Plant Physiology Preview
Published on October 9, 2003; 10.1104/pp.103.030379
Received July 18, 2003
Returned for revision July 30, 2003
Accepted August 7, 2003
Multiple Hormones Act Sequentially to Mediate a Susceptible Tomato Pathogen Defense Response
Philip J. O’Donnell , Eric Schmelz , Anna Block , Otto Miersch , Claus Wasternack , Jeffrey B. Jones , and Harry J. Klee *
Department of Horticultural Sciences (P.J.O., A.B., H.J.K.) and Department of Plant Pathology (J.B.J.), University of Florida, Gainesville, Florida 32611; United States Department of Agriculture-Agricultural Research Service, Center for Medical Agricultural and Veterinary Entomology, 1700 SW 23 Drive, Gainesville, Florida 32608 (E.S.); and Institute of Plant Biochemistry, D-06018 Halle, Germany (O.M., C.W.)
* Corresponding author; email: hjklee{at}ifas.ufl.edu.
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.
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