A Pectinase‐deficient Ralstonia solanacearum Strain Induces Reduced and Delayed Structural Defences in Tomato Xylem

Abstract

AbstractIt has been suggested that oligogalacturonides (OGAs) released by bacterial pectinases can induce plant defence responses. To test this hypothesis, resistant tomato cultivar LS‐89 and susceptible cultivar Ponderosa were inoculated with either wild‐type Ralstonia solanacearum strain K60 or a pectinase‐deficient triple mutant K60‐509, which lacks endo‐polygalacturonase PehA, exo‐poly‐alpha‐d‐galacturonosidase PehB, and pectin methylesterase Pme. K60 induced structural defence responses, including electron‐dense materials (EDMs) in vessels and apposition layers (ALs) in parenchyma cells adjacent to xylem vessels colonized by bacteria in LS‐89 stems. In contrast, LS‐89 infected with K60‐509 did not have any EDMs in vessels at 4 days after inoculation (DAI), and had them only rarely at 7 DAI. In LS‐89 infected with K60‐509, ALs were rarely observed in parenchyma cells adjacent to vessels at 4 DAI, and while they were present at 7 DAI, they were thinner than ALs induced by K60. The bacterial density in LS‐89 stems infected with K60‐509 was lower than in stems infected with K60 at 4 DAI, but the strains reached similar population sizes by 7 DAI, showing the pectinase‐deficient mutant colonized resistant stems more slowly than did the wild‐type strain. Vessels infected with K60‐509 contained fewer EDMs at 7 DAI than were observed at either 4 or 7 DAI in vessels colonized by K60, although bacterial density in the xylem tissues containing K60‐509 at 7 DAI was about the same as in the xylem tissues containing K60 at 4 DAI. Neither the wild‐type strain nor the pectinase‐deficient mutant induced these histopathological changes on susceptible cultivar Ponderosa. These results indicate that R. solanacearum pectinases play some role in eliciting histopathological changes in LS‐89, likely by releasing OGAs that trigger plant structural defences.