Low cell density regulator AphA upregulates the expression of Vibrio vulnificus iscR gene encoding the Fe-S cluster regulator IscR

IscR is a global transcriptional regulator that contributes to the pathogenesis of Vibrio vulnificus, a food-borne pathogen. In the present study, the regulatory mechanism for the iscR expression of V. vulnificus was evaluated. The expression of iscR was found to be upregulated by a transcriptional...

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Bibliographic Details
Published in:The journal of microbiology 2014, 52(5), , pp.413-421
Main Authors: Lim, Jong Gyu, Park, Jin Hwan, Choi, Sang Ho
Format: Article
Language:English
Subjects:
Agricultural biotechnology
autoregulation
Binding sites
Biomedical and Life Sciences
Biosynthesis
deoxyribonuclease I
DNA Footprinting
DNA Mutational Analysis
DNA, Bacterial - metabolism
Electrophoretic Mobility Shift Assay
food pathogens
Gene Expression Profiling
gene expression regulation
Gene Expression Regulation, Bacterial
Genes
Laboratories
Life Sciences
Microbial Pathogenesis and Host-Microbe Interaction
Microbiology
Pathogenesis
Pathogens
Plasmids
Promoter Regions, Genetic
Protein Binding
Toxicology
Transcription factors
Transcription Factors - genetics
Transcription Factors - metabolism
Vibrio
Vibrio vulnificus
Vibrio vulnificus - genetics
Vibrio vulnificus - growth & development
Virulence
생물학
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Summary:IscR is a global transcriptional regulator that contributes to the pathogenesis of Vibrio vulnificus, a food-borne pathogen. In the present study, the regulatory mechanism for the iscR expression of V. vulnificus was evaluated. The expression of iscR was found to be upregulated by a transcriptional regulator AphA, a homologue of the low cell density regulator AphA of the Vibrio species, in the exponential phase of growth. The promoter activity of iscR appeared to be activated and repressed by AphA and IscR, respectively. EMSA and DNase I protection assay showed that both AphA and IscR bind to the iscR regulatory region and the binding site for AphA overlapped with part of the binding site for IscR. Further mutational analysis suggested that AphA upregulates the iscR expression only in the presence of functional IscR. An examination of the roles of AphA and the binding sites revealed that the binding of AphA would hinder the IscR-mediated repression of the iscR transcription. The combined results show that V. vulnificus AphA upregulates iscR expression by antagonizing its negative autoregulation.
ISSN:1225-8873
1976-3794
DOI:10.1007/s12275-014-3592-4