Inactivating a β1 subunit of SnRK1 promotes broad-spectrum disease resistance in rice

Summary Rice is a staple crop for over half of the world’s population, and its sustainable production is vital to ensure global food security. However, rice is highly susceptible to several devastating fungal diseases 1 , including blast disease caused by Magnaporthe oryzae , sheath blight by Rhizoctonia solani , false smut by Ustilaginoidea virens , brown spot by Bipolaris oryzae , bakanae by Fusarium fujikuroi , and head blight by F. graminearum . The mechanisms underlying the susceptibility of rice to these fungal diseases remain unclear. Here, we report that the β subunit of SnRK1, SnRK1β1A, confers broad-spectrum susceptibility to these fungal diseases. Our findings reveal that diverse rice fungal pathogens have convergently evolved an effector, Gas2, which interacts with SnRK1β1A to prevent its ubiquitination-mediated degradation and promotes its nuclear translocation. While SnRK1 β 1A is expressed at low levels in healthy plants, its expression is markedly induced upon fungal infections, facilitating susceptibility by inhibiting SnRK1α1, the α subunit of SnRK1, whose overexpression has been shown to enhance broad-spectrum resistance in rice 2 . Notably, rice lines with disrupted SnRK1 β 1A are resistant to multiple fungal diseases without compromising growth and yield in the field. Together, this study demonstrates that broad-spectrum disease resistance in crops can be achieved by disrupting inducible susceptibility genes whose encoded proteins are targeted by effectors conserved in multiple pathogens.