The Role of Ethylene in PAMP-Triggered Immunity in Fusarium Crown Rot Disease Resistance in Wheat

Fusarium Crown Rot (FCR) is a devastating disease of cereal crops worldwide cause by necrotrophic fungal pathogens Fusarium graminearum and Fusarium pseudograminearum, resulting in 89% crop loss.  No-till cultivation conservation efforts have led to a resurgence of FCR.  Recently, our laboratory has shown that disease resistance to FCR can be enhanced in susceptible wheat cultivars by stimulating the ethylene-signaling pathway with ethylene biosynthetic precursor 1-aminocyclopropene-1carboxylic acid (ACC).  Additionally,  resistant cultivars become more susceptible when ethylene-signaling is inhibited by treatment with the competitive inhibitor 1-methylcylopropene (1-MCP).  Stimulating the ethylene-signaling pathway has also shown enhanced basal defense response to pathogen-associated molecular pattern flg22 in FCR-susceptible wheat cv ‘Kennedy’ and blocking ethylene perception appears to decrease basal defense response to flg22 in FCR-resistant wheat cv ‘Bobwhite’.  RNA-Seq analysis of FCR-susceptible wheat cv ‘Kennedy’ during enhanced resistant and genetically susceptible interactions has shown a significant difference in Differentially Expressed Genes (DEGs).  In the ACC-treated enhanced resistant interaction, 7466 and 6716 DEGs were uniquely up and down regulated, respectively.  Many of the DEGs identified by Biotic Stress MapMap analysis fall within disease-response categories such as peroxidases, pathogenesis-related proteins, WRKY transcription factors, plant hormone signaling, and ethylene response factors.  Further analysis of the RNA-Seq data paired with quantifiable disease responses to FCR and PAMPs will help to determine the role of ethylene signaling in defense responses in wheat.  Additional transcriptome analysis will be performed on genetically resistant wheat cv ‘Bobwhite’ to identify any correlation between induced and genetic resistance to FCR by evaluating shared DEGs and promoter sequences.