Pathogen-associated molecular patterns (PAMPs) elicit basal defense responses in plants, and, in turn, pathogens have evolved mechanisms to overcome these PAMP-induced defenses. To suppress immunity, the phytopathogenic bacterium Pseudomonas syringae secretes effector proteins, the biochemical function and virulence targets of which remain largely unknown. We show that HopAI1, an effector widely conserved in both plant and animal bacterial pathogens, inhibits the Arabidopsis mitogen-activated protein kinases (MAPKs) activated by exposure to PAMPs. HopAI1 inactivates MAPKs by removing the phosphate group from phosphothreonine through a unique phosphothreonine lyase activity, which is required for HopAI1 function. The inhibition of MAPKs by HopA1 suppresses two independent downstream events, namely the reinforcement of cell wall defense and transcriptional activation of PAMP response genes. The MAPKs MPK3 and MPK6 physically interact with HopAI1 indicating that they are direct targets of HopAI1. These findings uncover a mechanism by which Pseudomonas syringae overcomes host innate immunity to promote pathogenesis.

Salicylic acid (SA) is a defense hormone required for both local and systemic acquired resistance (SAR) in plants. Pathogen infections induce SA synthesis through up-regulating the expression of Isochorismate Synthase 1 (ICS1), which encodes a key enzyme in SA production. Here we report that both SAR Deficient 1 (SARD1) and CBP60g are key regulators for ICS1 induction and SA synthesis. Whereas knocking out SARD1 compromises basal resistance and SAR, overexpression of SARD1 constitutively activates defense responses. In the sard1-1 cbp60g-1 double mutant, pathogen-induced ICS1 upregulation and SA synthesis are blocked in both local and systemic leaves, resulting in compromised basal resistance and loss of SAR. Electrophoretic mobility shift assays showed that SARD1 and CBP60g represent a plant-specific family of DNA-binding proteins. Both proteins are recruited to the promoter of ICS1 in response to pathogen infections, suggesting that they control SA synthesis by regulating ICS1 at the transcriptional level.

Plants use receptor kinases, such as FLS2 and EFR, to perceive bacterial pathogens and initiate innate immunity. This immunity is often suppressed by bacterial effectors, allowing pathogen propagation. To counteract, plants have evolved disease resistance genes that detect the bacterial effectors and reinstate resistance. The Pseudomonas syringae effector AvrPto promotes infection in susceptible plants but triggers resistance in plants carrying the protein kinase Pto and the associated resistance protein Prf. Here we show that AvrPto binds receptor kinases, including Arabidopsis FLS2 and EFR and tomato LeFLS2, to block plant immune responses in the plant cell. The ability to target receptor kinases is required for the virulence function of AvrPto in plants. The FLS2-AvrPto interaction and Pto-AvrPto interaction appear to share similar sequence requirements, and Pto competes with FLS2 for AvrPto binding. The results suggest that the mechanism by which AvrPto recognizes virulence targets is linked to the evolution of Pto, which, in association with Prf, recognizes the bacterium and triggers strong resistance.

No abstract

Pathogen-associated molecular patterns (PAMPs) trigger plant defenses when perceived by surface-localized immune receptors. PAMP-triggered immunity (PTI) plays a vital role in the resistance of plants to numerous potential pathogens. MicroRNA (miRNA) biogenesis is known to be important for PTI, but miRNA species involved in this process have not been fully explored. Here we show that the Arabidopsis (Arabidopsis thaliana) miRNA effector protein, Argonaute1 (AGO1), is required for a number of PTI responses including PAMP-induced callose deposition, gene expression, and seedling growth inhibition. Deep sequencing of AGO1-bound small RNAs led to the identification of a number of miRNAs that are up-or down-regulated by flg22, a well-studied PAMP. Overexpression of selected miRNAs in stable transgenic plants demonstrated that miR160a positively regulate PAMP-induced callose deposition, whereas miR398b and miR773 negatively regulate PAMPinduced callose deposition and disease resistance to bacteria, suggesting a complexity of the miRNA regulation in plant innate immunity.