Abstract
Background: 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).
Results: 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 WCS417rtriggered 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 overexpression of an engineered cytosolic isoform of the disease resistance regulator NPR1 restores the impaired JAinduced disease resistance in ocp3 plants.
Conclusions: 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.
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).
Results: 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 WCS417rtriggered 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 overexpression of an engineered cytosolic isoform of the disease resistance regulator NPR1 restores the impaired JAinduced disease resistance in ocp3 plants.
Conclusions: 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.
Original language | English |
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Article number | 199 |
Pages (from-to) | 1-13 |
Number of pages | 13 |
Journal | BMC Plant Biology |
Volume | 10 |
DOIs | |
Publication status | Published - 13 Sept 2010 |