ArticleScientific reports2017
Genetic deficiency in neuronal peroxisomal fatty acid β-oxidation causes the interruption of dauer development in Caenorhabditis elegans.
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 14 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
14 citing papers in PubMed, 18 citations in OpenAlex.
- Loss of the fatty acid β-oxidation genebioRxiv : the preprint server for biology · 2026Article
- Article
- BMP-dependent mobilization of fatty acid metabolism promotes Caenorhabditis elegans survival on a bacterial pathogen.Disease models & mechanisms · 2025Article
- Robustness and variability inbioRxiv : the preprint server for biology · 2024Article
- Article
- Chemical Signaling Regulates Axon Regeneration via the GPCR-Gqα Pathway inThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2022Article
- Review
- An Untargeted Approach for Revealing Electrophilic Metabolites.ACS chemical biology · 2020Article
- Modeling tissue-relevant Caenorhabditis elegans metabolism at network, pathway, reaction, and metabolite levels.Molecular systems biology · 2020Article
- The peroxisomal fatty acid transporter ABCD1/PMP-4 is required in the C. elegans hypodermis for axonal maintenance: A worm model for adrenoleukodystrophy.Free radical biology & medicine · 2020Article
- A novel functional cross-interaction between opioid and pheromone signaling may be involved in stress avoidance in Caenorhabditis elegans.Scientific reports · 2020Article
- A Molecular Basis for Reciprocal Regulation between Pheromones and Hormones in Response to Dietary Cues inInternational journal of molecular sciences · 2020Article
- Ascaroside Pheromones: Chemical Biology and Pleiotropic Neuronal Functions.International journal of molecular sciences · 2019Review
- Article
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
Although peroxisomal fatty acid (FA) β-oxidation is known to be critical for animal development, the cellular mechanisms that control the manner in which its neuronal deficiency causes developmental defects remain unclear. To elucidate the potential cellular consequences of neuronal FA metabolic disorder for dauer development, an alternative developmental process in Caenorhabditis elegans that occurs during stress, we investigated the sequential effects of its corresponding genetic deficiency. Here, we show that the daf-22 gene in peroxisomal FA β-oxidation plays a distinct role in ASK neurons, and its deficiency interrupts dauer development even in the presence of the exogenous ascaroside pheromones that induce such development. Un-metabolized FAs accumulated in ASK neurons of daf-22 mutants stimulate the endoplasmic reticulum (ER) stress response, which may enhance the XBP-1 activity that promotes the transcription of neuronal insulin-like peptides. These sequential cell-autonomous reactions in ASK neurons then activate insulin/IGF-1 signaling, which culminates in the suppression of DAF-16/FOXO activity. This suppression results in the interruption of dauer development, independently of pheromone presence. These findings suggest that neuronal peroxisomal FA β-oxidation is indispensable for animal development by regulating the ER stress response and neuroendocrine signaling.
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.