Molecular Espionage in Plant Immunity: A Pathogen Effector Eavesdrops on Salicylic Acid to Hijack the Host Transcriptional Mediator Hub

Pathogens disrupt transcriptional hubs to subvert host immunity, yet the spatiotemporal mechanisms remain enigmatic. Here, we report a pathogen effector hijacks the core eukaryotic transcriptional machinery by acting as a molecular mimic of host repressors, deploying this sabotage in synchrony with the plant immune rhythm. We discover the Phytophthora sojae nuclear effector directly targets the host Mediator complex. Crucially, PsAvh109 emulates the host repressor TOPLESS (TPL), competitively occupying the Mediator subunit MED21 and locks the MED21-MED6 interaction interface, repressing SA-responsive defense genes without triggering degradation. Strikingly, PsAvh109 expression is induced by host-derived SA, the very signal displaces TPL from MED21 to activate immunity. This enables the pathogen to deploy its molecular trap precisely when the host initiates defense, perpetuating transcriptional repression during a critical vulnerability window. This work establishes a paradigm-shifting 'sensing-response' model in plant-pathogen interactions, wherein Phytophthora pathogens deploy a dynamically synchronized virulence strategy. By eavesdropping on host-derived salicylic acid (SA), the pathogen induces nuclear effector PsAvh109 expression to precisely coincide with TPL dissociation from MED21. Crucially, PsAvh109 executes non-degradative steric blockade of the MED21-MED6 interface through high-fidelity molecular mimicry, perpetuating transcriptional repression without triggering host surveillance systems. This dual-layered strategy redefines effector function as a rhythm-matched molecular sabotage agent.