Open AccessThe Type III Effector HsvG of the Gall-Forming Pantoea agglomerans Mediates Expression of the Host Gene HSVGT
Author(s) -
Gal Nissan,
Shulamit Manulis-Sasson,
Laura Chalupowicz,
Doron Teper,
Adva Yeheskel,
Metsada PasmanikChor,
Guido Sessa,
Isaac Barash
Publication year - 2012
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-06-11-0173
Subject(s) - pantoea agglomerans , biology , transcription factor , leucine zipper , effector , electrophoretic mobility shift assay , gene , microbiology and biotechnology , enhancer , dna , mutant , transcription (linguistics) , dna binding protein , zinc finger , genetics , bacteria , linguistics , philosophy
The type III effector HsvG of the gall-forming Pantoea agglomerans pv. gypsophilae is a DNA-binding protein that is imported to the host nucleus and involved in host specificity. The DNA-binding region of HsvG was delineated to 266 amino acids located within a secondary structure region near the N-terminus of the protein but did not display any homology to canonical DNA-binding motifs. A binding site selection procedure was used to isolate a target gene of HsvG, named HSVGT, in Gypsophila paniculata. HSVGT is a predicted acidic protein of the DnaJ family with 244 amino acids. It harbors characteristic conserved motifs of a eukaryotic transcription factor, including a bipartite nuclear localization signal, zinc finger, and leucine zipper DNA-binding motifs. Quantitative real-time polymerase chain reaction analysis demonstrated that HSVGT transcription is specifically induced in planta within 2 h after inoculation with the wild-type P. agglomerans pv. gypsophilae compared with the hsvG mutant. Induction of HSVGT reached a peak of sixfold at 4 h after inoculation and progressively declined thereafter. Gel-shift assay demonstrated that HsvG binds to the HSVGT promoter, indicating that HSVGT is a direct target of HsvG. Our results support the hypothesis that HsvG functions as a transcription factor in gypsophila.