A bacterial GW-effector directly targets Arabidopsis Argonaute 1 to suppress PAMP-triggered immunity and cause disease

Pseudomonas syringae ( P. syringae ) type-III effectors were previously found to suppress the Arabidopsis microRNA (miRNA) pathway through unknown mechanisms. Here, we first show that the P. syringae HopT1-1 effector promotes pathogenicity by suppressing the Arabidopsis Argonaute 1 (AGO1)-dependent miRNA pathway. We further demonstrate that HopT1-1 physically interacts with Arabidopsis AGO1 through conserved glycine/tryptophan (GW) motifs. Importantly, this AGO-binding platform was found to be essential for the ability of HopT1-1 to suppress both miRNA activity and PAMP-Triggered Immunity (PTI). These results therefore indicate that the RNA silencing suppression activity of HopT1-1 is intimately coupled to its virulence function. Overall, these findings provide the first evidence that a bacterial effector has evolved to directly target an AGO protein to suppress PTI and cause disease. ### Competing Interest Statement The authors have declared no competing interest.