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The Arabidopsis RESURRECTION1 Gene Regulates a Novel Antagonistic Interaction in Plant Defense to Biotrophs and Necrotrophs

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 Alternar...

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Published in:Plant physiology (Bethesda) 2009-09, Vol.151 (1), p.290-305
Main Authors: Mang, Hyung Gon, Laluk, Kristin A., Parsons, Eugene P., Kosma, Dylan K., Cooper, Bruce R., Park, Hyeong Cheol, AbuQamar, Synan, Boccongelli, Claudia, Miyazaki, Saori, Consiglio, Federica, Chilosi, Gabriele, Bohnert, Hans J., Bressan, Ray A., Mengiste, Tesfaye, Jenks, Matthew A.
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Language:English
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Summary: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 rstl correlate with higher levels of jasmonic acid (JA) and increased basal and B. cinerea-inauced expression of the plant defensin PDF1.2 gene but reduced E. cichoracearum-mducible salicylic acid levels and expression of pathogenesis-related genes PR1 and PR2. These results are consistent with rstl's varied resistance and susceptibility to pathogens of different life styles. Cuticular lipids, both cutin monomers and cuticular waxes, on rstl 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 coil mutation (causing defective JA signaling) is completely epista tic to rstl, whereas the ein2 mutation (causing defective ethylene signaling) is partially epista tic to rstl, 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.
ISSN:0032-0889
1532-2548
1532-2548
DOI:10.1104/pp.109.142158