Abstract
The plant pathogen Pseudomonas syringae secretes multiple effectors that modulate plant defenses. Some effectors trigger defenses due to specific recognition by plant immune complexes, whereas others can suppress the resulting immune responses. The HopZ3 effector of P. syringae pv. syringae B728a (PsyB728a) is an acetyltransferase that modifies not only components of plant immune complexes, but also the Psy effectors that activate these complexes. In Arabidopsis, HopZ3 acetylates the host RPM1 complex and the Psy effectors AvrRpm1 and AvrB3. This study focuses on the role of HopZ3 during tomato infection. In Psy-resistant tomato, the main immune complex includes PRF and PTO, a RIPK-family kinase that recognizes the AvrPto effector. HopZ3 acts as a virulence factor on tomato by suppressing AvrPto1Psy-triggered immunity. HopZ3 acetylates AvrPto1Psy and the host proteins PTO, SlRIPK and SlRIN4s. Biochemical reconstruction and site-directed mutagenesis experiments suggest that acetylation acts in multiple ways to suppress immune signaling in tomato. First, acetylation disrupts the critical AvrPto1Psy-PTO interaction needed to initiate the immune response. Unmodified residues at the binding interface of both proteins and at other residues needed for binding are acetylated. Second, acetylation occurs at residues important for AvrPto1Psy function but not for binding to PTO. Finally, acetylation reduces specific phosphorylations needed for promoting the immune-inducing activity of HopZ3’s targets such as AvrPto1Psy and PTO. In some cases, acetylation competes with phosphorylation. HopZ3-mediated acetylation suppresses the kinase activity of SlRIPK and the phosphorylation of its SlRIN4 substrate previously implicated in PTO-signaling. Thus, HopZ3 disrupts the functions of multiple immune components and the effectors that trigger them, leading to increased susceptibility to infection. Finally, mass spectrometry used to map specific acetylated residues confirmed HopZ3’s unusual capacity to modify histidine in addition to serine, threonine and lysine residues.
Highlights
The plant pathogen Pseudomonas syringae uses type III-secreted proteins to promote its growth during infection of plants
Our study emphasizes the importance of HopZ3-dependent acetylation of immune complexes and bacterial effectors across plant species in the suppression of effector-induced immunity
These effector proteins are injected into plant cells, where they often interfere with plant defense signaling either through binding, post-translational modifications (PTMs) and/or destabilization of host factors [1,2]
Summary
The plant pathogen Pseudomonas syringae uses type III-secreted proteins to promote its growth during infection of plants. These effector proteins are injected into plant cells, where they often interfere with plant defense signaling either through binding, post-translational modifications (PTMs) and/or destabilization of host factors [1,2]. AvrB or AvrRpm, from different P. syringae strains can strongly trigger RPM1 signaling and are considered avirulence factors. These effectors cause the cytoplasmic RIN4-INDUCED PROTEIN KINASE (RIPK and probably additional kinases) to phosphorylate RIN4. Immune responses are induced by phosphorylations of specific RIN4 residues that are triggered by recognition of effectors or microbial patterns [3,4,5,6]
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