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First published online September 28, 2007; 10.1104/pp.107.103325 Plant Physiology 145:890-904 (2007) © 2007 American Society of Plant Biologists OPEN ACCESS ARTICLE
Hydrogen Peroxide Generation by the Pepper Extracellular Peroxidase CaPO2 Activates Local and Systemic Cell Death and Defense Response to Bacterial Pathogens1,[W],[OA]College of Life Sciences and Biotechnology, Korea University, Seoul 136–713, Republic of Korea
Reactive oxygen species (ROS) are responsible for mediating cellular defense responses in plants. Controversy has existed over the origin of ROS in plant defense. We have isolated a novel extracellular peroxidase gene, CaPO2, from pepper (Capsicum annuum). Local or systemic expression of CaPO2 is induced in pepper by avirulent Xanthomonas campestris pv vesicatoria (Xcv) infection. We examined the function of the CaPO2 gene in plant defense using the virus-induced gene silencing technique and gain-of-function transgenic plants. CaPO2-silenced pepper plants were highly susceptible to Xcv infection. Virus-induced gene silencing of the CaPO2 gene also compromised hydrogen peroxide (H2O2) accumulation and hypersensitive cell death in leaves, both locally and systemically, during avirulent Xcv infection. In contrast, overexpression of CaPO2 in Arabidopsis (Arabidopsis thaliana) conferred enhanced disease resistance accompanied by cell death, H2O2 accumulation, and PR gene induction. In CaPO2-overexpression Arabidopsis leaves infected by Pseudomonas syringae pv tomato, H2O2 generation was sensitive to potassium cyanide (a peroxidase inhibitor) but insensitive to diphenylene iodonium (an NADPH oxidase inhibitor), suggesting that H2O2 generation depends on peroxidase in Arabidopsis. Together, these results indicate that the CaPO2 peroxidase is involved in ROS generation, both locally and systemically, to activate cell death and PR gene induction during the defense response to pathogen invasion.
1 This work was supported by the Crop Functional Genomics Center of the 21st Century Frontier Research Program (grant no. CG1133) funded by the Ministry of Science and Technology, Korea; a grant from the Center for Plant Genetics and Breeding Research, Seoul National University, Korea; and by the Biogreen21 Program (grant no. 20070401034028), Rural Development Administration, Korea. 2 Present address: Department of Plant and Microbial Biology, University of California, Berkeley, CA 94720. 3 Present address: Institute of Molecular Plant Sciences, School of Biological Sciences, University of Edinburgh, King's Buildings, Edinburgh EH9 3JR, UK. The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Byung Kook Hwang (bkhwang{at}korea.ac.kr). [W] The online version of this article contains Web-only data. [OA] Open Access articles can be viewed online without a subscription. www.plantphysiol.org/cgi/doi/10.1104/pp.107.103325 * Corresponding author; e-mail bkhwang{at}korea.ac.kr. Received June 4, 2007; accepted September 26, 2007; published September 28, 2007. This article has been cited by other articles:
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