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First published online March 10, 2006; 10.1105/tpc.105.039982

The Plant Cell 18:1038-1051 (2006)
© 2006 American Society of Plant Biologists

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Salicylic Acid–Independent ENHANCED DISEASE SUSCEPTIBILITY1 Signaling in Arabidopsis Immunity and Cell Death Is Regulated by the Monooxygenase FMO1 and the Nudix Hydrolase NUDT7[W]

Michael Bartscha, Enrico Gobbatoa, Pawel Bednareka, Svenja Debeyb, Joachim L. Schultzeb, Jaqueline Bautora and Jane E. Parkera,1

a Department of Plant–Microbe Interactions, Max Planck Institute for Plant Breeding Research, D-50829 Cologne, Germany
b Molecular Tumor Biology and Tumor Immunology, Clinic I, University of Cologne, D-50937 Cologne, Germany

1 To whom correspondence should be addressed. E-mail parker{at}mpiz-koeln.mpg.de; fax 49-221-5062-353.

Arabidopsis thaliana ENHANCED DISEASE SUSCEPTIBILITY1 (EDS1) controls defense activation and programmed cell death conditioned by intracellular Toll-related immune receptors that recognize specific pathogen effectors. EDS1 is also needed for basal resistance to invasive pathogens by restricting the progression of disease. In both responses, EDS1, assisted by its interacting partner, PHYTOALEXIN-DEFICIENT4 (PAD4), regulates accumulation of the phenolic defense molecule salicylic acid (SA) and other as yet unidentified signal intermediates. An Arabidopsis whole genome microarray experiment was designed to identify genes whose expression depends on EDS1 and PAD4, irrespective of local SA accumulation, and potential candidates of an SA-independent branch of EDS1 defense were found. We define two new immune regulators through analysis of corresponding Arabidopsis loss-of-function insertion mutants. FLAVIN-DEPENDENT MONOOXYGENASE1 (FMO1) positively regulates the EDS1 pathway, and one member (NUDT7) of a family of cytosolic Nudix hydrolases exerts negative control of EDS1 signaling. Analysis of fmo1 and nudt7 mutants alone or in combination with sid2-1, a mutation that severely depletes pathogen-induced SA production, points to SA-independent functions of FMO1 and NUDT7 in EDS1-conditioned disease resistance and cell death. We find instead that SA antagonizes initiation of cell death and stunting of growth in nudt7 mutants.




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