Date of Award

Spring 2008

Document Type

Thesis

Degree Name

Bachelor of Science

Department

Biology

First Advisor

Dr. Laura Runyen-Janecky

Abstract

Shigella flexneri is a facultative intracellular pathogen capable of causing dysentery, a condition that afflicts many around the world, especially in developing countries. There are several aspects of Shigella pathogenesis that are not well understood, including a number of genetic and cellular changes that allow Shigella to adapt to stresses encountered while invading and replicating within the eukaryotic cytosol. It was the goal of this research to examine the roles of iscSUA and suf, gene systems predicted to encode for iron-sulfur cluster biosynthesis proteins, in Shigella surviving exposure to oxidative stress agents and during Shigella invasion and plaque formation in a human colon cell line. An S. flexneri strain containing a deletion mutation in the iscSUA genes (UR022) was created and an earlier constructed S. flexneri strain containing a deletion mutation in the entire suf operon (UR011) was verified. Both mutant strains were less resistant to hydrogen peroxide and the superoxide-generator phenazine methosulfate than the wild-type strain. Although UR011 was able to grow at a comparable rate to the wild-type strain in both iron-replete and iron-limited media, UR022 showed reduced growth relative to the wild-type in both media. Furthermore, we found that although UR011 formed wild-type plaques in Henle cell monolayers, UR022 could not form plaques because the strain was noninvasive. Our data suggest that while suf oes not hinder growth or invasiveness, iscSUA is critical for S. flexneri invasion and normal growth.

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