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Plant Physiology Preview Published on March 20, 2009; 10.1104/pp.108.133678
OPEN ACCESS ARTICLE
Received December 3, 2008 The synthetic elicitor 3,5-Dichloroanthranillic acid (DCA) induces NPR1-dependent and NPR1-independent mechanisms of disease resistance in Arabidopsis thaliana
ChemGen IGERT program, Center for Plant Cell Biology, Institute for Integrative Genome Biology, Department of Botany and Plant Sciences, University of California at Riverside, CA 92521, USA * Corresponding author; email: thomas.eulgem{at}ucr.edu.
Immune responses of Arabidopsis thaliana are at least partially mediated by coordinated transcriptional upregulation of plant defense genes, such as the Late/sustained Upregulation 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 sub-sets 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 co-factor NPR1, 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 (associated with chemically induced defense) genes 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.
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