ArticlePLoS pathogens2015
mir-233 modulates the unfolded protein response in C. elegans during Pseudomonas aeruginosa infection.
Article in PLoS pathogens, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 56 citations in OpenAlex.
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- Pathogen infection induces sickness behaviors through neuromodulators linked to stress and satiety in C. elegans.Nature communications · 2025Article
- Unzipping the defense: a comprehensive review on bZIP transcription factors inFrontiers in cellular and infection microbiology · 2025Review
- Inheritance of Stress Responses via Small Non-Coding RNAs in Invertebrates and Mammals.Epigenomes · 2023Review
- The Interplay between Host Defense, Infection, and Clinical Status in Septic Patients: A Narrative Review.International journal of molecular sciences · 2022Review
- TOR functions as a molecular switch connecting an iron cue with host innate defense against bacterial infection.PLoS genetics · 2021Article
- ProbioticFrontiers in cellular and infection microbiology · 2021Article
- Endoplasmic Reticulum Homeostasis and Stress Responses in Caenorhabditis elegans.Progress in molecular and subcellular biology · 2021Article
- Innate immunity in C. elegans.Current topics in developmental biology · 2021Review
- MicroRNAs: An Update of Applications in Forensic Science.Diagnostics (Basel, Switzerland) · 2020Review
- Biomarkers in Cystic Fibrosis Lung Disease - A Review.Romanian journal of anaesthesia and intensive care · 2020Review
- Mycoplasma hyopneumoniae J elicits an antioxidant response and decreases the expression of ciliary genes in infected swine epithelial cells.Scientific reports · 2020Article
- Inhibition of the oligosaccharyl transferase in Caenorhabditis elegans that compromises ER proteostasis suppresses p38-dependent protection against pathogenic bacteria.PLoS genetics · 2020Article
- MANF deletion abrogates early larval Caenorhabditis elegans stress response to tunicamycin and Pseudomonas aeruginosa.European journal of cell biology · 2019Article
- Restoration of Proteostasis in the Endoplasmic Reticulum Reverses an Inflammation-Like Response to Cytoplasmic DNA inGenetics · 2019Article
- Article
- Recent Molecular Genetic Explorations ofGenetics · 2018Article
- Metabolic shift from glycogen to trehalose promotes lifespan and healthspan inProceedings of the National Academy of Sciences of the United States of America · 2018Article
- mir-355 Functions as An Important Link between p38 MAPK Signaling and Insulin Signaling in the Regulation of Innate Immunity.Scientific reports · 2017Article
Corrections and comments
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Authors and funding
5 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The unfolded protein response (UPR), which is activated by perturbations of the endoplasmic reticulum homeostasis, has been shown to play an important role in innate immunity and inflammation. However, little is known about the molecular mechanisms underlying activation of the UPR during immune responses. Using small RNA deep sequencing and reverse genetic analysis, we show that the microRNA mir-233 is required for activation of the UPR in Caenorhabditis elegans exposed to Pseudomonas aeruginosa PA14. P. aeruginosa infection up-regulates the expression of mir-233 in a p38 MAPK-dependent manner. Quantitative proteomic analysis identifies SCA-1, a C. elegans homologue of the sarco/endoplasmic reticulum Ca2+-ATPase, as a target of mir-233. During P. aeruginosa PA14 infection, mir-233 represses the protein levels of SCA-1, which in turn leads to activation of the UPR. Whereas mir-233 mutants are more sensitive to P. aeruginosa infection, knockdown of sca-1 leads to enhanced resistance to the killing by P. aeruginosa. Our study indicates that microRNA-dependent pathways may have an impact on innate immunity by activating the UPR.
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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.