Cell death induced by mycotoxin fumonisin B(1) is accompanied by oxidative stress and transcriptional modulation in Arabidopsis cell culture

KEY MESSAGE: Fumonisin B (1) induces rapid programmed cell death in Arabidopsis cells, oxidative and nitrosative bursts, and differentially modulates cell death responsive genes. Glutathione is the main antioxidant involved in the stress response. ABSTRACT: Fumonisin B(1) (FB(1)) is a fungal toxin produced by Fusarium spp. able to exert pleiotropic toxicity in plants. FB(1) is known to be a strong inducer of the programmed cell death (PCD); however, the exact mechanism underling the plant–toxin interactions and the molecular events that lead to PCD are still unclear. Therefore, in this work, we provided a comprehensive investigation of the response of the model organism Arabidopsis thaliana at the nuclear, transcriptional, and biochemical level after the treatment with FB(1) at two different concentrations, namely 1 and 5 µM during a time-course of 96 h. FB(1) induced oxidative and nitrosative bursts and a rapid cell death in Arabidopsis cell cultures, which resembled a HR-like PCD event. Different genes involved in the regulation of PCD, antioxidant metabolism, photosynthesis, pathogenesis, and sugar transport were upregulated, especially during the late treatment time and with higher FB(1) concentration. Among the antioxidant enzymes and compounds studied, only glutathione appeared to be highly induced in both treatments, suggesting that it might be an important stress molecule induced during FB(1) exposure. Collectively, these findings highlight the complexity of the signaling network of A. thaliana and provide information for the understanding of the physiological, molecular, and biochemical responses to counteract FB(1)-induced toxicity. SUPPLEMENTARY INFORMATION: The online version contains supplementary material available at 10.1007/s00299-022-02888-5.