Open AccessGenetic Organization of the hrp Gene Cluster and dspAE/BF Operon in Erwinia herbicola pv. gypsophilae
Author(s) -
Henia Mor,
Shulamit Manulis,
Michal Zuck,
Roni Nizan,
David L. Coplin,
Isaac Barash
Publication year - 2001
Publication title -
molecular plant-microbe interactions
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.565
H-Index - 153
eISSN - 1943-7706
pISSN - 0894-0282
DOI - 10.1094/mpmi.2001.14.3.431
Subject(s) - erwinia , operon , fire blight , biology , transposon mutagenesis , plasmid , gene , transposable element , genetics , mutant , mutagenesis , microbiology and biotechnology , gene cluster , pantoea agglomerans , bacteria
Erwinia herbicola pv. gypsophilae induces gall formation in gypsophila that is dependent on the existence of a pathogenicity plasmid (pPATH Ehg ). 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 pPATH Ehg 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.