Date of Award

1-1-2012

Document Type

Campus Access Thesis

Department

Chemistry and Biochemistry

Sub-Department

Chemistry

First Advisor

F Wayne Outten

Abstract

Iron is an essential cofactor for many biological processes. Due to the potential toxicity of iron as a result of Fenton chemistry, iron homeostasis in humans and other mammals is tightly controlled; this leaves only minute amounts of free iron available to invading pathogenic bacteria. This tight regulation forces pathogenic bacteria to scavenge for iron and has led to the development of complex iron acquisition systems (Andrews et al 2003, 216). In E. coli, ferric uptake regulator, Fur, regulates the transcription of several genes involved with iron acquisition (Hantke 2001, 172). One of these genes, yqjH, encodes the enzyme YqjH, a putative ferric reductase. Previous studies have shown that yqjH is also regulated by the divergently transcribed transcription factor YqjI. YqjI represses the transcription of itself and yqjH by binding to two specific sites on the gene promoters (Wang et al 2011, 563). Current studies were designed to characterize the regulation of the yqjH-yqjI intergenic region by Fur and YqjI. We will present how Fur and YqjI binding disruptions affect their regulatory abilities and how our results add to the understanding of the regulation within this complex intergenic region (Wang et al 2012, in preparation).

Rights

© 2012, Katherine Philipkosky

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