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

被引:50
作者
Mang, Hyung Gon [1 ]
Laluk, Kristin A. [2 ]
Parsons, Eugene P. [1 ]
Kosma, Dylan K. [1 ]
Cooper, Bruce R. [1 ]
Park, Hyeong Cheol [1 ]
AbuQamar, Synan [2 ]
Boccongelli, Claudia [3 ]
Miyazaki, Saori [4 ]
Consiglio, Federica [5 ]
Chilosi, Gabriele [3 ]
Bohnert, Hans J. [4 ]
Bressan, Ray A. [1 ,6 ]
Mengiste, Tesfaye [2 ]
Jenks, Matthew A. [1 ]
机构
[1] Purdue Univ, Dept Hort & Landscape Architecture, W Lafayette, IN 47907 USA
[2] Purdue Univ, Dept Bot & Plant Pathol, W Lafayette, IN 47907 USA
[3] Univ Tuscia, Dept Plant Protect, I-01100 Viterbo, Italy
[4] Univ Illinois, Dept Plant Biol & Crop Sci, Urbana, IL 61801 USA
[5] Inst Plant Genet, Consiglio Nazl Ric, Ist Genet Vegetale, I-80055 Portici, Italy
[6] Gyeongsang Natl Univ, Div Appl Life Sci, Jinju 660701, South Korea
关键词
SYSTEMIC ACQUIRED-RESISTANCE; F-SP HORDEI; SALICYLIC-ACID; BOTRYTIS-CINEREA; JASMONIC-ACID; PSEUDOMONAS-SYRINGAE; ABSCISIC-ACID; CROSS-TALK; DISEASE SUSCEPTIBILITY; TRANSCRIPTION FACTOR;
D O I
10.1104/pp.109.142158
中图分类号
Q94 [植物学];
学科分类号
071001 ;
摘要
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.
引用
收藏
页码:290 / 305
页数:16
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