INCOMPATIBLE INTERACTIONS BETWEEN CRUCIFERS AND XANTHOMONAS-CAMPESTRIS INVOLVE A VASCULAR HYPERSENSITIVE RESPONSE - ROLE OF THE HRPX LOCUS

The hrpXc locus of X. campestris pv. campestris is required for pathogenicity on crucifers and for hypersensitivity on nonhost plants (S. Kamoun and C. I. Kado, J. Bacteriol. 172:5165-5172, 1990). Southern blot hybridizations of total DNA with a 334-bp PstI probe internal to hrpXc was conducted on 14 independent X. campestris isolates from crucifers representing X. c. pv. campestris and X. c. pv. armoraciae. All strains contained sequences homologous to hrpXc located in an 11-kb EcoRI fragment. Electroporation of integrative plasmids, that carry small insert fragments internal to the hrpXc transcriptional unit, allowed the construction of HrpX mutants in 10 strains representing X. c. pv. campestris (four races, eight strains) and X. c. pv. armoraciae (two strains). All mutants were unable to induce disease symptoms on crucifers or cause a hypersensitive response on nonhosts. Chromosomal transcriptional fusions of hrpXc to gusA (beta-glucuronidase) and cal (chloramphenicol acetyltransferase) reporter genes were also constructed by marker-integration and used to confirm that hrpXc is expressed in X. c. pv. campestris only in plants. The response of crucifer plants to incompatible inoculations with X. campestris was also closely examined histochemically, and a localized and rapid vascular browning reminiscent of a hypersensitive response was found to correlate with incompatibility. Interestingly, all HrpX mutants induced this vascular hypersensitive response (VHR), suggesting that the plant response to these hrp mutants is not null. Coinoculation of HrpXc mutants with the wild-type parental strains suppressed in planta growth defection and the vascular browning response, and rescued HrpXc mutants. Our observations lead us to propose the hypothesis that hrpXc may function in suppression of defense response(s) in the compatible host plant.