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A Key Role for the Arabidopsis WIN3 Protein in Disease Resistance Triggered by Pseudomonas syringae That Secrete AvrRpt2

October 2007 , Volume 20 , Number  10
Pages  1,192 - 1,200

Min Woo Lee, Hua Lu, Ho Won Jung, and Jean T. Greenberg

Molecular Genetics and Cell Biology Department, The University of Chicago, 1103 East 57th Street, Chicago, IL 60637, U.S.A.

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Accepted 14 June 2007.

Effector proteins injected by the pathogenic bacteria Pseudomonas syringae into plants can have profound effects on the pathogen--host interaction due to their efficient recognition by plants and the subsequent triggering of defenses. The AvrRpt2 effector triggers strong local and systemic defense (called systemic acquired resistance [SAR]) responses in Arabidopsis thaliana plants that harbor a functional RPS2 gene that encodes an R protein in the coiled-coil, nucleotide-binding domain, leucine-rich repeat class. The newly identified win3-T mutant shows greatly reduced resistance to P. syringae carrying avrRpt2. In win3-T plants, RIN4 cleavage, an early AvrRpt2-induced event, is normal. However, salicylic acid accumulation is compromised, as is SAR induction and the local hypersensitive cell death response after infection by P. syringae carrying avrRpt2. WIN3 encodes a member of the firefly luciferase protein superfamily. Expression of WIN3 at an infection site partially requires PAD4, a protein known to play a quantitative role in RPS2-mediated signaling. WIN3 expression in tissue distal to an infection site requires multiple salicylic acid regulatory genes. Finally, win3-T plants show modestly increased susceptibility to virulent P. syringae and modestly reduced SAR in response to P. syringae carrying avrRpm1. Thus, WIN3 is a key element of the RPS2 defense response pathway and a basal and systemic defense component.

Additional keywords: avirulence, GH3, hypersensitive response, leaf spot disease.

© 2007 The American Phytopathological Society