Raka M. Mitra,1
Keegan D. Hasselmann,1
Jerry D. Cohen,3
Fumiaki Katagiri,1 and
1Department of Plant Biology, Microbial and Plant Genomics Institute, University of Minnesota, 1445 Gortner Avenue, St. Paul 55108, U.S.A.; 2Department of Life Sciences, Graduate School of Arts and Sciences, The University of Tokyo, Komaba 3-8-1, Meguro-ku, Tokyo 153-8902, Japan; 3Department of Horticultural Science, Microbial and Plant Genomics Institute, University of Minnesota, 1970 Folwell Avenue, St. Paul 55108, U.S.A.
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Accepted 11 August 2008.
Expression profiling of wild-type plants and mutants with defects in key components of the defense signaling network was used to model the Arabidopsis network 24 h after infection by Pseudomonas syringae pv. maculicola ES4326. Results using the Affymetrix ATH1 array revealed that expression levels of most pathogen-responsive genes were affected by mutations in coi1, ein2, npr1, pad4, or sid2. These five mutations defined a small number of different expression patterns displayed by the majority of pathogen-responsive genes. P. syringae pv. tomato strain DC3000 elicited a much weaker salicylic acid (SA) response than ES4326. Additional mutants were profiled using a custom array. Profiles of pbs3 and ndr1 revealed major effects of these mutations and allowed PBS3 and NDR1 to be placed between the EDS1/PAD4 node and the SA synthesis node in the defense network. Comparison of coi1, dde2, and jar1 profiles showed that many genes were affected by coi1 but very few were affected by dde2 or jar1. Profiles of coi1 plants infected with ES4326 were very similar to those of wild-type plants infected with bacteria unable to produce the phytotoxin coronatine, indicating that, essentially, all COI1-dependent gene expression changes in this system are caused by coronatine.
© 2008 The American Phytopathological Society