Powdery mildew (PM) leads to severe yield reduction in qingke (Hordeum vulgare L. var. nudum). Although studies have focused on identifying PM-related resistance genes, mechanistic insights into the metabolic regulation… Click to show full abstract
Powdery mildew (PM) leads to severe yield reduction in qingke (Hordeum vulgare L. var. nudum). Although studies have focused on identifying PM-related resistance genes, mechanistic insights into the metabolic regulation networks of resistance against PM have rarely been explored in qingke. Here, we integrated transcriptomic, proteomic and metabolomic data using PM-susceptible (G72) and PM-resistant (K69) accessions to systemically explore the mechanisms of PM resistance. The integrated results show that a rapidly transduction of jasmonic acid (JA) and (+)-7-iso-jasmonoyl-L-isoleucine (JA-Ile), and importantly, a inducing accumulation of aromatic PAs conferred qingke-specific resistance for PM stress. Functional analysis revealed that the four BAHD N-acyltransferase genes were responsible for the synthesis of aliphatic and aromatic PAs. The expression of the four genes are induced by methyl jasmonate (MeJA) and PM treatment. Co-expression network analysis shows that a histone lysine demethylase, JMJ705 gene, also induced by MeJA and PM treatment, had highly correlation with PAs biosynthesis. Chromatin immunoprecipitation (ChIP)-seq assays revealed that the level of trimethylated histone H3 lysine 27 (H3K27me3) of the four genes in MeJA and PM-treated plants was significantly reduced. Overall, our results suggest that a novel strategy for jasmonic acid signal-mediated demethylation controlling the accumulation of aromatic PAs to enhance plant immune resistance through removal of H3K27me3 and activating defense-related gene expression.
               
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