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Plant Physiol. 2014 Jul;165(3):1269-1284. doi: 10.1104/pp.114.242495. Epub 2014 May 28.

Enhanced Disease Susceptibility1 Mediates Pathogen Resistance and Virulence Function of a Bacterial Effector in Soybean.

Plant physiology

Jialin Wang, M B Shine, Qing-Ming Gao, Duroy Navarre, Wei Jiang, Chunyan Liu, Qingshan Chen, Guohua Hu, Aardra Kachroo

Affiliations

  1. College of Agriculture, Northeast Agricultural University, Harbin 150030, China (J.W., W.J., Q.C., G.H.);Department of Plant Pathology, University of Kentucky, Lexington, Kentucky 40546 (J.W., M.B.S., Q.-M.G., A.K.);United States Department of Agriculture-Agricultural Research Service, Washington State University, Prosser, Washington 99350 (D.N.); andLand Reclamation Research and Breeding Centre of Heilongjiang, Harbin 150090, China (C.L., G.H.).
  2. College of Agriculture, Northeast Agricultural University, Harbin 150030, China (J.W., W.J., Q.C., G.H.);Department of Plant Pathology, University of Kentucky, Lexington, Kentucky 40546 (J.W., M.B.S., Q.-M.G., A.K.);United States Department of Agriculture-Agricultural Research Service, Washington State University, Prosser, Washington 99350 (D.N.); andLand Reclamation Research and Breeding Centre of Heilongjiang, Harbin 150090, China (C.L., G.H.) [email protected] [email protected].

PMID: 24872380 PMCID: PMC4081336 DOI: 10.1104/pp.114.242495

Abstract

Enhanced disease susceptibility1 (EDS1) and phytoalexin deficient4 (PAD4) are well-known regulators of both basal and resistance (R) protein-mediated plant defense. We identified two EDS1-like (GmEDS1a/GmEDS1b) proteins and one PAD4-like (GmPAD4) protein that are required for resistance signaling in soybean (Glycine max). Consistent with their significant structural conservation to Arabidopsis (Arabidopsis thaliana) counterparts, constitutive expression of GmEDS1 or GmPAD4 complemented the pathogen resistance defects of Arabidopsis eds1 and pad4 mutants, respectively. Interestingly, however, the GmEDS1 and GmPAD4 did not complement pathogen-inducible salicylic acid accumulation in the eds1/pad4 mutants. Furthermore, the GmEDS1a/GmEDS1b proteins were unable to complement the turnip crinkle virus coat protein-mediated activation of the Arabidopsis R protein Hypersensitive reaction to Turnip crinkle virus (HRT), even though both interacted with HRT. Silencing GmEDS1a/GmEDS1b or GmPAD4 reduced basal and pathogen-inducible salicylic acid accumulation and enhanced soybean susceptibility to virulent pathogens. The GmEDS1a/GmEDS1b and GmPAD4 genes were also required for Resistance to Pseudomonas syringae pv glycinea2 (Rpg2)-mediated resistance to Pseudomonas syringae. Notably, the GmEDS1a/GmEDS1b proteins interacted with the cognate bacterial effector AvrA1 and were required for its virulence function in rpg2 plants. Together, these results show that despite significant structural similarities, conserved defense signaling components from diverse plants can differ in their functionalities. In addition, we demonstrate a role for GmEDS1 in regulating the virulence function of a bacterial effector.

© 2014 American Society of Plant Biologists. All Rights Reserved.

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