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Updated: Oct 12, 2025

Quantification of Fungal Colonization, Sporogenesis, and Production of Mycotoxins Using Kernel Bioassays
Published on: April 23, 2012
Lipid Signaling Modulates the Response to Fumonisin Contamination and Its Source, Fusarium verticillioides, in Maize
Laura Righetti1, Chiara Dall'Asta1, Luigi Lucini2
1Department of Food and Drug, University of Parma, Parma, Italy.
Abstract:
Fumonisin-contaminated maize (Zea mays L.) products are a major health concern because of their toxic effects in humans and animals. Breeding maize for increased mycotoxin resistance is one of the key sustainable strategies for mitigating the effects of fumonisin contamination. Recent studies suggest a link between fumonisin accumulation and plant lipid and oxylipin profiles. However, the data collected so far do not reveal a cause-and-effect relationship. In this study, to decipher the multifactorial nature of mycotoxin resistance and plant-pathogen interaction mechanisms, we examined the oxylipin and complex lipid profiles of two maize hybrids (H21 and H22, the latter showing significantly lower FBs content) grown in the open field in two locations over 3years. Untargeted ultra-high performance liquid chromatography coupled with quadrupole-time-of-flight (UHPLC-Q-TOF), together with chemometrics analysis, successfully distinguished between the two hybrids as having low- and high-level fumonisin contamination. Considering that H21 and H22 were exposed to the same environmental factors, the higher activation of lipid signaling systems in H22 suggests that other routes are enabled in the less susceptible hybrids to limit fumonisin B (FB) accumulation. Our results highlighted the crucial role played by oxylipin and sphingolipid signaling in modulating the complex maize response to F. verticillioides infection. Overall, our results returned a global view on the changes in lipid metabolites related to fumonisin accumulation under open field conditions, and revealed a strong activation of the lipid signaling cascade in maize in the presence of FB1.
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