ArticleScientific reports2017
Superoxide dismutase SOD-1 modulates C. elegans pathogen avoidance behavior.
Article in Scientific reports, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
28 citing papers in PubMed, 42 citations in OpenAlex.
- Article
- Egg Peptides From American Shad Extend Lifespan and Healthspan in Caenorhabditis elegans via Lipid Metabolism Remodeling and Antioxidant Defense.Chemistry & biodiversity · 2026Article
- Application ofBiomolecules & therapeutics · 2026Review
- Deep ocean bacterial metabolites improve host survival and modulate immune-associated responses in Caenorhabditis elegans during Pseudomonas pathogenesis.Archives of microbiology · 2026Article
- Superoxide dismutase impacts extracellular vesicle shedding and uptake.Free radical biology & medicine · 2026Article
- Superoxide dismutase impacts extracellular vesicle biogenesis and uptake.bioRxiv : the preprint server for biology · 2025Article
- Article
- Molecular requirements foreLife · 2025Article
- Review
- Behavioral adaptations ofPeerJ · 2025Review
- Ovalbumin promotes innate immune response of Caenorhabditis elegans through DAF-16 and SKN-1 pathways in insulin/IGF-1 signaling.Journal of physiology and biochemistry · 2024Article
- Modeling Host-Pathogen Interactions inInternational journal of molecular sciences · 2024Review
- Deciphering Microbiome, Transcriptome, and Metabolic Interactions in the Presence of ProbioticAntibiotics (Basel, Switzerland) · 2024Article
- Fused in sarcoma regulates glutamate signaling and oxidative stress response.Free radical biology & medicine · 2024Article
- Neuronal basis and diverse mechanisms of pathogen avoidance inFrontiers in immunology · 2024Review
- PNPLA3-I148M Variant Promotes the Progression of Liver Fibrosis by Inducing Mitochondrial Dysfunction.International journal of molecular sciences · 2023Article
- Potential Anti-Alzheimer Properties of Mogrosides in Vitamin B12-DeficientMolecules (Basel, Switzerland) · 2023Article
- Superoxide dismutase SOD-3 regulates redox homeostasis in the intestine.microPublication biology · 2023Article
- Simple models to understand complex disease: 10 years of progress fromFrontiers in neuroscience · 2023Review
- The gut efflux pump MRP-1 exports oxidized glutathione as a danger signal that stimulates behavioral immunity and aversive learning.Communications biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
The C. elegans nervous system mediates protective physiological and behavioral responses amid infection. However, it remains largely unknown how the nervous system responds to reactive oxygen species (ROS) activated by pathogenic microbes during infection. Here, we show superoxide dismutase-1 (SOD-1), an enzyme that converts superoxide into less toxic hydrogen peroxide and oxygen, functions in the gustatory neuron ASER to mediate C. elegans pathogen avoidance response. When C. elegans first encounters pathogenic bacteria P. aeruginosa, SOD-1 is induced in the ASER neuron. After prolonged P. aeruginosa exposure, ASER-specific SOD-1 expression is diminished. In turn, C. elegans starts to vacate the pathogenic bacteria lawn. Genetic knockdown experiments reveal that pathogen-induced ROS activate sod-1 dependent behavioral response non cell-autonomously. We postulate that the delayed aversive response to detrimental microbes may provide survival benefits by allowing C. elegans to temporarily utilize food that is tainted with pathogens as an additional energy source. Our data offer a mechanistic insight into how the nervous system mediates food-seeking behavior amid oxidative stress and suggest that the internal state of redox homeostasis could underlie the behavioral response to harmful microbial species.
Indexed as
Identifiers
What OpenQuestion holds
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.