ArticlePLoS genetics2014
Regulation of synaptic nlg-1/neuroligin abundance by the skn-1/Nrf stress response pathway protects against oxidative stress.
Article in PLoS genetics, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 31 papers.
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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
31 citing papers in PubMed, 48 citations in OpenAlex.
- The Nodding syndrome cerebrospinal fluid proteome: a lens into neurodevelopmental failure consistent with environmentally triggeredFrontiers in molecular neuroscience · 2026Article
- Protein sequence editing defines distinct and overlapping functions of SKN-1A/Nrf1 and SKN-1C/Nrf2.PLoS genetics · 2025Article
- Disrupting the SKN-1 homeostat: mechanistic insights and phenotypic outcomes.Frontiers in aging · 2024Review
- A dicer-related helicase opposes the age-related pathology from SKN-1 activation in ASI neurons.Proceedings of the National Academy of Sciences of the United States of America · 2023Article
- Patient-specific variants of NFU1/NFU-1 disrupt cholinergic signaling in a model of multiple mitochondrial dysfunctions syndrome 1.Disease models & mechanisms · 2023Article
- Deregulation of Mitochondrial Calcium Handling Due to Presenilin Loss Disrupts Redox Homeostasis and Promotes Neuronal Dysfunction.Antioxidants (Basel, Switzerland) · 2022Article
- Neuroligin-mediated neurodevelopmental defects are induced by mitochondrial dysfunction and prevented by lutein in C. elegans.Nature communications · 2022Article
- Kinesin-3 mediated axonal delivery of presynaptic neurexin stabilizes dendritic spines and postsynaptic components.PLoS genetics · 2022Article
- High-ContentCells · 2021Article
- Neuroligin-1 Is a Mediator of Methylmercury Neuromuscular Toxicity.Toxicological sciences : an official journal of the Society of Toxicology · 2021Article
- Mitochondrial hydrogen peroxide positively regulates neuropeptide secretion during diet-induced activation of the oxidative stress response.Nature communications · 2021Article
- Neuroligin-1 is altered in the hippocampus of Alzheimer's disease patients and mouse models, and modulates the toxicity of amyloid-beta oligomers.Scientific reports · 2020Article
- Stress-Induced Neuron Remodeling Reveals Differential Interplay Between Neurexin and Environmental Factors inGenetics · 2019Article
- WDR-23 and SKN-1/Nrf2 Coordinate with the BLI-3 Dual Oxidase in Response to Iodide-Triggered Oxidative Stress.G3 (Bethesda, Md.) · 2018Article
- Sphingosine Kinase Regulates Neuropeptide Secretion During the Oxidative Stress-Response Through Intertissue Signaling.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- The Claudin-like Protein HPO-30 Is Required to Maintain LAChRs at theThe Journal of neuroscience : the official journal of the Society for Neuroscience · 2018Article
- Identification of interneurons required for the aversive response of Caenorhabditis elegans to graphene oxide.Journal of nanobiotechnology · 2018Article
- Thrombospondin-1 secreted by human umbilical cord blood-derived mesenchymal stem cells rescues neurons from synaptic dysfunction in Alzheimer's disease model.Scientific reports · 2018Article
- Mutations in Caenorhabditis elegans neuroligin-like glit-1, the apoptosis pathway and the calcium chaperone crt-1 increase dopaminergic neurodegeneration after 6-OHDA treatment.PLoS genetics · 2018Article
- A Genetic Analysis of theGenetics · 2017Article
Corrections and comments
- Erratum issuedEgrafov, Oleg [corrected to Evgrafov, Oleg]
Authors and funding
5 authors at 1 institution in 1 country.
Funding
Abstract
The Nrf family of transcription factors mediates adaptive responses to stress and longevity, but the identities of the crucial Nrf targets, and the tissues in which they function in multicellular organisms to promote survival, are not known. Here, we use whole transcriptome RNA sequencing to identify 810 genes whose expression is controlled by the SKN-1/Nrf2 negative regulator WDR-23 in the nervous system of Caenorhabditis elegans. Among the genes identified is the synaptic cell adhesion molecule nlg-1/neuroligin. We find that the synaptic abundance of NLG-1 protein increases following pharmacological treatments that generate oxidative stress or by the genetic activation of skn-1. Increasing nlg-1 dosage correlates with increased survival in response to oxidative stress, whereas genetic inactivation of nlg-1 reduces survival and impairs skn-1-mediated stress resistance. We identify a canonical SKN-1 binding site in the nlg-1 promoter that binds to SKN-1 in vitro and is necessary for SKN-1 and toxin-mediated increases in nlg-1 expression in vivo. Together, our results suggest that SKN-1 activation in the nervous system can confer protection to organisms in response to stress by directly regulating nlg-1/neuroligin expression.
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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.