Location
University of Nevada, Las Vegas
Start Date
3-8-2010 9:00 AM
End Date
3-8-2010 12:00 PM
Description
Shigella species are gram-negative, rod-shaped bacteria that are closely related to Escherichia coli. Virulent Shigella spp. are intracellular pathogens that invade, replicate and spread through epithelial cells of the lower intestine and cause bacillary dysentery in humans. This disease is characterized by a robust inflammatory response that results in fever, abdominal pain, and bloody diarrhea (3). According to the CDC, approximately 14,000 cases are reported each year in the United States alone. This number however, does not reflect the actual incidence of this disease as many cases go unreported. The molecular pathogenesis of these bacteria lies in the large virulence plasmid (~230-kb) that is found in all virulent Shigella spp. Two key virulence determinants include the ability to invade colonic epithelia (mediated by the ipa-mxi-spa gene locus) and the ability to spread to adjacent cells, a process known as actin-based-motility (mediated and controlled by icsA and icsP respectively). These events are largely regulated by VirB, a transcription factor (2, 3). Canonically, transcription factors are known to bind sequences proximal to the transcriptional start site (within 200-bp). Recent work has focused on the regulation of icsP (encodes a protease of the outer membrane) by VirB and has shed light on a novel regulatory strategy, whereby VirB regulates the activation of icsP from sites located more than 1-kb upstream of the transcriptional start site (1). Nine putative VirB binding sites have been found upstream of the icsP gene. This work seeks to characterize the contribution made by these putative binding sites to the VirB-dependent regulation of icsP.
Keywords
Genetic code; Genetic transcription; Shigella flexneri
Disciplines
Bacteriology | Genetics and Genomics | Life Sciences | Microbiology
Language
English
Evaluation of VirB binding site contribution to the regulation of the icsP promoter in Shigella flexneri
University of Nevada, Las Vegas
Shigella species are gram-negative, rod-shaped bacteria that are closely related to Escherichia coli. Virulent Shigella spp. are intracellular pathogens that invade, replicate and spread through epithelial cells of the lower intestine and cause bacillary dysentery in humans. This disease is characterized by a robust inflammatory response that results in fever, abdominal pain, and bloody diarrhea (3). According to the CDC, approximately 14,000 cases are reported each year in the United States alone. This number however, does not reflect the actual incidence of this disease as many cases go unreported. The molecular pathogenesis of these bacteria lies in the large virulence plasmid (~230-kb) that is found in all virulent Shigella spp. Two key virulence determinants include the ability to invade colonic epithelia (mediated by the ipa-mxi-spa gene locus) and the ability to spread to adjacent cells, a process known as actin-based-motility (mediated and controlled by icsA and icsP respectively). These events are largely regulated by VirB, a transcription factor (2, 3). Canonically, transcription factors are known to bind sequences proximal to the transcriptional start site (within 200-bp). Recent work has focused on the regulation of icsP (encodes a protease of the outer membrane) by VirB and has shed light on a novel regulatory strategy, whereby VirB regulates the activation of icsP from sites located more than 1-kb upstream of the transcriptional start site (1). Nine putative VirB binding sites have been found upstream of the icsP gene. This work seeks to characterize the contribution made by these putative binding sites to the VirB-dependent regulation of icsP.
Comments
Poster research sponsored by NIH INBRE