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Coronatine inhibits stomatal closure and delays hypersensitive response cell death induced by nonhost bacterial pathogens
Author(s) -
Seonghee Lee,
Yasuhiro Ishiga,
Kristen Clermont,
Kirankumar S. Mysore
Publication year - 2013
Publication title -
peerj
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.927
H-Index - 70
ISSN - 2167-8359
DOI - 10.7717/peerj.34
Subject(s) - pseudomonas syringae , coronatine , phytotoxin , jasmonic acid , hypersensitive response , biology , pathogen , plant defense against herbivory , microbiology and biotechnology , botany , arabidopsis , defence mechanisms , systemic acquired resistance , plant disease resistance , gene , toxin , genetics , mutant
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.

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