A bacterial GW-effector targets Arabidopsis AGO1 to promote pathogenicity and induces Effector-triggered immunity by disrupting AGO1 homeostasis

Pseudomonas syringae type-III effectors were previously found to suppress the Arabidopsis miRNA pathway through elusive mechanisms. Here, we first show that HopT1-1 effector promotes pathogenicity by suppressing the Arabidopsis AGO1-dependent microRNA (miRNA) pathway. We further demonstrate that HopT1-1 interacts with, and suppresses the activity of, AGO1 through conserved glycine/tryptophan-(GW) motifs. HopT1-1 dampens PAMP-Triggered-Immunity (PTI) in a GW-dependent manner and its presence mimics the impaired PTI responses, which were also observed in ago1 mutants. In addition, the silencing suppression activity of HopT1-1 induces Effector-Triggered-Immunity (ETI), which is correlated with an over-accumulation of silencing factors that are controlled by miRNAs, including AGO1. Remarkably, alleviating miR168-directed silencing of AGO1 was sufficient to trigger an ETI-like response, orchestrated by typical disease resistance-immune signaling factors, suggesting that HopT1-1-induced perturbation of AGO1 homeostasis is a trigger of ETI activation. In summary, this study reports for the first time a strategy used by a bacterial effector to directly target an AGO protein and on how plants perceive its silencing suppression activity to trigger a host counter-counter defense.