Changes in the Wheat Primary Metabolism during Defense Against Fusarium graminearum

Wheat is commonly infected by Fusarium graminearum, causing Fusarium head blight, which leads to severe losses in grain yield and quality. A decisive factor in the mounted defense response is how plants counteract the effects of the F. graminearum toxin deoxynivalenol, which elicits oxidative stress and inhibits protein biosynthesis. In response plants generate secondary metabolites, inactivate the toxin by metabolization and try to compensate for the reduced levels of protein biosynthesis. All these incur at significant cost and require restructuring of the primary metabolism to meet the elevated needs in energy, carbon and nitrogen equivalents. We have investigated changes to the primary metabolism in response to the pathogen in transcriptomic and metabolomic datasets and additionally to the toxin in metabolomic datasets. These data have been generated by RNAseq and GC-MS from wheat near-isogenic lines segregating for the resistance QTL Fhb1 and Qfhs.ifa-5A in a series of time points after inoculation with the fungus or deoxynivalenol. We observed increased levels in the respiration including the pentose phosphate pathway, which produces also erythrose-4-phosphate, required as a precursor in the shikimate pathway, which ultimatively leads to the production of defense-associated phenylpropanoids. The detrimental effects on translation by the toxin are met by the increased synthesis of amino acids and tRNA ligases. Significant differences for Fhb1 were observed in metabolite levels after DON treatment and to a lesser extent for lines lacking Qfhs.ifa-5A after Fusarium graminearum treatment.