ArticleProceedings of the National Academy of Sciences of the United States of America2009
A genome-wide screen in Saccharomyces cerevisiae reveals a critical role for the mitochondria in the toxicity of a trichothecene mycotoxin.
Article in Proceedings of the National Academy of Sciences of the United States of America, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 23 papers.
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Who cites it
23 citing papers in PubMed, 69 citations in OpenAlex.
- Computational glycosyltransferases masked deoxynivalenol toxicity and halted FHB spread in wheat grains.Journal of advanced research · 2026Article
- mtIF3 is locally translated in axons and regulates mitochondrial translation for axonal growth.BMC biology · 2022Article
- Characterisation of two unique sesquiterpenoids fromMycology · 2022Article
- Genome-Wide Identification of Cellular Pathways and Key Genes That Respond to Sodium Bicarbonate Stress inFrontiers in microbiology · 2022Article
- Effects of trichothecene production byFrontiers in plant science · 2022Article
- The Ribosome-Binding Mode of Trichothecene Mycotoxins Rationalizes Their Structure-Activity Relationships.International journal of molecular sciences · 2021Article
- Verification ofFrontiers in microbiology · 2021Article
- Bidirectional titration of yeast gene expression using a pooled CRISPR guide RNA approach.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
- Trichothecin Inhibits Cancer-Related Features in Colorectal Cancer Development by Targeting STAT3.Molecules (Basel, Switzerland) · 2020Article
- Efflux pumps as an additional source of resistance to trichothecenes in Fusarium proliferatum and Fusarium oxysporum isolates.Journal of applied genetics · 2019Article
- Effect of deoxynivalenol on apoptosis, barrier function, and expression levels of genes involved in nutrient transport, mitochondrial biogenesis and function in IPEC-J2 cells.Toxicology research · 2017Article
- Screening of Deoxynivalenol Producing Strains and Elucidation of Possible Toxigenic Molecular Mechanism.Toxins · 2017Article
- Ribosome quality control is a central protection mechanism for yeast exposed to deoxynivalenol and trichothecin.BMC genomics · 2016Article
- Acetylated Deoxynivalenol Generates Differences of Gene Expression that Discriminate Trichothecene Toxicity.Toxins · 2016Article
- RNA-Seq Revealed Differences in Transcriptomes between 3ADON and 15ADON Populations of Fusarium graminearum In Vitro and In Planta.PloS one · 2016Article
- A Lipid Transfer Protein Increases the Glutathione Content and Enhances Arabidopsis Resistance to a Trichothecene Mycotoxin.PloS one · 2015Article
- Elimination of damaged mitochondria through mitophagy reduces mitochondrial oxidative stress and increases tolerance to trichothecenes.Proceedings of the National Academy of Sciences of the United States of America · 2014Article
- Cellular development associated with induced mycotoxin synthesis in the filamentous fungus Fusarium graminearum.PloS one · 2013Article
- On the trail of a cereal killer: recent advances in Fusarium graminearum pathogenomics and host resistance.Molecular plant pathology · 2012Review
- Trichothecene mycotoxins inhibit mitochondrial translation--implication for the mechanism of toxicity.Toxins · 2011Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
Trichothecene mycotoxins synthesized by Fusarium species are potent inhibitors of eukaryotic translation. They are encountered in both the environment and in food, posing a threat to human and animal health. They have diverse roles in the cell that are not limited to the inhibition of protein synthesis. To understand the trichothecene mechanism of action, we screened the yeast knockout library to identify genes whose deletion confers resistance to trichothecin (Tcin). The largest group of resistant strains affected mitochondrial function, suggesting a role for fully active mitochondria in trichothecene toxicity. Tcin inhibited mitochondrial translation in the wild-type strain to a greater extent than in the most resistant strains, implicating mitochondrial translation as a previously unrecognized site of action. The Tcin-resistant strains were cross-resistant to anisomycin and chloramphenicol, suggesting that Tcin targets the peptidyltransferase center of mitochondrial ribosomes. Tcin-induced cell death was partially rescued by mutants that regulate mitochondrial fusion and maintenance of the tubular morphology of mitochondria. Treatment of yeast cells with Tcin led to the fragmentation of the tubular mitochondrial network, supporting a role for Tcin in disruption of mitochondrial membrane morphology. These results provide genome-wide insight into the mode of action of trichothecene mycotoxins and uncover a critical role for mitochondrial translation and membrane maintenance in their toxicity.
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