SUMMARYPseudomonas 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.
Faculty Opinions recommendation of Arabidopsis RIN4 negatively regulates disease resistance mediated by RPS2 and RPM1 downstream or independent of the NDR1 signal modulator and is not required for the virulence functions of bacterial type III effectors AvrRpt2 or AvrRpm1.
