OsASA2 Loss-of-Function Confers Broad-Spectrum Disease Resistance and Triggers Cell Death by Regulating Anthranilate...

Lesion mimic mutants are valuable for studying plant cell death and defence mechanisms. Here, we identify a rice lesion mimic mutant, osasa2-1, which exhibits spontaneous cell death and enhanced disease resistance. The mutant displays white spots on leaves that develop into large brown lesions. Histological analysis reveals increased cell death and H₂O₂ accumulation. Map-based cloning identified the causal gene as OsASA2 (LOC_Os03g15780). The osasa2-1 mutant carries a G496 deletion that introduces a premature stop codon, likely resulting in nonsense-mediated decay of the mutant transcript. We demonstrate that OsASA2 interacts with OsASA1, OsASB1 and OsASB2. Its loss-of-function leads to hyperactivation of anthranilate synthase (AS) activity, enhancing tryptophan biosynthesis and metabolic flux into downstream pathways. The osasa2-1 mutant exhibits elevated reactive oxygen species (ROS) levels, increased callose deposition and upregulation of defence-related genes, contributing to enhanced resistance against both the rice blast fungus Magnaporthe oryzae and the bacterial blight pathogen Xanthomonas oryzae pv. oryzae. Our findings highlight a novel regulatory role for OsASA2 in conferring broad-spectrum disease resistance by modulating AS activity and the tryptophan biosynthetic pathway in rice.