Faculty
Timothy
R. Hoover,
Ph.D.
Associate Professor of Microbiology, Associate
Head of Microbiology, and Undergraduate Coordinator
Ph.D.
(1988) University of Wisconsin-Madison
Address: Department of Microbiology
548 Biological Sciences
Building
Athens, GA 30602-2605
Phone: (706)
542-2675
E-mail: trhoover@uga.edu
COS CV: http://myprofile.cos.com/hoovert44
PubMed: hoover
tr
Research Interests:
Helicobacter pylori is a microaerophilic,
gram-negative bacterium that is a significant human pathogen of
the gastric mucosa. Colonization of the gastric mucosa by H.
pylori leads to a chronic inflammation that can progress
to a variety of diseases, including chronic gastritis, peptic
ulcer disease or gastric cancer. My research examines H.
pylori factors that are potentially important for colonization
and how the expression of these genes is controlled. One factor
required for colonization is motility, which is achieved in H.
pylori through a cluster of polar flagella. Flagellar
biosynthesis in H. pylori involves all three
sigma factors found in this bacterium (RpoD, RpoN and FliA) and
over 40 flagellar genes. Recent work from my lab and other researchers
suggests a transcriptional hierarchy for flagellar genes in H.
pylori that is coordinated with flagellar assembly through
the activity of the export apparatus. The flagellar protein export
apparatus is a type III secretion system responsible for translocating
many of the flagellar proteins across the cell membrane and mutations
in genes encoding export apparatus components often interfere
with transcription of RpoN-dependent and FliA-dependent flagellar
genes. Current work in the lab is directed at identifying the
mechanism by which the export apparatus controls expression of
these flagellar genes. A second project in the lab examines the
metabolism acetone and other ketone bodies (acetoacetate and ß-hydroxybutyrate)
by H. pylori. Ketone bodies are produced by
the body in high amounts during fasting or prolonged exercise,
and these compounds may represent an important energy source for
H. pylori. Our preliminary results indicate
that inactivation of at least one of the genes involved in acetone
metabolism interferes with host colonization. It is hoped that
the results of our studies will lead to new strategies for the
detection or treatment of H. pylori infection.
