Authors
Xiurong Yang, Shuangyong Yan, Zhongchi Cui, Yuejiao Li, Ruixiang Wang, Shuqin Sun, Guangsheng Li, Fei Zhao, Jingping Su, Shengjun Wang
Published in
Plant disease. Pages PDIS07251546RE. Sep 30, 2026. Epub Sep 30, 2026.
Abstract
Rice blast, caused by Magnaporthe oryzae, severely threatens global rice production. This study deciphers the molecular basis of blast resistance through comparative transcriptomics of resistant (403) and susceptible (402) rice cultivars. Resistant plants exhibited limited symptom development, accompanied by targeted transcriptional reprogramming with only 393 differentially expressed genes (DEGs) versus 1,336 DEGs in susceptible plants. Kyoto Encyclopedia of Genes and Genomics (KEGG) analysis revealed preferential activation of defense-centric pathways in resistant cultivars, including diterpenoid biosynthesis (12 DEGs), phenylpropanoid metabolism (5 upregulated genes: prx15, poxN, OsPAL04, POXgX9, and 4CL5), and MAPK signaling. Notably, conserved upregulation of terpenoid/lipid metabolism genes (93 DEGs) and resistant-specific induction of key regulators (LOX-L2 for jasmonic acid [JA] biosynthesis and BOR2/UGD1 for cell wall reinforcement) formed a coordinated defense network. Contrastingly, susceptible plants showed inefficient activation of DNA replication and cell cycle pathways. Transcription factor (TF) dynamics further highlighted this divergence, with resistant plants displaying focused TF regulation (23 DEGs) versus widespread changes in susceptible plants (105 DEGs). Quantitative real-time PCR (qPCR) validation confirmed resistant-specific upregulation of phenylpropanoid (prx128, prx15, OsPAL04, poxN, and POXgX9) and phenylalanine metabolism genes (OsAMI2, TDC1, and OsTDC3), while susceptibility-associated genes (prx27 and prx17) were upregulated in susceptible varieties. This study uncovers the diterpenoid biosynthesis pathway as a central hub in rice blast resistance, providing theoretical foundations for improving resistance through genetic engineering or molecular breeding.
PMID:
42814898
Bibliographic data and abstract were imported from PubMed on 01 Oct 2026.
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