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Open Access Research article

OCP3 is an important modulator of NPR1-mediated jasmonic acid-dependent induced defenses in Arabidopsis

Vicente Ramírez1, Sjoerd Van der Ent2, Javier García-Andrade1, Alberto Coego1, Corné MJ Pieterse2 and Pablo Vera1*

Author Affiliations

1 Instituto de Biología Molecular y Celular de Plantas (IBMCP), Universidad Politécnica de Valencia-Consejo Superior de Investigaciones Científicas (CSIC). Camino de Vera s/n, Valencia, Spain

2 Plant-Microbe Interactions, Department of Biology, Faculty of Science, Utrecht University, 3508 TB Utrecht, The Netherlands

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BMC Plant Biology 2010, 10:199  doi:10.1186/1471-2229-10-199

Published: 13 September 2010



Upon appropriate stimulation, plants increase their level of resistance against future pathogen attack. This phenomenon, known as induced resistance, presents an adaptive advantage due to its reduced fitness costs and its systemic and broad-spectrum nature. In Arabidopsis, different types of induced resistance have been defined based on the signaling pathways involved, particularly those dependent on salicylic acid (SA) and/or jasmonic acid (JA).


Here, we have assessed the implication of the transcriptional regulator OCP3 in SA- and JA-dependent induced defenses. Through a series of double mutant analyses, we conclude that SA-dependent defense signaling does not require OCP3. However, we found that ocp3 plants are impaired in a Pseudomonas fluorescens WCS417r-triggered induced systemic resistance (ISR) against both Pseudomonas syrinagae DC3000 and Hyaloperonospora arabidopsidis, and we show that this impairment is not due to a defect in JA-perception. Likewise, exogenous application of JA failed to induce defenses in ocp3 plants. In addition, we provide evidence showing that the over-expression of an engineered cytosolic isoform of the disease resistance regulator NPR1 restores the impaired JA-induced disease resistance in ocp3 plants.


Our findings point to a model in which OCP3 may modulate the nucleocytosolic function of NPR1 in the regulation of JA-dependent induced defense responses.