RT Journal Article
SR Electronic
T1 A bacterial GW-effector targets Arabidopsis AGO1 to promote pathogenicity and induces Effector-triggered immunity by disrupting AGO1 homeostasis
JF bioRxiv
FD Cold Spring Harbor Laboratory
SP 215590
DO 10.1101/215590
A1 Odon Thiébeauld
A1 Magali Charvin
A1 Meenu Singla Rastogi
A1 Fan Yang
A1 Dominique Pontier
A1 Cécile Pouzet
A1 Laure Bapaume
A1 Guangyong Li
A1 Laurent Deslandes
A1 Thierry Lagrange
A1 James R. Alfano
A1 Lionel Navarro
YR 2017
UL http://biorxiv.org/content/early/2017/11/07/215590.abstract
AB 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.