Omics study reveals the regulation network of CEBiP in rice defense against Magnaporthe oryzae
Rice blast disease is regarded as a major threat to rice yields. The efficient and sustainable strategies for disease control mainly rely on the use of resistant crop varieties. Plants initiate basal defense responses upon pathogen detection by cell surface-localized pattern recognition receptors (PRRs), which consist of receptor-like kinases (RLKs) and receptor-like proteins (RLPs). CEBiP is a typical RLP in rice and requires the RLK CERK to activate the chitin-induced defense response against rice blast-causing fungal pathogen, Magnaporthe oryzae. However, our knowledge about the broader signaling and metabolomic pathways associated with CEBiP activation remains partial. Here, we performed an integrated transcriptomic and metabolomic analysis of rice ZH11 genotype and CEBiP knockout mutant plants. Both plants were infected with M. oryzae and infected leaves were harvested at 24, 48, and 72 hpi for RNA sequencing and LC-MS/MS analysis. Comparative transcriptomic analysis reveals a total of 655 genes that were specifically differentially regulated upon knockout of CEBiP , they were mainly related to diterpenoid biosynthesis, phenylpropanoid biosynthesis, nitrogen metabolism, MAPK signaling pathway, plant-pathogen interaction, and plant hormone signal transduction. Comparative metabolomic analysis uncovers a total of 962 specifically regulated metabolites, and caffeine metabolism and glutathione metabolism appear to be essential for the CEBiP-mediated defense response. Through integrated transcriptomic and metabolomic analyses, we propose that salicylic acid (SA) signaling plays a dominant role in the CEBiP immune function.