Submitted to: Applied and Environmental Microbiology
Publication Type: Peer reviewed journal
Publication Acceptance Date: 3/18/2002
Publication Date: N/A
Citation: 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 previously found a gene that protects the mold from its own toxins while they are being made. In this study we characterized a Fusarium gene that converts trichothecenes into more toxic products. We showed that this gene is essential for the production and release of T-2 toxin and vomitoxin.
Technical Abstract: Mutant strains of Fusarium graminearum Z3639 produced by disruption of Tri8 were altered in their ability to biosynthesize 15-acetyldeoxynivalenol (15-ADON) and instead accumulated 3,15-diacetyldeoxynivalenol, 7,8-dihydroxycalonectrin, and calonectrin. The accumulation of these C-3-acetylated compounds suggests that Tri8 encodes an esterase responsible for the final step in Fusarium trichothecene biosynthesis, deacetylation at C-3. This was confirmed with both cell-free enzyme assays, heterologous expression of Tri8 in yeast and disruption of Tri8 in Fusarium sporotrichioides. F. sporotrichioides Tri8 mutants accumulated 3-acetyl T-2 toxin, 3-acetyl neosolaniol and 3,4,15-triacetoxyscripenol rather than T-2 toxin, neosolaniol and 4,15-diacetoxyscirpenol (DAS). The presence of a free C-3 hydroxyl group is a key component of Fusarium trichothecene toxicity. Tri101 encodes a C-3 transacetylase that acts as a self-protection or resistance factor during biosynthesis. Since Tri8 encodes the esterase that removes this protecting group, it may be considered a toxicity factor.