021Review
- Elevated mitochondrial DNA copy number found in ubiquinone-deficient clk-1 mutants is not rescued by ubiquinone precursor 2-4-dihydroxybenzoate.Mitochondrion · 2021Article
31 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
5 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
When mitochondrial respiration or ubiquinone production is inhibited in Caenorhabditis elegans, behavioral rates are slowed and lifespan is extended. Here, we show that these perturbations increase the expression of cell-protective and metabolic genes and the abundance of mitochondrial DNA. This response is similar to the response triggered by inhibiting respiration in yeast and mammalian cells, termed the "retrograde response". As in yeast, genes switched on in C. elegans mitochondrial mutants extend lifespan, suggesting an underlying evolutionary conservation of mechanism. Inhibition of fstr-1, a potential signaling gene that is up-regulated in clk-1 (ubiquinone-defective) mutants, and its close homolog fstr-2 prevents the expression of many retrograde-response genes and accelerates clk-1 behavioral and aging rates. Thus, clk-1 mutants live in "slow motion" because of a fstr-1/2-dependent pathway that responds to ubiquinone. Loss of fstr-1/2 does not suppress the phenotypes of all long-lived mitochondrial mutants. Thus, although different mitochondrial perturbations activate similar transcriptional and physiological responses, they do so in different ways.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.