Partner und Internationale Organisationen
(Englisch)
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A, B, CY, CZ, DK, FIN, F, D, H, IRL, I, NL, N, P, RO, SK, E, S, CH, GB T. Rhis, Swiss federal research station for animal production H.R. Forrer, Swiss federal research station for agroecology and agriculture V. Michel, Swiss federal research station for plant production
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Abstract
(Englisch)
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Fusarium head blight on wheat is caused by several mycotoxigenic Fusarium species (e.g., F. culmorum and F. graminearum). These fungi survive and sporulate on crop residues, and infect subsequent crops at the flowering stage. Due to changes in agricultural practices (e.g., no-tillage) and in climatic conditions, this disease and the resultant mycotoxins such as deoxynivalenol (DON) are posing an increasing risk to animal and human health. Trichoderma strains are well known for their biocontrol activity against several plant pathogens through chitinase production and are potential antagonists against F. graminearum and F. culmorum. It has been shown that DON inhibits expression of the nag1-chitinase gene of T. atroviride on agar plates and on maize residues. The combination of Trichoderma with a bacterial antagonist could be a useful method to enhance biocontrol activity against mycotoxigenic Fusarium. Fluorescent pseudomonads are established biocontrol agents against several soilborne pathogens. Production of the polyketide 2, 4-diacetylphloroglucinol (Phl) contributes substantially to the antimicrobial activity of many biocontrol pseudomonads. The expression of the phlACBDE biosynthetic operon of strain CHA0 was measured by using a translational phlA'-'lacZ fusion. phlA-expression is insensitive to DON. The effect of the combination of Pseudomonas fluorescens CHA0 and Trichoderma atroviride P1 on the expression of important biocontrol genes of T. atroviride P1 and P. fluorescens CHA0 was studied to evaluate the feasibility to combine these antagonists against mycotoxigenic Fusarium. Phl enhanced nag1 expression, whereas an unidentified substance from P. fluorescens CHA0 repressed expression of both chitinases studied. Addition of T. atroviride P1 culture filtrates to the growing medium of P. fluorescens enhanced in the exponential growing phase b-galactosidase-activity. When both antagonists were grown together on residues of two maize cultivars, expression of a phlA'-'lacZ fusion was significantly repressed. Although negative interactions between P. fluorescens and T. atroviride occurred, the combination could be a useful tool to overcome negative signaling between mycotoxigenic fungi and potential antagonists.
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