Acetylation of an NB-LRR Plant Immune-Effector Complex Suppresses Immunity

• HopZ3 targets the RPM1 immune complex and effectors that activate this complex
• HopZ3 acetylates Ser, Thr, Lys, as well as His
• HopZ3 acetylates residues important for multiple facets of plant immune signaling
• Bacterial effector-effector interactions are implicated in the outcome of infection

SummaryModifications of plant immune complexes by secreted pathogen effectors can trigger strong immune responses mediated by the action of nucleotide binding-leucine-rich repeat immune receptors. Although some strains of the pathogen Pseudomonas syringae harbor effectors that individually can trigger immunity, the plant’s response may be suppressed by other virulence factors. This work reveals a robust strategy for immune suppression mediated by HopZ3, an effector in the YopJ family of acetyltransferases. The suppressing HopZ3 effector binds to and can acetylate multiple members of the RPM1 immune complex, as well as two P. syringae effectors that together activate the RPM1 complex. These acetylations modify serine, threonine, lysine, and/or histidine residues in the targets. Through HopZ3-mediated acetylation, it is possible that the whole effector-immune complex is inactivated, leading to increased growth of the pathogen.

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