Rice is a staple crop feeding over half of the global population, yet it faces severe yield losses due to devastating diseases, including those caused by hemibiotrophic pathogens, such as Magnaporthe oryzae (the causative agent of blast disease) and Xanthomonas oryzae pv. oryzae (the bacterial leaf blight pathogen). While resistance genes are a cornerstone of crop protection, many nucleotide-binding leucine-rich receptor (NLR)-type resistance genes are prone to breakdown and often impose yield penalties. In this study, we report that the cross-species transfer of the maize NAM-ATAF1/2-CUC2 transcription factor ZmNAC2 into rice confers resistance to both blast and bacterial leaf blight diseases without compromising yield. Mechanistically, ZmNAC2 interacts with OsNAC2, a negative regulator of salicylic acid (SA) biosynthesis, and disrupts its association with the APETALA2/ethylene-responsive element binding protein OsEREBP1 in the OsZmNAC2 transgenic rice, thereby quenching repression and promoting SA production. Moreover, ZmNAC2 binds to the cis-regulatory elements within the promoter of the SA biosynthetic gene phenylalanine ammonia lyase 6, transactivating its expression and further enhancing SA accumulation. The resulting elevated SA levels impart broad-spectrum resistance in the transgenic rice against M. oryzae and X. oryzae pv. oryzae. Together, our findings provide a proof of concept for leveraging non-NLR genes from staple food crops to boost disease resistance without incurring yield penalties.
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