ArticleNucleic acids research2017
The non-stop decay mRNA surveillance pathway is required for oxidative stress tolerance.
Article in Nucleic acids research, 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
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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.
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Who cites it
28 citing papers in PubMed, 58 citations in OpenAlex.
- The function of mRNA quality control in aging and age-related diseases.The Journal of biological chemistry · 2026Review
- A predictive framework for stop-loss variants with C-terminal extensions.Nucleic acids research · 2026Article
- Mitochondrial Dysfunction in the Development and Progression of Cardiometabolic Diseases: A Narrative Review.Journal of clinical medicine · 2025Review
- o8G-modified circPLCE1 inhibits lung cancer progression via chaperone-mediated autophagy.Molecular cancer · 2025Article
- A Comparative Overview of the Role of Human Ribonucleases in Nonsense-Mediated mRNA Decay.Genes · 2024Article
- HBS1L deficiency causes retinal dystrophy in a child and in a mouse model associated with defective development of photoreceptor cells.Disease models & mechanisms · 2024Article
- Sequestrase chaperones protect against oxidative stress-induced protein aggregation and [PSI+] prion formation.PLoS genetics · 2024Article
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- Epitranscriptomic modifications in mesenchymal stem cell differentiation: advances, mechanistic insights, and beyond.Cell death and differentiation · 2024Review
- Genetic deficiency of ribosomal rescue factor HBS1L causes retinal dystrophy associated with Pelota and EDF1 depletion.bioRxiv : the preprint server for biology · 2023Article
- Dihydromyricetin functions as a tumor suppressor in hepatoblastoma by regulating SOD1/ROS pathway.Frontiers in oncology · 2023Article
- Ferroptosis and its emerging role in esophageal cancer.Frontiers in molecular biosciences · 2022Review
- A comprehensive coverage insurance for cells: revealing links between ribosome collisions, stress responses and mRNA surveillance.RNA biology · 2022Review
- Mining novelFrontiers in microbiology · 2022Article
- LISTERIN E3 Ubiquitin Ligase and Ribosome-Associated Quality Control (RQC) Mechanism.Molecular neurobiology · 2021Review
- RNA degradation is required for the germ-cell to maternal transition in Drosophila.Current biology : CB · 2021Article
- Zebrafish Ski7 tunes RNA levels during the oocyte-to-embryo transition.PLoS genetics · 2021Article
- Consequences for Pancreatic β-Cell Identity and Function of Unregulated Transcript Processing.Frontiers in endocrinology · 2021Review
- Article
- The emerging role of RNA modifications in the regulation of mRNA stability.Experimental & molecular medicine · 2020Review
Corrections and comments
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Authors and funding
3 authors at 1 institution in 2 countries.
Funding
Abstract
Reactive oxygen species (ROS) are toxic by-products of normal aerobic metabolism. ROS can damage mRNAs and the translational apparatus resulting in translational defects and aberrant protein production. Three mRNA quality control systems monitor mRNAs for translational errors: nonsense-mediated decay, non-stop decay (NSD) and no-go decay (NGD) pathways. Here, we show that factors required for the recognition of NSD substrates and components of the SKI complex are required for oxidant tolerance. We found an overlapping requirement for Ski7, which bridges the interaction between the SKI complex and the exosome, and NGD components (Dom34/Hbs1) which have been shown to function in both NSD and NGD. We show that ski7 dom34 and ski7 hbs1 mutants are sensitive to hydrogen peroxide stress and accumulate an NSD substrate. We further show that NSD substrates are generated during ROS exposure as a result of aggregation of the Sup35 translation termination factor, which increases stop codon read-through allowing ribosomes to translate into the 3΄-end of mRNAs. Overexpression of Sup35 decreases stop codon read-through and rescues oxidant tolerance consistent with this model. Our data reveal an unanticipated requirement for the NSD pathway during oxidative stress conditions which prevents the production of aberrant proteins from NSD mRNAs.
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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.