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Fusarium head blight (FHB) caused by Fusarium graminearum is a devastating disease of wheat, barley and other grain cereals worldwide.It not only causes severe yield losses but also contaminates infected grains with harmful mycotoxins such as trichothecene deoxynivalenol (DON), which is inhibitory to protein synthesis in eukaryotes by binding with L3.Although its molecular target is conserved, F.graminearum is highly tolerant against DON.However, like in many other mycotoxin-producing fungi, the molecular mechanism conferring self-protection against DON in F.graminearum is not clear.Two genes in the trichothecene biosynthesis clusters, TRI12 and TRI101, have been implicated in providing some degree of DON-tolerance but the tri12 and tri101 mutants still produce DON.Other genes must exist to be responsible for conferring self-protection against DON in F.graminearum.In this study,we firstly generated the T512101triple mutant by deletion of the TRI5, TRI12, and TRI101genes simultaneously.The T512101 mutant was defected in DON production and plant infection but still resistant to exogenous DON.We then used the RNA-seq approach to identify genes induced by DON treatment.Because DON is inhibitory to protein synthesis, cycloheximide (CHX) treatment was used as the control.We screened 264 genes specifically induced by DON but not CHX treatment.Through gene annotation and GO enrichment analysis, we selected 21 genes that were likely involved in DON resistance for further functional characterization.First, their expression profiles were verified by qRT-PCR.Candidate genes were then selected for determining their functions related to self-protection against DON in F.graminearum.Results from these on-going functional studies will be presented and discussed for their potentials for developing transgenic plants with improved FHB resistance and reduced DON contamination.