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Metabolic profiling of wheat rachis node infection by Fusarium graminearum – decoding deoxynivalenol-dependent susceptibility

Fusarium graminearum is a filamentous ascomycete and the causal agent of Fusarium head blight on wheat that threatens food and feed production worldwide as infection reduces crop yield both quantitatively by interfering with kernel development and qualitatively by poisoning any remaining kernels wit...

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Bibliographic Details
Published in:The New phytologist 2019-01, Vol.221 (1), p.459-469
Main Authors: Bönnighausen, Jakob, Schauer, Nicolas, Schäfer, Wilhelm, Bormann, Jörg
Format: Article
Language:English
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Summary:Fusarium graminearum is a filamentous ascomycete and the causal agent of Fusarium head blight on wheat that threatens food and feed production worldwide as infection reduces crop yield both quantitatively by interfering with kernel development and qualitatively by poisoning any remaining kernels with mycotoxins. In wheat, F. graminearum infects spikelets and colonizes the entire head by growing through the rachis node at the bottom of each spikelet. Without the mycotoxin deoxynivalenol (DON), the pathogen cannot penetrate the rachis node and wheat is able to resist colonization. Using a global metabolite profiling approach we compared the metabolic profile of rachis nodes inoculated with either water, the Fusarium graminearum wild-type or the DON-deficient Δtri5 mutant. Extensive metabolic rearrangements mainly affect metabolites for general stress perception and signaling, reactive oxygen species (ROS) metabolism, cell wall composition, the tricarbonic acid (TCA) cycle and c-aminobutyric acid (GABA) shunt as well as sugar alcohols, amino acids, and storage carbohydrates. The results revealed specific, DON-related susceptibility factors. Wild-type infection resulted in an oxidative burst and the induction of plant programmed cell death, while spread of the DON-deficient mutant was blocked in a jasmonate (JA)-related defense reaction in concert with other factors. Hence, the Δtri5 mutant is prone to defense reactions that are, in the case of a wild-type infection, not initiated.
ISSN:0028-646X
1469-8137
DOI:10.1111/nph.15377