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PLANTS INTERACTING WITH OTHER ORGANISMS

The Arabidopsis RESURRECTION1 Gene Regulates a Novel Antagonistic Interaction in Plant Defense to Biotrophs and Necrotrophs^1,[W],[OA]

Department of Horticulture and Landscape Architecture (H.G.M., E.P.P., D.K.K., B.R.C., H.C.P., R.A.B., M.A.J.) and Department of Botany and Plant Pathology (K.A.L., S.A., T.M.), Purdue University, West Lafayette, Indiana 47907–2054; Department of Plant Protection, Università degli Studi Della Tuscia, 01100 Viterbo, Italy (C.B., G.C.); Department of Plant Biology and Crop Science, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801 (S.M., H.J.B.); Consiglio Nazionale delle Ricerche-Istituto di Genetica Vegetale, Institute of Plant Genetics, 80055 Portici, Italy (F.C.); and Division of Applied Life Science, Gyeongsang National University, Jinju 660–701, Korea (R.A.B.)

We report a role for the Arabidopsis (Arabidopsis thaliana) RESURRECTION1 (RST1) gene in plant defense. The rst1 mutant exhibits enhanced susceptibility to the biotrophic fungal pathogen Erysiphe cichoracearum but enhanced resistance to the necrotrophic fungal pathogens Botrytis cinerea and Alternaria brassicicola. RST1 encodes a novel protein that localizes to the plasma membrane and is predicted to contain 11 transmembrane domains. Disease responses in rst1 correlate with higher levels of jasmonic acid (JA) and increased basal and B. cinerea-induced expression of the plant defensin PDF1.2 gene but reduced E. cichoracearum-inducible salicylic acid levels and expression of pathogenesis-related genes PR1 and PR2. These results are consistent with rst1's varied resistance and susceptibility to pathogens of different life styles. Cuticular lipids, both cutin monomers and cuticular waxes, on rst1 leaves were significantly elevated, indicating a role for RST1 in the suppression of leaf cuticle lipid synthesis. The rst1 cuticle exhibits normal permeability, however, indicating that the disease responses of rst1 are not due to changes in this cuticle property. Double mutant analysis revealed that the coi1 mutation (causing defective JA signaling) is completely epistatic to rst1, whereas the ein2 mutation (causing defective ethylene signaling) is partially epistatic to rst1, for resistance to B. cinerea. The rst1 mutation thus defines a unique combination of disease responses to biotrophic and necrotrophic fungi in that it antagonizes salicylic acid-dependent defense and enhances JA-mediated defense through a mechanism that also controls cuticle synthesis.

The author responsible for distribution of materials integral to the findings presented in this article in accordance with the policy described in the Instructions for Authors (www.plantphysiol.org) is: Matthew A. Jenks (jenksm{at}purdue.edu).

^[W] The online version of this article contains Web-only data.

^[OA] Open Access articles can be viewed online without a subscription.

www.plantphysiol.org/cgi/doi/10.1104/pp.109.142158

^* Corresponding author; e-mail jenksm{at}purdue.edu.

Received May 28, 2009; accepted July 17, 2009; published July 22, 2009.