Plant Physiol. Journal of Pharmacology and Experimental Therapeutics
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Published on September 24, 2008; 10.1104/pp.108.127605

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Received August 4, 2008
Accepted September 5, 2008

Powdery Mildew Resistance Conferred by Loss of the EDR1 Protein Kinase is Suppressed by a Missense Mutation in KEG, a Regulator of ABA Signaling

Anna Wawrzynska , Katy M. Christiansen , Yinan Lan , Natalie L. Rodibaugh , and Roger W. Innes *

Department of Biology, Indiana University, Bloomington, IN 47405, USA

* Corresponding author; email: rinnes{at}indiana.edu.

Loss-of-function mutations in the Arabidopsis ENHANCED DISEASE RESISTANCE 1 (EDR1) gene confer enhanced resistance to infection by powdery mildew (Golovinomyces cichoracearum). EDR1 encodes a protein kinase, but its substrates, and the pathways regulated by EDR1 are unknown. To identify components of the EDR1 signal transduction pathway(s) we conducted a forward genetic screen for mutations that suppressed edr1-mediated disease resistance. Genetic mapping and cloning of one of these suppressor mutations revealed a recessive missense mutation in the KEEP ON GOING gene (KEG; At5g13530), which we designated keg-4. KEG encodes a multi-domain protein that includes a RING E3 ligase domain, a kinase domain, ankyrin repeats and HERC2-like repeats. The KEG protein has previously been shown to have ubiquitin ligase activity and to negatively regulate protein levels of the transcription factor ABCISIC ACID INSENSITIVE 5 (ABI5). KEG mRNA levels were found to be three fold higher in edr1 mutant plants compared to wild type. Loss-of-function mutations in KEG are seedling lethal and are hypersensitive to glucose and abscisic acid (ABA). The keg-4 mutation, in contrast, conferred resistance to 6% glucose, and suppressed edr1-mediated hypersensitivity to ABA, suggesting that the keg-4 mutation suppresses ABA signaling by altering KEG function. Several ABA-responsive genes were found to be further upregulated in the edr1 mutant following ABA treatment, and this upregulation was suppressed by the keg-4 mutation. We conclude that edr1-mediated resistance to powdery mildew is mediated, in part, by enhanced ABA signaling.




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