Silicon-induced basal resistance in tomato against Ralstonia solanacearum is related to modification of pectic cell wall polysaccharide structure

Bacterial wilt incidence was reduced by 38.1% and 100% in silicon-treated plants of the moderately resistant tomato genotype King Kong 2 and the resistant genotype Hawaii 7998 grown in peat substrate. At 5 days post inoculation the bacterial population was significantly reduced in stems and roots of genotype Hawaii 7998, and in stems of King Kong 2 in silicon-treated plants compared to non-treated plants, indicating a silicon-induced resistance, since silicon accumulated in roots, but not in stems, while a tolerance effect was observed in the susceptible genotype L390. Characterization of possible molecular mechanisms involved in silicon-mediated resistance by immuno-histochemical analysis of stem cell walls indicated silicon-induced changes in the pectic polysaccharide structure. After infection homogalacturonan with non-blockwise degradation of methyl-esters was increased in vessel walls in non-silicon-treated plants, but not in silicon-treated plants, possibly indicating the action of pathogen pectinmethylesterase. Also the staining of vessel walls for arabinogalactan-protein in infected, non-silicon-treated plants was not observed in silicon-treated plants. In inoculated, silicon-treated plants, staining for arabinan side chains of rhamnogalacturonan I (RG I) was increased in some vessel walls, and fluorescence of antibodies for galactan side chains of RG I overall increased in the xylem parenchyma compared to non-silicon-amended plants. These observations suggest an induced basal resistance on cell wall level after silicon treatment, while the yellow or brown autofluorescence occurring in inoculated, non-silicon-treated plants disappeared.