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XopD SUMO Protease Affects Host Transcription, Promotes Pathogen Growth, and Delays Symptom Development in Xanthomonas-Infected Tomato Leaves^[W],[OA]

^a Department of Biology, Stanford University, Stanford, California 94305
^b Department of Microbiology and Immunology, Stanford University, Stanford, California 94305
^c U.S. Department of Agriculture–Agricultural Research Service, Gainesville, Florida 32608

¹ Address correspondence to mudgett{at}stanford.edu.

We demonstrate that XopD, a type III effector from Xanthomonas campestris pathovar vesicatoria (Xcv), suppresses symptom production during the late stages of infection in susceptible tomato (Solanum lycopersicum) leaves. XopD-dependent delay of tissue degeneration correlates with reduced chlorophyll loss, reduced salicylic acid levels, and changes in the mRNA abundance of senescence- and defense-associated genes despite high pathogen titers. Subsequent structure-function analyses led to the discovery that XopD is a DNA binding protein that alters host transcription. XopD contains a putative helix-loop-helix domain required for DNA binding and two conserved ERF-associated amphiphilic motifs required to repress salicylic acid– and jasmonic acid–induced gene transcription in planta. Taken together, these data reveal that XopD is a unique virulence factor in Xcv that alters host transcription, promotes pathogen multiplication, and delays the onset of leaf chlorosis and necrosis.

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Effector XopD Suppresses Tissue Degeneration in Xanthomonas-Infected Tomato Leaves

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Plant Cell 2008 20: 1731. [Full Text]  

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