ArticleNature2014
Caenorhabditis elegans pathways that surveil and defend mitochondria.
Article in Nature, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 208 papers.
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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
208 citing papers in PubMed, 315 citations in OpenAlex.
- A multilayered stress-response circuit: The mammalian mitochondrial UPR.The FEBS journal · 2026Review
- InsP3R signaling and actomyosin-dependent mitochondrial dynamics play essential roles in mitochondrial stress-induced longevity.Nature communications · 2026Article
- The Nematicide Tioxazafen Disrupts Proteasome Function via Cytochrome P450 Bioactivation.bioRxiv : the preprint server for biology · 2026Article
- A lipid-sensitive food choice behavior influences aging outcomes from a longevity-promoting diet.The FEBS journal · 2026Article
- Mitochondrial redox homeostasis links organellar stress surveillance to germline and somatic integrity in Caenorhabditis elegans.Redox biology · 2026Article
- Article
- A Stress-Responsive Nuclear Factor, GLDI-8, Mediates Mitochondrial Stress Responses to ETC Dysfunction.International journal of molecular sciences · 2026Article
- Interplay between proteostasis pathways and innate immune responses inInfection and immunity · 2026Review
- Light sensing enhances thermotolerance and competitive fitness via serotonergic signaling in an eyeless organism.Cell research · 2026Article
- Longevity-promoting mitochondrial unfolded protein response activation requires elements of the PeBoW complex.Genes & development · 2026Article
- 6-PPD induces mitochondrial dysfunction and reduces healthspan and lifespan through SKN-1 in Caenorhabditis elegans.Journal of hazardous materials · 2025Article
- Synergistic Effects of Rotenone and Abamectin on Physiological Suppression, Population Inhibition, and Ion Disruption ofInternational journal of molecular sciences · 2025Article
- InsP3R signaling mediates mitochondrial stress-induced longevity through actomyosin-dependent mitochondrial dynamics.bioRxiv : the preprint server for biology · 2025Article
- Patterns of pathogenesis in innate immunity: insights from C. elegans.Nature reviews. Immunology · 2025Review
- Biological and clinical implications of a model of surveillance immunity.The Journal of clinical investigation · 2025Review
- Immuno-metabolic stress responses control longevity from mitochondrial translation inhibition in C. elegans.Nature communications · 2025Article
- Polyketide synthase-derived sphingolipids mediate microbiota protection against a bacterial pathogen in C. elegans.Nature communications · 2025Article
- Intercellular sphingolipid signaling mediates aversive learning in C. elegans.Current biology : CB · 2025Article
- Mitochondrial fission surveillance is coupled to Caenorhabditis elegans DNA and chromosome segregation integrity.PLoS genetics · 2025Article
- Diversity-disease relationships in natural microscopic nematode communities.Royal Society open science · 2025Article
148 more citing papers are in PubMed but not listed here.
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Mitochondrial function is challenged by toxic by-products of metabolism as well as by pathogen attack. Caenorhabditis elegans normally responds to mitochondrial dysfunction with activation of mitochondrial-repair, drug-detoxification and pathogen-response pathways. Here, from a genome-wide RNA interference (RNAi) screen, we identified 45 C. elegans genes that are required to upregulate detoxification, pathogen-response and mitochondrial-repair pathways after inhibition of mitochondrial function by drug-induced or genetic disruption. Animals defective in ceramide biosynthesis are deficient in mitochondrial surveillance, and addition of particular ceramides can rescue the surveillance defects. Ceramide can also rescue the mitochondrial surveillance defects of other gene inactivations, mapping these gene activities upstream of ceramide. Inhibition of the mevalonate pathway, either by RNAi or statin drugs, also disrupts mitochondrial surveillance. Growth of C. elegans with a significant fraction of bacterial species from their natural habitat causes mitochondrial dysfunction. Other bacterial species inhibit C. elegans defence responses to a mitochondrial toxin, revealing bacterial countermeasures to animal defence.
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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.