Decreased Expression of a Phosphoribosylanthranilate Transferase-Encoding Gene, OsPAT1, Causes Lesion Mimics in Rice

Lesion mimic mutants (LMMs) represent valuable biological tools for investigating plant defense mechanisms and cell death. Although multiple genes triggering lesion mimic formation have been identified, the connection between the lesion mimic phenotype and primary nutrient biosynthesis remains poorly understood. In our study, we characterized a novel rice LMM, <i>lmm9</i>, which exhibited persistent reddish-brown necrotic lesions from seedling stage to maturity, coupled with compromised agronomic traits and increased mortality rates. Map-based cloning and whole-genome sequencing identified a causal insertion in the promoter of <i>Os03g03450/OsPAT1</i>, the sole homolog of <i>Arabidopsis PAT1</i> in rice, resulting in reduced gene expression. Genetic complementation and RNAi assays confirmed that downregulation of <i>OsPAT1</i> led to lesion mimic formation in <i>lmm9</i>. <i>OsPAT1</i> could translate into two variants-the predominant OsPAT1.1 and the C-terminal variant OsPAT1.2. Structural modeling demonstrated high conservation between OsPAT1 and yeast TRP4, and OsPAT1.1 combining the plastid signal sequence of Arabidopsis PAT1 successfully complemented the <i>trp4</i> mutant in yeast. Notably, OsPAT1.1 and OsPAT1.2 showed different localization patterns, with OsPAT1.1 targeted to mitochondria and OsPAT1.2 localized to chloroplasts. Transcription analysis showed significant upregulation of tryptophan biosynthesis pathway genes in <i>lmm9</i>, consequently increasing the relative abundance of tryptophan and associated metabolites. Our findings provided further evidence that mutations in tryptophan biosynthetic genes can induce lesion mimic phenotypes in rice and would enhance the understanding of metabolic homeostasis in plant stress responses and cell death regulation.