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Aflatoxins are carcinogenic secondary metabolites produced by Aspergillus flavus and other closely related species. Many internal and external factors, such as nutrition, environment and interaction with the host (Zea mays) can affect aflatoxin biosynthesis. Host defence-related compounds, like oxylipins, may induce sporulation and modulate mycotoxins biosynthesis in several pathogenic fungi, apparently by replacing fungal endogenous oxylipins, produced by lipoperoxidative processes of lipoxygenase (LOX) and dioxygenase enzymes. In A. flavus, these oxylipins are crucial signals for the regulation of mycotoxins biosynthesis, conidiogenesis and sclerotia formation. To study how inhibition of oxylipins formation may affect the A. flavus metabolism and its relation with the host (maize kernels), we obtained a mutant (AfΔlox strain) presenting a knock-out of the lox1 gene, encoding a homologue of the human arachidonate 15-lipoxygenase. Onto liquid and solid media, the mutant displayed a different colony morphology in comparison with 3357 wild-type strain, i.e. absence of conidia, lack of aflatoxins biosynthesis and a lower basal activity of LOX enzyme. Interestingly, its conidiation and aflatoxins production was recovered by growing the strain onto maize seeds. To better understand the involvement of the crosstalk Z. mays-A. flavus, we performed an oxylipin profile of the two strains (WT and AfΔlox) and of the maize seeds after host colonization using an LC-TOF based lipidomic approach followed by a PCA statistical analysis. The results will contribute to the current knowledge on the role of lipid peroxidation governed by the lox1 gene in the morphogenesis, aflatoxins biosynthesis, and in host-pathogen interaction.

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