A bacterial GW-effector directly targets Arabidopsis Argonaute 1 to suppress PAMP-triggered immunity and cause disease
Thiebeauld, O.; Charvin, M.; Singla Rastogi, M.; Yang, F.; Pontier, D.; Pouzet, C.; Bapaume, L.; Amsefe, D.; Li, G.; Deslandes, L.; Lagrange, T.; Alfano, J. R.; Navarro, L.
Show abstract
Pseudomonas syringae type III effectors were previously shown to suppress the Arabidopsis microRNA (miRNA) pathway through unknown mechanisms. Here, we first show that the HopT1-1 effector promotes bacterial growth by suppressing the Arabidopsis Argonaute 1 (AGO1)-dependent miRNA pathway. We further demonstrate that HopT1-1 interacts with Arabidopsis AGO1 through conserved glycine/tryptophan (GW) motifs, and in turn suppresses miRNA function. This process is not associated with a general decrease in miRNA accumulation. Instead, HopT1-1 reduces the level of AGO1-associated miRNAs in a GW-dependent manner. Therefore, HopT1-1 alters AGO1-miRISC activity, rather than miRNA biogenesis or stability. In addition, we show that the AGO1-binding platform of HopT1-1 is essential to suppress the production of reactive oxygen species (ROS) and of callose deposits during Pattern-triggered immunity (PTI). These data imply that the RNA silencing suppression activity of HopT1-1 is intimately coupled with its virulence function. Overall, these findings provide sound evidence that a bacterial effector has evolved to directly target a plant AGO protein to suppress PTI and cause disease.
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