Date of Award

5-14-2012

Document Type

Thesis

Degree Name

Bachelor of Arts

First Advisor

Slonczewski, Joan

Abstract

In order for pathogenic E. coli to colonize the human intestine they must pass through the stomach (pH 2-4) which is at least 1000 times more acidic than optimal growth conditions (pH 5-9). Certain mechanisms for maintaining intracellular pH are unique to anoxic conditions and are not apparent when oxygen is present. It was hypothesized that ArcA and FNR‰ÛÓthe regulators that transition E. coli to anaerobic metabolism‰ÛÓare implicated in the organism‰Ûªs ability to utilize these anoxic-specific mechanisms. We conducted extreme-acid survival assays in aerated conditions, anoxic conditions, or a mixture of the two depending on stage of the experiment. We observed that FNR expression is associated with anoxic extreme-acid sensitivity. This association is dependent on the presence of tryptone in the extreme pH exposure medium. We hypothesize that FNR-associated acid sensitivity is caused by the regulator repressing expression of key acid resistance mechanisms. We tested how genetic knockouts for two acid resistance mechanisms survive in anoxic extreme acid. We determined that hydrogenase-3 contributes to anoxic acid resistance, but glutamate decarboxylase does not.

Comments

Includes bibliographical references (p. 33-39)

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