Different salicylic and jasmonic acids imbalances are involved in the oxidative stress-mediated cell death, induced by fumonisin B1 in maize seedlings with contrasting resistance to Fusarium verticillioides ear rot in the field.

Abstract

Background and aimFungal and plant secondary metabolites modulate the plant-pathogen interactions. However, the participation of fumonisins in the Fusarium verticillioides-maize pathosystem is unclear. In this work was studied the cell death, and the reactive oxygen species (ROS) - phytohormone imbalance interplay underlying the phytotoxicity of fumonisin B1 (FB1) in maize germplasms with contrasting resistance to Fusarium ear rot in the field. MethodsResistant (RH) and susceptible hybrid (SH) maize seedlings, grown from uninoculated seeds irrigated with FB1 (1 and 20 ppm), were harvested at 7, 14 and 21 days after planting, and were examined for electrolyte leakage (aerial parts); and for oxidative stress biomarkers (aerial parts and roots). The phytohormone (salicylic and jasmonic acids) imbalance interplay underlying the FB1-induced cell death were further explored in seedlings exposed 24 h to the mycotoxin (1 ppm) in hydroponics. ResultsCell death increased in RH and SH watered with 1 and 20 ppm of mycotoxin, respectively. Both toxin concentrations were pro-oxidant, and the major perturbations were found in roots. An Integrated Biomarker Response index was calculated suggesting that phytotoxicity occurs in a redox context more efficiently controlled by RH. ConclusionThe pre-treatment with the antioxidant ascorbic acid led to the conclusion that cell death in RH was related to a salicylic acid increase mediated by ROS. Nevertheless, FB1 induced two different phytohormonal regulatory mechanisms mediated by oxidative stress in both maize hybrids.