Involvement of a vascular hypersensitive response in quantitative resistance to Ralstonia solanacearum on tomato rootstock cultivar LS-89

Ralstonia solanacearum causes bacterial wilt disease in Solanaceae spp. Expression of the Phytophthora inhibitor protease 1 (PIP1) gene, which encodes a papain-like extracellular cysteine protease, is induced in R. solanacearum-inoculated stem tissues of quantitatively resistant tomato cultivar LS-89, but not in susceptible cultivar Ponderosa. Phytophthora inhibitor protease 1 is closely related to Rcr3, which is required for the Cf-2-mediated hypersensitive response (HR) to the leaf mould fungus Cladosporium fulvum and manifestation of HR cell death. However, up-regulation of PIP1 in R. solanacearum-inoculated LS-89 stems was not accompanied by visible HR cell death. Nevertheless, upon electron microscopic examination of inoculated stem tissues of resistant cultivar LS-89, several aggregated materials associated with HR cell death were observed in xylem parenchyma and pith cells surrounding xylem vessels. In addition, the accumulation of electron-dense substances was observed within the xylem vessel lumen of inoculated stems. Moreover, when the leaves of LS-89 or Ponderosa were infiltrated with 10 6 cells mL(-1) R. solanacearum, cell death appeared in LS-89 at 18 and 24 h after infiltration. The proliferation of bacteria in the infiltrated leaf tissues of LS-89 was suppressed to approximately 10-30% of that in Ponderosa, and expression of the defence-related gene PR-2 and HR marker gene hsr203J was induced in the infiltrated tissues. These results indicated that the response of LS-89 is a true HR, and induction of vascular HR in xylem parenchyma and pith cells surrounding xylem vessels seems to be associated with quantitative resistance of LS-89 to R. solanacearum.