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First published online March 20, 2009; 10.1104/pp.108.133678 Plant Physiology 150:333-347 (2009) © 2009 American Society of Plant Biologists OPEN ACCESS ARTICLE
The Synthetic Elicitor 3,5-Dichloroanthranilic Acid Induces NPR1-Dependent and NPR1-Independent Mechanisms of Disease Resistance in Arabidopsis1,[W],[OA]ChemGen Integrative Graduate Education and Research Traineeship Program, Center for Plant Cell Biology, Institute for Integrative Genome Biology, Department of Botany and Plant Sciences, University of California at Riverside, Riverside, California 92521
Immune responses of Arabidopsis (Arabidopsis thaliana) are at least partially mediated by coordinated transcriptional up-regulation of plant defense genes, such as the Late/sustained Up-regulation in Response to Hyaloperonospora parasitica (LURP) cluster. We found a defined region in the promoter of the LURP member CaBP22 to be important for this response. Using a CaBP22 promoter-reporter fusion, we have established a robust and specific high-throughput screening system for synthetic defense elicitors that can be used to trigger defined subsets of plant immune responses. Screening a collection of 42,000 diversity-oriented molecules, we identified 114 candidate LURP inducers. One representative, 3,5-dichloroanthranilic acid (DCA), efficiently induced defense reactions to the phytopathogens H. parasitica and Pseudomonas syringae. In contrast to known salicylic acid analogs, such as 2,6-dichloroisonicotinic acid (INA), which exhibit a long-lasting defense-inducing activity and are fully dependent on the transcriptional cofactor NPR1 (for Nonexpresser of Pathogenesis-Related genes1), DCA acts transiently and is only partially dependent on NPR1. Microarray analyses revealed a cluster of 142 DCA- and INA-responsive genes that show a pattern of differential expression coinciding with the kinetics of DCA-mediated disease resistance. These ACID genes (for Associated with Chemically Induced Defense) constitute a core gene set associated with chemically induced disease resistance, many of which appear to encode components of the natural immune system of Arabidopsis.
1 This work was supported by the National Science Foundation-Integrative Organismal Biology (grant no. 0449439 to T.E.), by the U.S. Department of Agriculture Cooperative State Research, Education, and Extension Service (grant no. 2008–35301–19264 to T.E.), and by a predoctoral fellowship to C.K. from the National Science Foundation-funded ChemGen Integrative Graduate Education and Research Traineeship program (fellowship no. DGE 0504249). 2 Present address: Kelley Scientific Resources, La Jolla, CA 92121. 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: Thomas Eulgem (thomas.eulgem{at}ucr.edu). [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.108.133678 * Corresponding author; e-mail thomas.eulgem{at}ucr.edu. Received December 3, 2008; accepted March 17, 2009; published March 20, 2009.
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