Maize kernel metabolome involved in resistance to fusarium ear rot and fumonisin contamination

poses a threat to worldwide maize production due to its ability to infect maize kernel and synthesize fumonisins that can be accumulated above safety levels for humans and animals. Maize breeding has been proposed as key tool to decrease kernel contamination with fumonisins, but metabolic studies complementary to genomic approaches are necessary to disclose the complexity of maize resistance. An untargeted metabolomic study was proposed using inbreds genetically related but with contrasting levels of resistance in order to uncover pathways implicated in resistance to Fusarium ear rot (FER) and fumonisin contamination in the maize kernel and to look for possible biomarkers. Metabolite determinations were performed in kernels collected at 3 and 10 days after inoculation with (dat). Discriminant metabolites between resistant and susceptible RILs were rather found at 10 than 3 dat, although metabolite differences at later stages of colonization could be driven by subtle variations at earlier stages of infection. Within this context, differences for membrane lipid homeostasis, methionine metabolism, and indolacetic acid conjugation seemed highly relevant to distinguish between resistant and susceptible inbreds, confirming the polygenic nature of resistance to FER and fumonisin contamination in the maize kernels. Nevertheless, some specific metabolites such as the polyamine spermidine and/or the alkaloid isoquinoline seemed to be promising indirect selection traits to improve resistance to FER and reduce fumonisin accumulation. Therefore, and experiments will be necessary to validate the inhibitory effects of these compounds on fumonisins biosynthesis.