1.7.2
INTERACTIONS OF XANTHOMONAS AXONOPODIS PV. VESICATORIA 75-3hrp MUTANTS, THE PATHOGENIC PARENT AND THE HOST PLANT

W MOSS1, U BONAS2, JB JONES3 and M WILSON1

1Auburn University, Auburn, AL, USA; 2Institut des Sciences Vegetales, CNRS, Gif-sur-Yvette, France; 3GCREC, University of Florida, Bradenton, FL, USA

Background and objectives
Bacterial spot of tomato, caused by Xanthomonas axonopodis pv. vesicatoria, is a serious disease of fresh-market tomato [1]. Resistance to this pathogen is not available in commercial cultivars, and the efficacy of copper bactericides has declined due to copper resistance. Hypersensitive response and pathogenicity (hrp) mutants of X. a. pv. vesicatoria 75-3R may be effective biocontrol agents of bacterial spot caused by the pathogenic homologous parent. Pre-inoculation with X. a. pv. vesicatoria 75-3hrpG, Xv, F and E mutants differentially suppressed development of bacterial spot of tomato caused by the pathogenic parent in the greenhouse or by naturally occurring pathogenic strains in the field [2]. Experiments are being conducted to determine the mechanism of differential disease suppression.

Results and conclusions
Although all of the mutants significantly suppressed disease in the greenhouse when applied 48 h prior to pathogen inoculation, significant differences in disease suppression were observed among the mutants. The greatest reduction in disease severity was obtained with 75-3hrpG, while 75-3hrpE reduced disease severity less than the other mutants. Under field conditions in Alabama the mutants were inoculated weekly onto tomato, and significant season-long reductions in disease severity were obtained with all of the mutants. However, 75-3hrpG suppressed disease development more than the other mutants. A field experiment in Florida produced similar results. In other systems, pre-inoculation with bacterial antagonists has resulted in suppression of disease severity by reducing pathogen population sizes. Surprisingly, although 75-3hrpG suppressed disease severity to a greater degree than the other mutants in the current study, there were no differences in pathogen population sizes between the pathogen-only control and the 75-3hrpG-treated plants when population sizes were determined by sonication and dilution plating. Conversely, when inoculated following 75-3hrpE, pathogen population sizes were significantly larger than the control after 48 h. No other differences in pathogen population sizes were observed. Additionally, the mutants do not appear to induce a systemic host defence response when lower leaves of tomato are pre-inoculated with the mutants prior to challenge of distal leaves with the pathogen. We believe that the 75-3hrp mutants differ in an early non-specific host defence response, possibly involving differential activation of one or more signal transduction pathways. Alternatively, the hrp mutants may have different abilities to suppress the host response.

References
1. Bauske E, Zehnder G, Sikora E, Kemble J, 1996. http://ipmwww.ncsu.edu/Southern_Region/tomato.htm
2. Moss W, Byrne J, Wilson M, 1997. Phytopathology 87, S68 (abstr.).