A prominent role for RCAR3-mediated ABA signaling in response to Pseudomonas syringae pv. tomato DC3000 infection in Arabidopsis.

In plant-pathogen interaction, the plant hormone ABA can serve as a crucial modulator of plant responses to biotic as well as abiotic stress. Recent studies have identified pyrabactin resistance (PYR) 1/PYR1-like (PYL)/regulatory component of ABA receptor (RCAR) proteins as an ABA receptor that interacts with the protein phosphatase type 2C (PP2C) family. Here, we examined the functional involvement of ABA signaling components in pre- and post-invasive defense responses of Arabidopsis against the virulent pathogen Pseudomonas syringae pv. tomato (Pst) DC3000. Overexpression of the ABA receptor, RCAR3, enhanced susceptibility to Pst DC3000 by suppressing callose deposition and induction of salicylic acid (SA)-mediated pathogenesis-related (PR) genes, such as PR1 and NPR1, after syringe infiltration. In contrast, a dip inoculation assay revealed that RCAR3-overexpression mutants inhibited stomatal reopening during Pst DC3000 infection and coronatine (COR) treatment, leading to enhanced resistance to Pst DC3000, which was not accompanied by differential expression of PR1 and NPR1 genes. As a negative regulator of ABA signaling, PP2CA interacted with RCAR3 and its loss-of-function and overexpression mutants revealed that ABA sensitivity was positively correlated with stomatal immunity, similar to RCAR3 overexpression mutants. Taken together, these results suggest that RCAR3- and PP2CA-mediated ABA signaling antagonistically or synergistically contributes to the plant immune system throughout different phases of Pst DC3000 attack by SA or COR signaling cross-talk.