Abstract
Plant resistance (R) proteins provide a robust surveillance system to defend against potential pathogens. Despite their importance in plant innate immunity, relatively few of the ∼170 R proteins in Arabidopsis have well-characterized resistance specificity. In order to identify the R protein responsible for recognition of the Pseudomonas syringae type III secreted effector (T3SE) HopZ1a, we assembled an Arabidopsis R gene T–DNA Insertion Collection (ARTIC) from publicly available Arabidopsis thaliana insertion lines and screened it for plants lacking HopZ1a-induced immunity. This reverse genetic screen revealed that the Arabidopsis R protein HOPZ-ACTIVATED RESISTANCE 1 (ZAR1; At3g50950) is required for recognition of HopZ1a in Arabidopsis. ZAR1 belongs to the coiled-coil (CC) class of nucleotide binding site and leucine-rich repeat (NBS–LRR) containing R proteins; however, the ZAR1 CC domain phylogenetically clusters in a clade distinct from other related Arabidopsis R proteins. ZAR1–mediated immunity is independent of several genes required by other R protein signaling pathways, including NDR1 and RAR1, suggesting that ZAR1 possesses distinct signaling requirements. The closely-related T3SE protein, HopZ1b, is still recognized by zar1 Arabidopsis plants indicating that Arabidopsis has evolved at least two independent R proteins to recognize the HopZ T3SE family. Also, in Arabidopsis zar1 plants HopZ1a promotes P. syringae growth indicative of an ancestral virulence function for this T3SE prior to the evolution of recognition by the host resistance protein ZAR1. Our results demonstrate that the Arabidopsis resistance protein ZAR1 confers allele-specific recognition and virulence attenuation of the Pseudomonas syringae T3SE protein HopZ1a.
Highlights
The retaliatory arms race between host and pathogen has molded the evolution of host immune responses and bacterial virulence strategies
Pseudomonas syringae is a model bacterial pathogen that can infect a broad range of plant species, including important crop plants, as well as the model plant Arabidopsis thaliana
We show that ZAR1–mediated immunity is independent of known Arabidopsis resistance-related genes suggesting that ZAR1 possesses novel signaling requirements
Summary
The retaliatory arms race between host and pathogen has molded the evolution of host immune responses and bacterial virulence strategies. The primary virulence mechanism of Gramnegative bacteria such as Pseudomonas syringae is the type III secretion system (T3SS) that allows for the translocation of type III secreted effector (T3SE) proteins directly into plant cells [1]. T3SEs can betray the bacteria to the plant host by activating effector triggered immunity (ETI) [7]. ETI is a branch of plant immunity in which Resistance (R) proteins recognize specific effector proteins resulting in an effective immune response which is often accompanied by a rapid, localized cell death termed the hypersensitive response (HR) [8,9]. The resistance protein indirectly recognizes the T3SE by interacting with a host target of the T3SE [9]. Evolutionary pressure by pathogens has caused the expansion of several R protein families and the diversification of the signaling components which they employ [14]
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