EDM2 is required for RPP7-dependent disease resistance in Arabidopsis and affects RPP7 transcript levels
Specific disease resistance of Arabidopsis thaliana against the Hyaloperonospora parasitica isolate Hiks1 (HpHiks1) is mediated by RPP7. Although this disease resistance gene encodes a typical nucleotide binding site leucine-rich repeat (NB-LRR) disease resistance protein, its function is independent of the defense hormone salicylic acid and most known genes required for plant immune responses. We identified EDM2 (enhanced downy mildew 2) in a genetic screen for RPP7 suppressors. Mutations of EDM2 phenocopy RPP7 mutations, but do not affect other tested disease resistance genes. We isolated EDM2 by map-based cloning. The predicted EDM2 protein is structurally unrelated to previously identified components of the plant immune system, bears typical features of transcriptional regulators, including plant homeodomain (PHD)-finger-like domains, and defines a plant-specific protein family. In edm2 mutants both constitutive and HpHiks1-induced RPP7 transcript levels are reduced, suggesting that EDM2 is either a direct or an indirect regulator of RPP7 expression. Microarray analyses defined a set of defense-associated genes, the expression of which is suppressed during successful HpHiks1 colonization of either rpp7 or edm2 plants. This transcriptional phenotype is counteracted by an EDM2/RPP7-dependent mechanism.
Document Type: Research Article
Affiliations: 1: Center for Plant Cell Biology, Department of Botany and Plant Sciences, University of California at Riverside, CA 92521, USA, 2: Department of Plant Pathology, Physiology, and Weed Science, and Fralin Biotechnology Center, Virginia Polytechnic Institute and State University, Blacksburg, VA 24061-0346, USA, 3: Department of Biology, CB#3280 University of North Carolina at Chapel Hill, NC 27599, USA, 4: Warwick-HRI, University of Warwick, Warwick CV35 9EF, UK, 5: Syngenta Biotechnology, Inc., 3054 Cornwallis Road, Research Triangle Park, NC 27709, USA, and
Publication date: March 1, 2007