Transgenic expression of the TRI101 or PDR5 gene increases resistance of tobacco to the phytotoxic effects of the trichothecene 4,15-diacetoxyscirpenol.

Mycotoxins are fungal secondary compounds that are toxic to vertebrates. Their presence in food and feeds, as the result of fungal disease in crops, can present a danger to animal or human health. Many mycotoxins have also been shown to be phytotoxic and in some cases, such as with trichothecenes produced by the wheat head blight fungus Fusarium graminearum, mycotoxins may act as virulence factors. Antibiotic-producing organisms, including fungi, protect themselves from their own toxins by metabolic alteration of the compound, modification of the target site of action or by exporting the compound to the extracellular space. We have tested the effectiveness of adapting two of these strategies, metabolic alteration and extracellular transport, to protect plant cells from the deleterious effects of the trichothecene 4,15-diacetoxyscirpenol (DAS). Tobacco plants were transformed with either the Saccharomyces cerevisiae gene PDR5, which encodes a multi-drug transporter, or with the Fusarium sporotrichioides gene TRI101, which encodes a trichothecene 3-O-acetyltransferase. Both genes conferred significant increased tolerance to DAS as measured by a sensitive seed germination assay. Expression of PDR5 or TRI101 in a seed-specific manner in crop plants such as wheat could lower the incidence of head blight as well as reduce mycotoxin levels within the seed.