Analysis of resistance gene-mediated defense responses in Arabidopsis thaliana plants carrying a mutation in CPR5

In resistant plants, pathogen attack often leads to rapid activation of defense responses that limit multiplication and spread of the pathogen. To investigate the signaling mechanisms underlying this process, we carried out a screen for mutants in the signaling pathway governing resistance in Arabid...

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Published in:Molecular plant-microbe interactions Vol. 11; no. 12; pp. 1196 - 1206
Main Authors: Boch, J, Verbsky, M.L, Robertson, T.L, Larkin, J.C, Kunkel, B.N
Format: Journal Article
Language:English
Published: St Paul, MN APS Press 01-12-1998
The American Phytopathological Society
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Summary:In resistant plants, pathogen attack often leads to rapid activation of defense responses that limit multiplication and spread of the pathogen. To investigate the signaling mechanisms underlying this process, we carried out a screen for mutants in the signaling pathway governing resistance in Arabidopsis thaliana to the bacterial pathogen Pseudomonas syringae. This involved screening for suppressor mutations that restored resistance to a susceptible line carrying a mutation in the RPS2 resistance gene. A mutant that conferred resistance by activating defense responses in the absence of pathogens was isolated. This mutant, which carries a mutation at the CPR5 locus and was thus designated cpr5-2, exhibited resistance to P. syringae, spontaneous development of necrotic lesions, elevated PR gene expression in the absence of pathogens, and abnormal trichomes. Resistance gene-mediated defenses, including the hypersensitive response, restriction of pathogen growth, and induction of defense-related gene expression, were functional in cpr5-2 mutant plants. Additionally, in cpr5-2 plants RPS2-mediated induction of PR-1 expression was enhanced, whereas RPM1- mediated induction of ELI3 was not. These findings suggest that CPR5 encodes a negative regulator of the RPS2 signal transduction pathway.
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ISSN:0894-0282
1943-7706
DOI:10.1094/mpmi.1998.11.12.1196