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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 independen...

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Published in:The Plant journal : for cell and molecular biology 2007-03, Vol.49 (5), p.829-839
Main Authors: Eulgem, Thomas, Tsuchiya, Tokuji, Wang, Xiao-Jun, Beasley, Britt, Cuzick, Alayne, Tör, Mahmut, Zhu, Tong, McDowell, John M, Holub, Eric, Dangl, Jeffery L
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Language:English
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Summary: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.
ISSN:0960-7412
1365-313X
DOI:10.1111/j.1365-313X.2006.02999.x