The Magnaporthe oryzae effector MoCHT1 targets and stabilizes rice OsLLB to suppress jasmonic acid synthesis and enhance infection.

Rice blast disease caused by Magnaporthe oryzae (M. oryzae) poses a serious threat to rice security worldwide. This filamentous pathogen modulates rice defense responses by secreting effectors to facilitate infection. The phytohormone jasmonic acid (JA) plays crucial roles in the response to rice blast fungus. However, how M. oryzae disrupts JA-mediated resistance in rice is not well understood. In this study, we identify a new effector, a chloroplast-targeting protein (MoCHT1), from M. oryzae. Knocking out MoCHT1 decreases virulence, whereas heterologous expression of MoCHT1 in rice compromises disease resistance. MoCHT1 interacts with a rice LESION AND LAMINA BENDING (OsLLB) protein, a negative regulator of JA biosynthesis in the chloroplast. Loss-of-function of OsLLB leads to increased JA accumulation, thereby improving resistance to rice blast. The interaction between MoCHT1 and OsLLB results in the inhibition of OsLLB degradation, consequently reducing JA accumulation, thereby impairing JA content and decreasing plant disease resistance. Overall, this study reveals the molecular mechanism by which M. oryzae utilizes MoCHT1 to subvert rice JA signaling, broadening our understanding of how pathogens circumvent host immune responses by manipulating plant defense hormone biosynthesis.