OPEN ACCESS ARTICLE

This Article Free via Open Access: OA OA Full Text Full Text (PDF) Supplemental Data OA All Versions of this Article: 20/7/1915    most recent tpc.108.058529v1 Alert me when this article is cited Alert me if a correction is posted Services Email this article to a friend Related articles in Plant Cell Similar articles in this journal Similar articles in PubMed Alert me to new issues of the journal Download to citation manager Citing Articles Citing Articles via HighWire Citing Articles via CrossRef Citing Articles via Google Scholar Google Scholar Articles by Kim, J.-G. Articles by Mudgett, M. B. Search for Related Content PubMed PubMed Citation Articles by Kim, J.-G. Articles by Mudgett, M. B. Agricola Articles by Kim, J.-G. Articles by Mudgett, M. B.

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.

Related articles in Plant Cell:

Effector XopD Suppresses Tissue Degeneration in Xanthomonas-Infected Tomato Leaves

Jennifer Mach
Plant Cell 2008 20: 1731. [Full Text]  

This article has been cited by other articles:

				J.-G. Kim, X. Li, J. A. Roden, K. W. Taylor, C. D. Aakre, B. Su, S. Lalonde, A. Kirik, Y. Chen, G. Baranage, et al. Xanthomonas T3S Effector XopN Suppresses PAMP-Triggered Immunity and Interacts with a Tomato Atypical Receptor-Like Kinase and TFT1 PLANT CELL, April 1, 2009; 21(4): 1305 - 1323. [Abstract] [Full Text] [PDF]

				N. Kocal, U. Sonnewald, and S. Sonnewald Cell Wall-Bound Invertase Limits Sucrose Export and Is Involved in Symptom Development and Inhibition of Photosynthesis during Compatible Interaction between Tomato and Xanthomonas campestris pv vesicatoria Plant Physiology, November 1, 2008; 148(3): 1523 - 1536. [Abstract] [Full Text] [PDF]

				J. Mach Effector XopD Suppresses Tissue Degeneration in Xanthomonas-Infected Tomato Leaves PLANT CELL, July 1, 2008; 20(7): 1731 - 1731. [Full Text] [PDF]