|Mudgett, Mary Beth|
Submitted to: The Plant Cell
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: 7/3/2008
Publication Date: 7/29/2008
Citation: Kim, J., Taylor, K.W., Hotson, A., Keegan, M., Schmelz, E.A., Mudgett, M. 2008. XopD SUMO protease affects host transcription, promotes pathogen growth, and delays symptom development in Xanthomonas-infected tomato leaves. The Plant Cell. www.plantcell.org/cgi/doi/10.1105/tpc.108.058529 Interpretive Summary: Crop plants, such as tomato, often suffer from bacterial spot disease caused by the leaf pathogen Xanthomonas campestris pathovar vesicatoria (Xcv). Xcv bacteria are known to secrete effector proteins into tomato cells that modify their environment by reducing plant defenses and promoting high levels of bacterial growth. Despite this basic knowledge, the precise mechanism of specific Xcv effector proteins, their intracellular targets, and ultimately modifications to host plant physiology, have remained mysterious. In collaboration with researchers from Stanford University, scientists at the Center for Medical, Agricultural and Veterinary Entomology in Gainesville, FL, have discovered that the bacterial effector protein XopD is critical for reducing plant defenses and maximizing pathogen growth. XopD is a highly multifunctional protein that acts in part by directly binding plant DNA, suppressing host transcriptional defense responses and delaying leaf senescence. XopD also suppresses both the accumulation defense-related phytohormones and the activation of phytohormone-based signal transduction. Using XopD, Xcv bacteria prolong the normal life span of infected tissues resulting in what visually appears to be plant tolerance; however, the plant is not in control. This work provides fundamental insight to the mechanisms used by bacterial pathogens to maximally colonize crop plants and will eventually will lead to targeted transgenic strategies to recuperate effective plant defense responses to pathogen attack.
Technical Abstract: We demonstrate that XopD, a type III effector from Xanthomonas campestris pathovar vesicatoria, promotes plant tolerance to infection by suppressing leaf senescence. XopD-dependent delay of tissue degeneration correlates with reduced chlorophyll loss, reduced salicylic acid levels, and changes in mRNA abundance for senescence- and defense-associated genes, despite high pathogen titers relative to a xopD' null mutant. To genetically uncover mechanisms of XopD action, a yeast suppressor screen was performed to identify mutants altered in sensitivity to XopD growth inhibition. Mutants with defects in transcriptional regulation and chromatin remodeling were isolated. This led to the discovery that XopD is a DNA-binding protein that alters transcription of SNF2-regulated genes in yeast. XopD structure-function analyses identified a helix-loop-helix domain required for DNA-binding and two conserved ERF-associated amphiphilic motifs required to repress hormoneinduced. gene transcription in planta. Thus, XopD promotes plant tolerance by repressing host gene transcription altered in response to Xanthomonas infection.