Location
University of Nevada, Las Vegas
Start Date
9-8-2011 10:15 AM
End Date
9-8-2011 12:00 PM
Description
Shigella flexneri is a gram-negative, invasive bacterial pathogen that afflicts the human colonic epithelium, causing shigellosis, an illness triggering severe dysentery. The World Health Organization cites the disease burden of shigellosis near 90 million episodes and 108,000 deaths per year.
The motility and spread of Shigella is modulated by icsP, a virulence gene. The transcription factor VirB positively regulates many virulence genes encoded by the Shigella virulence plasmid. Two distal binding sites of VirB have been shown to regulate the promoter activity of icsP, despite their location of more than 1 kb upstream of the transcription start site. Five VirB binding sites are located between these two sites and the transcription start site, and two are located in close proximity downstream of the transcription start site.
Investigation into the impact of the VirB binding sites is part of a larger effort to understand the workings of VirB, which is the major switch that controls virulence gene expression in Shigella.
Keywords
Gene expression; Genetic transcription; Shigella flexneri; Virulence (Microbiology) — Genetic aspects
Disciplines
Bacteriology | Diseases | Genetics and Genomics | Molecular Genetics
Language
English
Combination of VirB binding site mutations to evaluate collective impact on icsP promoter activity in Shigella flexneri
University of Nevada, Las Vegas
Shigella flexneri is a gram-negative, invasive bacterial pathogen that afflicts the human colonic epithelium, causing shigellosis, an illness triggering severe dysentery. The World Health Organization cites the disease burden of shigellosis near 90 million episodes and 108,000 deaths per year.
The motility and spread of Shigella is modulated by icsP, a virulence gene. The transcription factor VirB positively regulates many virulence genes encoded by the Shigella virulence plasmid. Two distal binding sites of VirB have been shown to regulate the promoter activity of icsP, despite their location of more than 1 kb upstream of the transcription start site. Five VirB binding sites are located between these two sites and the transcription start site, and two are located in close proximity downstream of the transcription start site.
Investigation into the impact of the VirB binding sites is part of a larger effort to understand the workings of VirB, which is the major switch that controls virulence gene expression in Shigella.
Comments
Research sponsored by: NIH grants # P20 RR-016464 and # R15 Al090573-01