1Department of Plant Sciences, Faculty of Life Sciences, Tel-Aviv University, Tel-Aviv 69978, Israel; 2Department of Plant Pathology, ARO, Volcani Center, Bet Dagan 50250, Israel; 3Department of Plant Pathology, Ohio State University, Columbus 43210-1087, U.S.A.
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Accepted 13 November 2000.
Erwinia herbicola pv. gypsophilae induces gall formation in gypsophila that is dependent on the existence of a pathogenicity plasmid (pPATHEhg). We previously demonstrated the presence of several hrp genes on this plasmid. By employing transposon mutagenesis and sequencing, a functional hrp gene cluster on the pPATHEhg has now been characterized completely. The hrp genes of E. herbicola pv. gypsophilae are remarkably similar to and colinear with those of Erwinia amylovora and Pantoea stewartii and generally showed 60 to 90% nucleotide or deduced amino acid identity. E. herbicola pv. gypsophilae, however, lacks hrpW, which is present in E. amylovora. Additionally, E. herbicola pv. gypsophilae mutants deficient in harpin production retained pathogenicity and were slightly reduced in their ability to elicit a hypersensitive response (HR) in tobacco. The “disease specific ” region, dspA/EB/F, exhibited 60 to 74% identity with the dspA/EB/F loci of E. amylovora and P. stewartii, respectively. Mutations in dspA/E abolished pathogenicity of E. herbicola pv. gypsophilae but not HR elicitation on tobacco. Inactivation of HrpL reduced plant-induced transcription of dspA/E by three orders, indicating Hrp-dependent regulation.
© 2001 The American Phytopathological Society