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Plant‐pathogenic Ralstonia strains cause bacterial wilt disease by colonizing xylem vessels of many crops, including tomato. Host resistance is the best control for bacterial wilt, but resistance mechanisms of the widely used Hawaii 7996 tomato breeding line (H7996) are unknown. Using growth in ex vivo xylem sap as a proxy for host xylem, we found that Ralstonia strain GMI1000 grows in sap from both healthy plants and Ralstonia‐infected susceptible plants. However, sap from Ralstonia‐infected H7996 plants inhibited Ralstonia growth, suggesting that in response to Ralstonia infection, resistant plants increase inhibitors in their xylem sap. Consistent with this, reciprocal grafting and defence gene expression experiments indicated that H7996 wilt resistance acts in both above‐ and belowground plant parts. Concerningly, H7996 resistance is broken by Ralstonia strain UW551 of the pandemic lineage that threatens highland tropical agriculture. Unlike other Ralstonia, UW551 grew well in sap from Ralstonia‐infected H7996 plants. Moreover, other Ralstonia strains could grow in sap from H7996 plants previously infected by UW551. Thus, UW551 overcomes H7996 resistance in part by detoxifying inhibitors in xylem sap. Testing a panel of xylem sap compounds identified by metabolomics revealed that no single chemical differentially inhibits Ralstonia strains that cannot infect H7996. However, sap from Ralstonia‐infected H7996 contained more phenolic compounds, which are known to be involved in plant antimicrobial defence. Culturing UW551 in this sap reduced total phenolic levels, indicating that the resistance‐breaking Ralstonia strain degrades these chemical defences. Together, these results suggest that H7996 tomato wilt resistance depends in part on inducible phenolic compounds in xylem sap. [ABSTRACT FROM AUTHOR]

Sources of resistance to tropical race 1 strains of Ralstonia solanacearum, the causative agent of bacterial wilt, have been identified in the tomato germplasm. Till now, no experimental data are available on Lycopersicon spp. (now Solanum spp.) sources for resistance to temperate race 3, biovar 2 strains. Eighty-two accessions belonging to different Lycopersicon spp. were evaluated for resistance to a race 3 strain endemic to Réunion Island. Evaluation was conducted in growth chambers, and included the Lycopersicon esculentum cv. Roma as susceptible control. No immunity or complete resistance was observed in any accession tested under our experimental conditions. Therefore, race 3 strain was demonstrated to be highly pathogenic on all the Lycopersicon accessions tested. Partial resistance was significantly detected in only one accession belonging to the species Lycopersicon peruvianum, and one L. esculentum var. cerasiforme tomato line. Five other genotypes from the species L. esculentum, Lycopersicon hirsutum and L. peruvianum were noteworthy. The Hawaii 7996 line represented the best source of partial resistance to race 3 with 52% of wilting. It can therefore be used as a starting point for introducing resistance to bacterial wilt caused by R. solanacearum race 3 in tomato and studying its genetic control. [ABSTRACT FROM AUTHOR]

The distribution and appearance of Ralstonia solanacearum in the upper hypocotyl tissues of root-inoculated tomato seedlings of resistant rootstock cultivar LS-89 (a selection from Hawaii 7998) and susceptible cultivar Ponderosa were compared to clarify the mechanism that limits the movement of the bacterial pathogen in resistant tomato tissues. In stems of wilted Ponderosa plants, bacteria colonized both the primary and the secondary xylem tissues. Bacteria were abundant in vessels, of which the pit membranes were often degenerated. All parenchyma cells adjacent to vessels with bacteria were necrotic and some of them were colonized with bacteria. In stems of LS-89 plants showing no discernible wilting symptoms, bacteria were observed in the primary xylem tissues but not in the secondary xylem tissues. Necrosis of parenchyma cells adjacent to vessels with bacteria was observed occasionally. The pit membranes were often thicker with high electron density. The inner electron-dense layer of cell wall of parenchyma cells and vessels was thicker and more conspicuous in xylem tissues of infected LS-89 than in xylem of infected Ponderosa or mock-inoculated plants. Electron-dense materials accumulated in or around pit cavities in parenchyma cells next to vessels with bacteria, and in vessels with bacteria. Many bacterial cells appeared normal in vessels, except for those in contact with the pit membranes. These results indicate that R. solanacearum moves from vessel to vessel in infected tissues through degenerated pit membranes and that restricted movement in xylem tissues was the characteristic feature in LS-89. The limitation in bacterial movement may be related to the thickening of the pit membranes and/or the accumulations of electron-dense materials in vessels and parenchyma cells. [ABSTRACT FROM AUTHOR]