Integrated Transcriptomic and Metabolomic Analyses Reveal the Importance of the Terpenoid, Fatty Acid, and Flavonoid Pathways in Rice Cell Death and Defense

Lesion mimic mutants provide unique tools to investigate plant-pathogen interactions, often exhibiting hypersensitive responses in the absence of biotic or abiotic stresses. The overexpression of the S-domain receptor-like kinase gene, SPL11 cell-death suppressor 2 (SDS2), in rice leads to constitutive programmed cell death and enhanced resistance to fungal and bacterial pathogens. However, the mechanisms underlying this broad-spectrum resistance remain unclear. This study integrates transcriptomic and metabolomic analyses of the SDS2-ACT mutant to uncover gene expression and metabolic shifts associated with disease resistance. To identify SDS2-specific physiological changes related to pathogen resistance, leaf tissues from the SDS2-ACT mutant and the Kitkaake WT line were subjected to both transcriptomic and non-targeted metabolic profiling. Transcriptomic analyses identified 1497 differentially expressed genes (DEGs), including up-regulated genes involved in terpenoid and flavonoid biosynthesis, phytohormone signaling, and defense-related pathways (including pathogenesis-related [PR] genes). Metabolomic profiling revealed significant alterations in the accumulation of several compound classes, including putative: terpenoids, phenylpropanoids, phytohormones, fatty acids, and sugars. These changes are likely correlated with the observed cell death and resistance phenotypes in the SDS2-ACT mutant. This study provides an overall landscape of the transcriptomic and metabolomic alterations in a lesion mimic mutant, identifying candidate defense-related genes and metabolites for functional analysis in rice.