Fusarium proliferatum is a common hemi-biotrophic pathogen that infect a wide range of host plants, often leading to substantial crop loss and yield reduction. F. proliferatum synthesizes various mycotoxins, and fumonisins B are the most prevalent. They act as virulence factors and specific effectors that elicit host resistance. The effects of selected plant metabolites on the metabolism of the F. proliferatum strain were analyzed in this study. Quercetin-3-glucoside (Q-3-Glc) and kaempferol-3-rutinoside (K-3-Rut) induced the pathogen's growth, while DIMBOA, isorhamnetin-3-O-rutinoside (Iso-3-Rut), ferulic acid (FA), protodioscin, and neochlorogenic acid (NClA) inhibited fungal growth. The expression of seven F. proliferatum genes related to primary metabolism and four FUM genes was measured using RT-qPCR upon plant metabolite addition to liquid cultures. The expression of CPR6 and SSC1 genes was induced 24 h after the addition of chlorogenic acid (ClA), while DIMBOA and protodioscin reduced their expression. The transcription of FUM1 on the third day of the experiment was increased by all metabolites except for Q-3-Glc when compared to the control culture. The expression of FUM6 was induced by protodioscin, K-3-Rut, and ClA, while FA and DIMBOA inhibited its expression. FUM19 was induced by all metabolites except FA. The highest concentration of fumonisin B1 (FB1) in control culture was 6.21 µg/mL. Protodioscin did not affect the FB content, while DIMBOA delayed their synthesis/secretion. Flavonoids and phenolic acids displayed similar effects. The results suggest that sole metabolites can have lower impacts on pathogen metabolism and mycotoxin synthesis than when combined with other compounds present in plant extracts. These synergistic effects require additional studies to reveal the mechanisms behind them.
Keywords: Fusarium; gene expression; metabolites; mycotoxins; plant-pathogen interaction; qPCR.