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ARS Home » Pacific West Area » Wapato, Washington » Temperate Tree Fruit and Vegetable Research » Research » Publications at this Location » Publication #306560

Title: EDS1 mediates pathogen resistance and virulence function of a bacterial effector in soybean

item WANG, J - University Of Kentucky
item SHINE, M - University Of Kentucky
item GAO, Q - University Of Kentucky
item Navarre, Duroy - Roy
item JIANG, W - Northeast Agricultural University
item CHEN, Q - Northeast Agricultural University
item HU, G - Northeast Agricultural University
item KACHROO, A - University Of Kentucky

Submitted to: Plant Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 5/28/2014
Publication Date: 7/15/2014
Citation: Wang, J., Shine, M.B., Gao, Q., Navarre, D.A., Jiang, W., Chen, Q., Hu, G., Kachroo, A. 2014. EDS1 mediates pathogen resistance and virulence function of a bacterial effector in soybean. Plant Physiology. 165:1269-1284.

Interpretive Summary: Crop yields and quality can be severely affected by disease and require costly pesticide treatments. Plants have innate ability to resist many diseases, but the mechanisms are not fully understood and so cannot be fully deployed. This work shows that two proteins, EDS1 and PAD4, have key roles in plant defense. The GMEDS1 protein directly interacted with AvrA1, a bacterial effector protein that enhances pathogen virulence and was required for its virulence. This research increases understanding of how plants resist disease and can contribute to the development of plants with superior resistance.

Technical Abstract: Enhanced disease susceptibility 1 (EDS1) and phytoalexin deficient 4 (PAD4) are well known regulators of both basal and resistance (R) protein-mediated plant defense. We identified two EDS1- (GmEDS1a/b) and one PAD4-like (GmPAD4) protein that are required for resistance signaling in soybean. Consistent with their significant structural conservation to Arabidopsis 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/b proteins were unable to complement the turnip crinkle virus coat protein-mediated activation of the Arabidopsis R protein HRT, even though both interacted with HRT. Silencing GmEDS1a/b or GmPAD4 reduced basal and pathogen-inducible SA accumulation and enhanced soybean susceptibility to virulent pathogens. The GmEDS1a/b and GmPAD4 genes were also required for Rpg2-mediated resistance to Pseudomonas syringae. Notably the GmEDS1a/b 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.