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ARS Home » Midwest Area » Peoria, Illinois » National Center for Agricultural Utilization Research » Mycotoxin Prevention and Applied Microbiology Research » Research » Publications at this Location » Publication #276454
Title: Trichothecene mycotoxins inhibit mitochondrial translation- Implication for FHB resistance

Author
item BIN-UMER, MOHAMED - Rutgers University
item MCLAUGHLIN, JOHN - Rutgers University
item BASU, DEBALEENA - Rutgers University
item McCormick, Susan
item TUMER, NILGUN - Rutgers University

Submitted to: National Fusarium Head Blight Forum
Publication Type: Abstract Only
Publication Acceptance Date: 12/6/2011
Publication Date: 12/6/2011
Citation: Bin-Umer, M.A., Mclaughlin, J., Basu, D., Mccormick, S.P., Tumer, N.E. 2011. Trichothecene mycotoxins inhibit mitochondrial translation- Implication for FHB resistance. National Fusarium Head Blight Forum Proceedings. Session3,p.81.

Interpretive Summary:

Technical Abstract: Trichothecenes are foodborne toxins produced by various fungi including the plant pathogen Fusarium graminearum, which causes head blight (FHB) or scab of wheat and barley, resulting in yield reduction and contamination of grains with trichothecene mycotoxins. Conventional approaches have not yet yielded effective resistance in the field. Identifying molecular mechanisms underlying trichothecene toxicity will therefore aid in understanding Fusarium pathology and engineering effective resistance against FHB. Trichothecenes first identified as inhibitors of translation are known to have multiple effects on eukaryotes, including inhibition of DNA, RNA synthesis, cell division, membrane structure and integrity and mitochondrial function. It is not clear if these are primary or secondary effects of inhibition of cytosolic translation. We previously showed that mitochondria play a critical role in the toxicity of a type B trichothecene, trichothecin. In this study, we investigated the direct effects of type A and type B trichothecenes on mitochondrial translation and membrane integrity in Saccharomyces cerevisiae. Sensitivity to trichothecenes increased when yeast cells required functional mitochondria for growth, while cells devoid of mitochondria ('0) showed increased tolerance. T-2, DAS and Tcin inhibited translation in isolated yeast mitochondria by 67% (T-2), 54% (DAS) and 70% (Tcin). Trichothecenes caused fragmentation of mitochondrial membrane when yeast cells were treated for 6 h with high doses at which total translation was inhibited by 44% (T-2), 33% (DAS) and 91% (Tcin). A corresponding drop in mitochondrial membrane fragmentation ('mito) and ROS levels was also observed. Trichothecenes, at low doses, did not promote severe membrane fragmentation or affect mitochondrial membrane integrity. Mitochondrial translation was significantly inhibited by 48% (T-2), 42% (DAS), and 34% (Tcin) at the low doses, but not total translation. These results indicate that trichothecenes directly target mitochondrial translation. Inhibition of mitochondrial translation is a primary target of trichothecenes and is not secondary to the disruption of mitochondrial membranes or cytosolic translation inhibition.