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Published on July 22, 2009; 10.1104/pp.109.142158

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Received May 28, 2009
Accepted July 17, 2009

The Arabidopsis RESURRECTION1 gene regulates a novel antagonistic interaction in plant defense to biotrophs and necrotrophs

Hyung Gon Mang , Kristin A. Laluk , Eugene P. Parsons , Dylan K. Kosma , Bruce R. Cooper , Hyeong Cheol Park , Synan AbuQamar , Claudia Boccongelli , Saori Miyazaki , Federica Consiglio , Gabriele Chilosi , Hans J. Bohnert , Ray A. Bressan , Tesfaye Mengiste , and Matthew A. Jenks *

Department of Horticulture and Landscape Architecture, Purdue University, West Lafayette, Indiana, 47907-2054, USA; Department of Botany and Plant Pathology, Purdue University, West Lafayette, Indiana, 47907-2054, USA; Department of Plant Protection, Universita degli Studi Della Tuscia, Via S. Cammillo de Lellis I-01100 Viterbo, Italy; Department of Plant Biology and Crop Science, University of Illinois at Urbana-Champaign, Urbana, Illinois 61801, USA; CNR-IGV Institute of Plant Genetics, Via Universita 133, 80055 Portici, Italy; Division of Applied Life Science, Gyeongsang National University, Jinju, 660-701, Korea

* Corresponding author; email: jenksm{at}purdue.edu.

We report a role for the Arabidopsis 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 eleven 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 (SA) 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 SA dependent defense and enhances JA mediated defense, through a mechanism that also controls cuticle synthesis.






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