Abstract
Trichothecenes are a closely related family of phytotoxins produced by a phytopathogenic fungi. Type A trichothecenes, such as T-2 toxin, caused rapid and prolonged activation of MAPKs, and triggered the cell death by activation of an elicitor-like signaling pathway in Arabidopsis. However, a MAP kinase cascade in the response to trichothecenes is unknown. Novel MAPKKK (MKD1) was identified as a subunit of an AtNFXL1 protein complex. We had revealed that AtNFXL1 functions as a negative regulator of the trichothecene-induced defense response. mkd1 mutant growing on a medium without trichothecenes showed no phenotype, whereas a resistant phenotype was observed in T-2 toxin-treated mkd1 mutant compared with wild type. In addition, the expression of MKD1 was induced by application of T-2 toxin. In gel kinase assays showed that the activation of MPK3 and MPK6 by T-2 toxin in mkd1 mutant was decreased compared with wild type.
