1Division of Functional Genomics, Advanced Science Research Center, Kanazawa University, 13-1 Takaramachi, Kanazawa 920-0934, Japan; 2Plant Functions Laboratory, RIKEN Institute, 2-1 Hirosawa, Wako, Saitama 351-0198, Japan; 3Laboratory for Plant Molecular Biology, RIKEN Tsukuba Institute, 3-1-1, Koyadai, Tsukuba 305-0074, Japan; 4Laboratory for Remediation Research, Plant Science Center, RIKEN, Yokohama 230-0045, Japan
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Accepted 9 January 2006.
Phytopathogenic fungi such as Fusarium spp. synthesize trichothecene family phytotoxins. Although the type B trichothecene, deoxynivalenol (DON), is thought to be a virulence factor allowing infection of plants by their trichothecene-producing Fusarium spp., little is known about effects of trichothecenes on the defense response in host plants. Therefore, in this article, we investigated these effects of various trichothecenes in Fusarium-susceptible Arabidopsis thaliana. Necrotic lesions were observed in Arabidopsis leaves infiltrated by 1 μM type A trichothecenes such as T-2 toxin. Trichothecene-induced lesions exhibited dead cells, callose deposition, generation of hydrogen peroxide, and accumulation of salicylic acids. Moreover, infiltration by trichothecenes caused rapid and prolonged activation of two mitogen-activated protein kinases and induced expression of both PR-1 and PDF1.2 genes. Thus, type A trichothecenes trigger the cell death by activation of an elicitor-like signaling pathway in Arabidopsis. Although DON did not have such an activity even at 10 μM, translational inhibition by DON was observed at concentrations above 5 μM. These results suggested that DON is capable of inhibiting translation in Arabidopsis cells without induction of the elicitor-like signaling pathway.
MAP kinase cascadesymbiosis.
© 2006 The American Phytopathological Society