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

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.