Location

University of Nevada Las Vegas, Student Union Ball Room

Start Date

6-8-2009 9:30 AM

End Date

6-8-2009 12:00 PM

Description

Iron is an essential element in the metabolism of many organisms, including bacteria. In many pathogenic bacteria, the levels of iron present trigger the expression of many virulence genes. In Shigella, a gram-negative bacterium that causes dysentery in humans, the expression of a small regulatory RNA, ryhB, is blocked in the presence of iron. Studies have revealed that ryhB represses virB, a global regulator of virulence genes in Shigella.

The icsP gene is under the direct control of VirB. icsP encodes an outer membrane protease that cleaves a protein necessary for the actin tail assembly of Shigella in vitro. In vivo, this actin tail enables the pathogenic Shigella to spread intracellularly. Because most of the iron is complexed inside host cells, the intracellular compartment is considered an iron-poor environment. The aim of this project is to determine whether iron levels influence the regulation of icsP through VirB.

Based on previous studies done on ryhB, I hypothesize that ryhB regulates icsP through VirB. Beta-galactosidase assays and Western blots will allow for determination of whether the activity of the icsP promoter and gene expression significantly differ in the presence and absence of iron.

Keywords

Dysentery; Free iron; Shigella flexneri

Disciplines

Bacteriology | Pathogenic Microbiology

Language

English

Comments

Abstract & poster


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Aug 6th, 9:30 AM Aug 6th, 12:00 PM

The Regulation of the icsP promoter of Shigella flexneri by ryhB

University of Nevada Las Vegas, Student Union Ball Room

Iron is an essential element in the metabolism of many organisms, including bacteria. In many pathogenic bacteria, the levels of iron present trigger the expression of many virulence genes. In Shigella, a gram-negative bacterium that causes dysentery in humans, the expression of a small regulatory RNA, ryhB, is blocked in the presence of iron. Studies have revealed that ryhB represses virB, a global regulator of virulence genes in Shigella.

The icsP gene is under the direct control of VirB. icsP encodes an outer membrane protease that cleaves a protein necessary for the actin tail assembly of Shigella in vitro. In vivo, this actin tail enables the pathogenic Shigella to spread intracellularly. Because most of the iron is complexed inside host cells, the intracellular compartment is considered an iron-poor environment. The aim of this project is to determine whether iron levels influence the regulation of icsP through VirB.

Based on previous studies done on ryhB, I hypothesize that ryhB regulates icsP through VirB. Beta-galactosidase assays and Western blots will allow for determination of whether the activity of the icsP promoter and gene expression significantly differ in the presence and absence of iron.