PsAvh109 suppresses SA-triggered immunity by mimicking TPL function to disrupt mediator complex assembly

Pathogens disrupt transcriptional hubs to subvert host immunity, yet the spatiotemporal mechanisms remain enigmatic. Here, we report a pathogen effector interferes with the core eukaryotic transcriptional machinery by acting as a functional mimic of host repressors, deploying this suppression 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 salicylic acid (SA)-responsive defense genes. Strikingly, PsAvh109 expression is induced by host-derived SA, the very signal displaces TPL from MED21 to activate immunity. This enables the pathogen to release the essential effector PsAvh109 precisely when the host initiates defense, perpetuating transcriptional repression during a critical vulnerability window. Our findings reveal a previously unrecognized strategy where pathogens exploit host signaling dynamics to release effectors that enforce sustained repression of defense programs. Tan et al. demonstrate that a P. sojae effector mimics a plant transcriptional repressor to block immune gene activation. Induced by host salicylic acid, PsAvh109 targets the Mediator complex, thereby sustaining suppression of defense responses during infection.