The Magnaporthe oryzae effector MoBys1 suppresses rice immunity by targeting OsCAD2 to manipulate host jasmonate and lignin metabolism.

Rice blast disease caused by Magnaporthe oryzae poses a severe threat to rice production. To counteract M. oryzae, plants synthesize jasmonate (JA) and lignin, two primary defense-related metabolites, to initiate defense programs. However, the mechanism through which M. oryzae modulates JA- and lignin-mediated plant immunity remains unclear. In this study, a novel M. oryzae effector, MoBys1, was identified as being involved in pathogenesis. Knockout of MoBys1 in M. oryzae significantly reduced its infection ability. Conversely, overexpression of MoBys1 in rice impaired the rice defense response. MoBys1 localizes to the plant cytoplasm and nucleus and interacts with rice cinnamyl alcohol dehydrogenase 2 (OsCAD2), an enzyme that catalyzes lignin biosynthesis. While OsCAD2 mutants exhibited weakened defenses, overexpression lines demonstrated enhanced resistance, highlighting the critical role of OsCAD2 in blast resistance. Furthermore, OsCAD2 functions as a transcription factor regulating a wide range of biological processes, including JA and lignin signaling pathways. The interaction between MoBys1 and OsCAD2 promotes OsCAD2 degradation, leading to reduced lignin and JA accumulation. These findings uncover a novel counter-defense mechanism by which M. oryzae employs the effector MoBys1 to degrade OsCAD2 and suppress host defense-related metabolite accumulation during infection.