Regulation of the phytotoxic response of Arabidopsis thaliana to the Fusarium mycotoxin deoxynivalenol

Abstract

Phytopathogenic fungi, such as Fusarium spp., synthesize trichothecene family phytotoxins. The type B trichothecene, namely deoxynivalenol (DON), is highly prevalent in small-grain cereals, such as wheat, corn and barley. DON is thought to be a virulence factor allowing plant infections and has an elicitor activity. We used the model plant Arabidopsis thaliana to evaluate the phytotoxic effects of DON in host plants. The growth of A. thaliana on media was significantly inhibited by DON. Moreover, DON induced cell death in detached leaves was observed by trypan blue staining. This is consistent with the phenomenon of organelle changes observed at the ultrastructural level. In our study, DON exposure stimulated oxidative bursts in the leaves, resulting in the concomitant down-regulation of antioxidant enzyme defense responses and up-regulation of lipid peroxidation. In addition, a real-time PCR analysis revealed that the DON treatment rapidly induced the transcription of defense genes, like AtrbohC and AtrbohD, and up-regulated the transcriptional level of the ascorbic acid peroxidase gene. These results suggested that DON phytotoxicity might result from reactive oxygen species pathways, and that DON production by the plant pathogen Fusarium graminearum can act as an elicitor influencing plant cell fate.