文档介绍：Powdery Mildew Resistance Conferred by Loss of the
ENHANCED DISEASE RESISTANCE1 Protein Kinase Is
Suppressed by a Missense Mutation in KEEP ON GOING,
a Regulator of Abscisic Acid Signaling1[W][OA]
Anna Wawrzynska2, Katy M. Christiansen, Yinan Lan, Natalie L. Rodibaugh, and Roger W. Innes*
Department of Biology, Indiana University, Bloomington, Indiana 47405
Loss-of-function mutations in the Arabidopsis (Arabidopsis thaliana) ENHANCED DISEASE RESISTANCE1 (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 ponents of the EDR1 signal transduction
pathway(s), we conducted a forward ic screen for mutations that suppressed edr1-mediated disease resistance. ic
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 multidomain 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 INSENSITIVE5.
KEG mRNA levels were found to be 3-fold higher in edr1 mutant pared 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 up-regulated in the edr1
mutant following ABA treatment, and this up-regulation was suppressed by the keg-4 mutation. We conclude that edr1-
mediated resistance to powdery mildew is mediated, in part, by enhanced ABA signaling.
Powdery mil