Fusarium species present ubiquitously in the environment are capable of infecting a wide range of plant species. They produce several mycotoxins targeted to weaken the host plant. While infecting some resistant plants, the host can alter the expression of toxin-related genes and accumulate no/very low amounts of mycotoxins. The ability of the host plant to modulate the biosynthesis of these toxins is entirely depending on the secondary metabolites produced by the plant, often as a part of systemic acquired resistance (SAR). A major role plays in the family of metabolites called phenyl propanoids, consisting of thousands of natural products, synthesized from the phenylalanine or tyrosine amino acids through a cascade of enzymatic reactions. They are also famous for inhibiting or limiting infection through their antioxidant characteristics. The current study was aimed at identifying the differentially expressed secondary metabolites in resistant (Sokolik) and susceptible (Santana) cultivars of pea (Pisum sativum L.) and understanding their roles in the growth and mycotoxin biosynthesis of two different Fusarium species. Although metabolites such as coumarin, spermidine, p-coumaric acid, isoorientin, and quercetin reduced the growth of the pathogen, a higher level of p-coumaric acid was found to enhance the growth of F. proliferatum strain PEA1. It was also noticeable that the growth of the pathogen did not depend on their ability to produce mycotoxins, as all the metabolites were able to highly inhibit the biosynthesis of fumonisin B1 and beauvericin.
Keywords: Fusarium; mycotoxins; secondary metabolites.