Submitted to: Applied and Environmental Microbiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 9/10/1999
Publication Date: N/A
Citation: N/A Interpretive Summary: The mold Fusarium is a common contaminant of grain and other livestock feeds. Several species of Fusarium produce trichothecene toxins such as T-2 toxin and vomitoxin which cause adverse effects on human and animal health. These toxins are also important factors in determining the severity of some plant diseases such as wheat head scab. We characterized a Fusarium gene that changes trichothecene toxins into less toxic products. We showed that this gene is essential for the production of T-2 toxin. This gene increases the resistance of yeast to trichothecenes. Wheat breeders and seed companies may be able to insert this gene into wheat to reduce yield losses due to wheat scab and to improve the quality of the wheat.
Technical Abstract: Trichothecenes are sesquiterpenoid antibiotics that occur as mycotoxins in corn and wheat products. To characterize the mechanisms of trichothecene self-protection we screened a Fusarium sporotrichioides NRRL 3299 cDNA expression library in a toxin sensitive Saccharomyces cerevisiae strain lacking a functional PDR5 gene. Over 45 yeast transformants were identified as resistant to the trichothecene, 4,15- diacetoxyscirpenol, and 14 of these transformants were subsequently shown to carry a cDNA encoding the trichothecene 3-O-acetyltransferase that was recently identified as the Fusarium sporotrichioides homolog (Kimura et al. FEBS Lett. 435:163-168, 1998) of the F. graminearum resistance gene Tri101 (Kimura et al. J. Biol. Chem. 273:1654-1661, 1998). FsTRI101 expressed in E. coli was capable of using a variety of C-3 hydroxylated trichothecenes as substrates. Mutant strains of F. sporotrichioides NRRL 3299 produced by disruption of FsTRI101 were shown to be altered in their ability to biosynthesize T-2 toxin. These mutants accumulated isotrichodermol, didecalonectrin, and 3-decalonectrin, trichothecenes that are not observed in cultures of the parent strain. Our results suggest that TRI101 converts isotrichodermol to isotrichodermin in the biosynthesis of T-2 toxin. The demonstration that FsTRI101 functions both to catalyze a required biosynthetic step and as a component of Fusarium trichothecene self-protection suggests this enzyme has played a critical role in the evolution of Fusarium trichothecene biosynthesis.