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

• Published in: New Phytologist
• Main Authors: Bönnighausen, Jakob, Schauer, Nicolas, Schäfer, Wilhelm, Bormann, Jörg
• Other Authors: Kompetenzzentrum Nachhaltige Universität’ of the University Hamburg
• Format: Article in Journal/Newspaper
• Language: English
• Published: Wiley 2018
• Subjects: Carbonic acid
• Online Access: http://dx.doi.org/10.1111/nph.15377; https://api.wiley.com/onlinelibrary/tdm/v1/articles/10.1111%2Fnph.15377; https://nph.onlinelibrary.wiley.com/doi/pdf/10.1111/nph.15377

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 ∆ tri5 mutant. Extensive metabolic rearrangements mainly affect metabolites for general stress perception and signaling, reactive oxygen species ( ROS ) metabolism, cell wall composition, the tri‐carbonic acid ( TCA) cycle and γ‐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 ∆ tri5 mutant is prone to defense reactions that are, in the case of a wild‐type infection, not initiated.