Vm00799 enhances pathogenicity through the MdTCP7–MdERF1B–ethylene signaling module and drives virulence differences between Valsa mali and V. pyri on apple

Apple Valsa canker (AVC), a destructive fungal disease caused primarily by Valsa mali (= Cytospora mali), poses a major threat to apple production. Its close relative, V. pyri, also infects apples but exhibits substantially weaker virulence than V. mali, and the molecular basis underlying this difference remains unclear. Here, we identified a V. mali-specific effector, Vm00799, as a key determinant of enhanced virulence on apple. Vm00799 targets the apple transcription factor MdTCP7 to enhance its binding to the MdERF1B promoter, thereby activating the MdTCP7-MdERF1B module and suppressing ethylene-mediated defense responses. Consistently, MdTCP7 and MdERF1B negatively regulate apple resistance, whereas ethylene signaling positively contributes to immunity against V. mali. Importantly, ectopic expression of Vm00799 significantly increased the virulence of V. pyri on apple in an MdTCP7-dependent manner. Collectively, our findings reveal that Vm00799 promotes V. mali infection by hijacking host transcriptional regulation to suppress ethylene-dependent immunity. This study uncovers the molecular basis of virulence divergence among closely related Valsa species and identifies potential target for AVC control.