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Activation of a COI1‐dependent pathway in Arabidopsis by Pseudomonas syringae type III effectors and coronatine
Author(s) -
He Ping,
Chintamanani Satya,
Chen Zhongying,
Zhu Lihuang,
Kunkel Barbara N.,
Alfano James R.,
Tang Xiaoyan,
Zhou JianMin
Publication year - 2004
Publication title -
the plant journal
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 3.058
H-Index - 269
eISSN - 1365-313X
pISSN - 0960-7412
DOI - 10.1111/j.1365-313x.2003.01986.x
Subject(s) - coronatine , pseudomonas syringae , effector , phytotoxin , virulence , arabidopsis , type three secretion system , biology , microbiology and biotechnology , secretion , mutant , virulence factor , pathogen , gene , genetics , biochemistry , toxin
Summary Gram‐negative bacteria use a variety of virulence factors including phytotoxins, exopolysaccharides, effectors secreted by the type III secretion system, and cell‐wall‐degrading enzymes to promote parasitism in plants. However, little is known about how these virulence factors alter plant cellular responses to promote disease. In this study, we show that virulent Pseudomonas syringae strains activate the transcription of an Arabidopsis ethylene response factor ( ERF ) gene, RAP2.6 , in a coronatine insensitive 1 (COI1)‐dependent manner. A highly sensitive RAP2.6 promoter‐firefly luciferase ( RAP2.6‐LUC ) reporter line was developed to monitor activities of various bacterial virulence genes. Analyses of P. syringae pv. tomato DC3000 mutants indicated that both type III secretion system and the phytotoxin coronatine are required for RAP2.6 induction. We show that at least five individual type III effectors, avirulence B (AvrB), AvrRpt2, AvrPphB, HopPtoK, and AvrPphE Pto , contributed to RAP2.6 induction. Gene‐for‐gene recognition was not involved in RAP2.6 induction because plants lacking RPM1 and RPS2 responded normally to AvrB and AvrRpt2 in RAP2.6 expression. Interestingly, the role of coronatine in RAP2.6 induction can be partially substituted by the addition of avrB in DC3000, suggesting that AvrB may mimic coronatine. These results suggest that P. syringae type III effectors and coronatine act by augmenting a COI1‐dependent pathway to promote parasitism.