Abstract The fungal phytotoxin pyriculol, produced by Magnaporthe oryzae, is potentially implicated in rice blast pathogenesis due to its necrosis-inducing activity. However, its functional role remained enigmatic. Here, we demonstrate that pyriculol does not act as a virulence factor for M. oryzae, as pathogenicity assays using transgenic fungal strains with altered pyriculol biosynthesis showed no correlation between pyriculol levels and disease severity across diverse rice genotypes. Strikingly, exogenous application of pyriculol or its isomer pyriculariol significantly enhanced rice resistance to M. oryzae, reducing lesion expansion by 30% and amplifying oxidative burst and defence-related gene expression (OsPR1a, OsPBZ1, and OsCPS4). Mechanistically, pyriculol mimicked salicylic acid (SA) by suppressing early jasmonate (JA) biosynthesis genes (OsAOS1/2 and OsAOC) and JA-responsive JAZ transcripts post-wounding, yet uniquely spared OsJAR1, enabling systemic JA-Ile conversion from methyl jasmonate. This selective modulation decoupled local JA–SA antagonism, promoting SA-driven defence priming while permitting systemic JA signalling. Histological analyses revealed that pyriculol-induced host cell death restricted fungal hyphal progression, synergizing with pathogen-triggered phytoalexin biosynthesis. Our findings redefine pyriculol as a fungal metabolite that paradoxically bolsters rice immunity via phytohormone crosstalk, offering novel insights into host–pathogen co-evolution and potential applications in plant defence potentiation.
Ma et al. (Tue,) studied this question.