Abstract

Pseudomonas syringae is the most widespread bacterial pathogen in plants. Several strains of P. syringae produce a phytotoxin, coronatine (COR), which acts as a jasmonic acid mimic and inhibits plant defense responses and contributes to disease symptom development. In this study, we found that COR inhibits early defense responses during nonhost disease resistance. Stomatal closure induced by a nonhost pathogen, P. syringae pv. tabaci, was disrupted by COR in tomato epidermal peels. In addition, nonhost HR cell death triggered by P. syringae pv. tabaci on tomato was remarkably delayed when COR was supplemented along with P. syringae pv. tabaci inoculation. Using isochorismate synthase (ICS)-silenced tomato plants and transcript profiles of genes in SA- and JA-related defense pathways, we show that COR suppresses SA-mediated defense during nonhost resistance.

Highlights

  • Plants possess a natural innate immune system that efficiently detects potential pathogens

  • Five days after spray inoculation of P. syringae pv. tomato DC3000, a number of bacterial leaf spots at infection sites were observed in tomato

  • We found that most stomata on tomato epidermal peels remained closed after inoculation of a nonhost pathogen, P. syringae pv. tabaci (Fig. 1)

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Summary

Introduction

Plants possess a natural innate immune system that efficiently detects potential pathogens. The initial stage of this defense system is based on the perception of pathogen- or microbe-associated molecular patterns (PAMPs or MAMPs) through pattern recognition receptors present at the plant cell surface (Boller & Felix, 2009). A significant induction of stomatal closure was observed within the first hour of contact with both host and nonhost bacterial pathogens (Melotto, Underwood & He, 2008). Bacterial pathogens have evolved to acquire specific virulence factors such as coronatine (COR) to overcome PAMPtriggered immunity (PTI) and stomata-based defense (Underwood, Melotto & He, 2007). Tomato DC3000 produces COR three hours after infection in the apoplast and on the plant surface to reopen closed stomata, How to cite this article Lee et al (2013), Coronatine inhibits stomatal closure and delays hypersensitive response cell death induced by nonhost bacterial pathogens. Chlorosis associated with disease caused by several pathovars of P. syringae has been attributed mainly to the phytotoxin COR (Bender et al, 1987; Zhao et al, 2003)

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