|O'Donnell, Phillip - DEPT HORT. SCI., UF|
|Block, Anna - DEPT HORT.SCI., UF|
|Miersch, Otto - HALLE GE, INS PLANT BIOCH|
|Wasternack, Claus - HALLE GE, INS PLANT BIOCH|
|Jones, Jeffery - DEPT PLANT PATH, UF|
|Klee, Harry - DEPT HORT. SCI., UF|
Submitted to: Plant Physiology
Publication Type: Peer Reviewed Journal
Publication Acceptance Date: August 7, 2003
Publication Date: November 20, 2003
Citation: O'Donnell, P.J., Schmelz, E.A., Block, A., Miersch, O., Wasternack, C., Jones, J.B., Klee, H.J. 2003. Multiple hormones act sequentially to mediate a susceptible tomato pathogen defense response. Plant Physiology. 133:1-9. Interpretive Summary: Dramatic and harmful forms of plant stress, such as disease, are mediated by interactions between pathogens and plant hormones. It was hypothesized that targeted interference with the production plant hormones could inhibit the growth of pathogens in plants. Working with the University of Florida (Department of Horticultural Sciences), scientists at the Center for Medical, Agricultural and Veterinary Entomology in Gainesville, FL, have discovered that the growth of a bacterial pathogen was inhibited in plants with defective hormone signaling pathways. Moreover, a series of plant hormones are required to act sequentially for typical disease progression to occur. An understanding of how pathogens manipulate plant hormones to increase the level of infection should lead to the development of plants with improved self-defense mechanisms to resist the spread of disease.
Technical Abstract: Phytohormones regulate plant responses to a wide range of biotic and abiotic stresses. How a limited number of hormones differentially mediate individual stress responses is not understood. We have used one such response, the compatible interaction of tomato (Lycopersicon esculentum) and Xanthomonas campestris pv vesicatoria (Xcv), to examine the interactions of jasmonic acid (JA), ethylene, and salicylic acid (SA). The role of JA was assessed using an antisense allene oxide cyclase transgenic line and the def1 mutant to suppress Xcv-induced biosynthesis of jasmonates. Xcv growth was limited in these lines as was subsequent disease symptom development. No increase in JA was detected before the onset of terminal necrosis. The lack of a detectable increase in JA may indicate that an oxylipin other than JA regulates basal resistance and symptom proliferation. Alternatively, there may be an increase in sensitivity to JA or related compounds following infection. Hormone measurements showed that the oxylipin signal must precede subsequent increases in ethylene and SA accumulation. Tomato thus actively regulates the Xcv-induced disease response via the sequential action of at least three hormones, promoting expansive cell death of its own tissue. This sequential action of jasmonate, ethylene, and SA in disease symptom development is different from the hormone interactions observed in many other plant-pathogen interactions.