Biocontrol agents such as Trichoderma were applied in many different environments. These habitats were potentially also occupied by mycotoxin producing fungi. This indicates that Trichoderma will likely encounter an array of mycotoxins. But little is known how these fungal toxins affect biocontrol efficacies. Any competitive advantage conferred by mycotoxins would complicate efforts to control mycotoxigenic fungi. We examined the influence of important mycotoxins on expression of Trichoderma chitinase genes using ech42-goxA or nag1-goxA reporter gene fusions in T. atroviride P1. Production of chitinases, such as the ECH 42 endochitinase and the N-acetyl--glucosaminidase NAG1, is a primary mechanism of action for T. atroviride P1. Recently, the molecular interaction between the Fusarium mycotoxin deoxynivalenol (DON) was evaluated in detail. It was found that DON down-regulates nag1 gene expression in the fungal antagonist Trichoderma atroviride P1. Using a broader approach, additional mycotoxins that are prevalent in various crops and environments were evaluated in vitro for their ability to interact with the antagonistic fungus Trichoderma atroviride strain P1. Three different patterns were identified with certain mycotoxins having no impact on expression of either chitinase gene (patulin, fumonisin B1, and beauvericin); others reduced significantly nag1, but not ech42 expression (DON, ochratoxin A), and a third group induced ech42, but had no influence on nag1 expression in T. atroviride P1 (aflatoxin and -zearalenol). As sole mycotoxin beauvericin reduced significantly Trichoderma growth. Implications for the understanding of ecological functions of mycotoxin production and for deployment of biocontrol strategies are discussed.
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