Asymmetric selection of a rice immune module and rebuild of disease resistance

Artificial selection has greatly shaped crop agronomic traits^1-3; however, the mechanistic basis of how immunity is selected remains unclear. Here we identify the Oryza sativa nucleotide-binding site and leucine-rich repeat (NLR) receptor XA48 and downstream transcription factors OsVOZ1 and OsVOZ2 (OsVOZ1/2), which confer resistance to bacterial blight. XA48 perceives the ancient pathogen effector XopG, activating effector-triggered immunity by degrading the negative regulator OsVOZ1/2. The XA48-OsVOZ1 module has undergone subspecies-specific selection: Xa48 is retained only in Oryza sativa indica and was lost in Oryza sativa japonica. By contrast, OsVOZ1 has diverged into two haplotypes-O. s. indica retains both OsVOZ1^A/S alleles compatible with Xa48, whereas O. s. japonica has only OsVOZ1^A. Reintroducing Xa48 into O. s. japonica severely compromises yield owing to the XA48-OsVOZ1^A-mediated immune incompatibility. Stacking XA48-mediated effector-triggered immunity with XA21-mediated pattern-triggered immunity reconstitutes the broad-spectrum resistance from wild rice. Our study therefore reveals how asymmetric selection of an NLR-transcription factor module shapes disease resistance and reproductive development, providing a strategy for breeding crops by harnessing the relative immunity of wild rice.