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First published online May 27, 2005; 10.1105/tpc.105.032375

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The Plant Cell 17:2123-2137 (2005)
© 2005 American Society of Plant Biologists

An Arabidopsis Homeodomain Transcription Factor, OVEREXPRESSOR OF CATIONIC PEROXIDASE 3, Mediates Resistance to Infection by Necrotrophic Pathogens

Alberto Coegoa, Vicente Ramireza, M. José Gila, Victor Florsb, Brigitte Mauch-Manic and Pablo Veraa,1

a Instituto de Biología Molecular y Celular de Plantas, Universidad Politécnica de Valencia–Consejo Superior de Investigaciones Científicas, 46022 Valencia, Spain
b Plant Physiology Section, Department of Experimental Sciences, Universidad Jaime I, Castellón 12071, Spain
c University of Neuchâtel, Faculty of Sciences, Institute of Botany, Biochemistry, CH-2007 Neuchâtel, Switzerland

1 To whom correspondence should be addressed. E-mail vera{at}ibmcp.upv.es; fax 34-96-3877859.

The mechanisms controlling plant resistance to necrotrophic fungal pathogens are poorly understood. We previously reported on Ep5C, a gene shown to be induced by the H2O2 generated during a plant–pathogen interaction. To identify novel plant components operating in pathogen-induced signaling cascades, we initiated a large-scale screen using Arabidopsis thaliana plants carrying the ß-glucuronidase reporter gene under control of the H2O2-responsive Ep5C promoter. Here, we report the identification and characterization of a mutant, ocp3 (for overexpressor of cationic peroxidase 3), in which the reporter construct is constitutively expressed. Healthy ocp3 plants show increased accumulation of H2O2 and express constitutively the Glutathione S-transferase1 and Plant Defensine 1.2 marker genes, but not the salicylic acid (SA)–dependent pathogenesis-related PR-1 gene. Strikingly, the ocp3 mutant shows enhanced resistance to the necrotrophic pathogens Botrytis cinerea and Plectosphaerella cucumerina. Conversely, resistance to virulent forms of the biotrophic oomycete Hyaloperonospora parasitica and the bacterial pathogen Pseudomonas syringae pv tomato DC3000 remains unaffected in ocp3 plants when compared with wild-type plants. Consistently with this, ocp3 plants are not affected in SA perception and express normal levels of PR genes after pathogen attack. To analyze signal transduction pathways where ocp3 operates, epistasis analyses between ocp3 and pad4, nahG, npr1, ein2, jin1, or coi1 were performed. These studies revealed that the resistance signaling to necrotrophic infection in ocp3 is fully dependent on appropriate perception of jasmonic acid through COI1 and does not require SA or ethylene perception through NPR1 or EIN2, respectively. The OCP3 gene encodes a homeodomain transcription factor that is constitutively expressed in healthy plants but repressed in response to infection by necrotrophic fungi. Together, these results suggest that OCP3 is an important factor for the COI1-dependent resistance of plants to infection by necrotrophic pathogens.




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