| Pre-inoculation with Xanthomonas campestris pv. vesicatoria 75-3hrpG, hrpXv, and hrpE1 mutants consistently suppressed development of bacterial spot disease of tomato under greenhouse and field conditions with the 75-3hrpG mutant treatment resulting in significantly greater suppression. In the field none of the hrp mutants achieved population sizes comparable to the pathogenic strain, 75-3RS, and no large population differences among the mutants were observed. When tomato plants were spray-inoculated in the greenhouse with the hrp mutants 48 h prior to pathogen challenge, significant reductions in external pathogen population sizes were not observed. However, in the growth chamber spray inoculation with the hrpG mutant significantly reduced internal pathogen population sizes when the pathogen was infiltrated into leaf tissue 48 h later.;None of the hrp mutant treatments reduced disease intensity when lower leaves of tomato were pre-inoculated with the mutants and distal leaves were challenged 48 h later with 75-3RS. Experiments were then conducted to determine whether plant defense pathways were differentially activated by the hrp mutants. Wild-type tomato plants and plants deficient in accumulation of salicylic acid (SA), sensing of ethylene, or accumulation of jasmonic acid (JA) were pre-inoculated with the hrp mutants and challenged 48 h later with 75-3RS. As in previous experiments, hrp mutants significantly suppressed disease on the wild-type tomato lines. However, in all experiments treatment with the hrpG mutant failed to suppress disease on any of the mutant or transgenic tomato lines, while treatment with the hrpXv or hrpE1 mutants failed to produce large or consistent effects on disease on the mutant or transgenic tomato lines. Since SA, JA, and ethylene are implicated in expression of host defenses, it is concluded that induction of hrpG is a critical event in suppression of the local host defense response to X. campestris pv. vesicatoria leading to suppression of bacterial spot. |
