| Description: | Deoxynivalenol (DON, vomitoxin), a trichothecene mycotoxin, mainly produced by Gibberella zeae, inhibits protein synthesis via binding to the ribosome and interfering with peptidyltransferase. DON causes apoptosis (cytotoxicity) and immunotoxicity to eukaryotic organisms. In animal cells, trichothecene activates mitogen-activated protein kinases(MAPKs) (including SAPK/JNK,p38MAPK and ERK) (Yang et al, 2000). DON appears to be unique in that other classes of trichothecenes do not activate these protein kinases. In plant, DON is a virulence factor in the pathogenesis of G. zeae on wheat (Desjardins et al 1996). Our primary work on the mechanism of DON toxicity to Arabidopsis (unpublished) also showed that DON inhibits germination dramatically. However we still have little data about the molecular mechanism of DON toxicity to plants. What pathways in the plant are involved in responding to the toxin? What genes are turned on or off during cell apoptosis by the toxin? To further understand overall gene profiling of plants in response to DON, we propose to utilize the Arabidopsis Functional Genomics Consortium microarray to compare the Arabidopsis response to DON treatment. This genome-wide study will provide important clues to facilitate the improvement of plant resistance to DON. As a first step, we will prepare RNAs from young seedlings of Columbia wild type treated with DON and water. These microarray data from the treated and untreated with DON will be useful for further understanding of toxicology of DON to plants. |
NASCArrays Information at The BAR
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