Southern Research scientists are currently engaged in the following basic research initiatives in bacteriology:
Purine Metabolism in Mycobacterium Tuberculosis, William B. Parker, Ph.D
Currently, little is known about purine metabolism in mycobacteria. It is hoped that further study will lead to the discovery of differences in utilization of substrates by the enzymes involved in purine salvage. This information could lead to the creation of new agents to selectively treat Mycobacterium tuberculosis infections.
Global Regulatory Networks Controlling Bacterial Behavior, Jorge Antonio Benitez, Ph.D.
The focus of this research is to understand how bacteria sense, integrate, and respond to overlapping environmental stimuli using the cholera bacterium as a model. Vibrio cholerae is a Gram-negative, highly motile bacterium that causes the diarrheal disease, cholera. Cholera is a paradigm waterborne disease transmitted by the fecal-oral route. Infecting Vibrios colonize the human small bowel, where secretion of cholera toxin triggers a profuse rice-watery diarrhea. Late in infection, cholera bacteria down-regulate the expression of virulence factors and activate the production of protease and motility to detach from the intestinal mucosa and return to the aquatic environment. The cholera bacterium can also switch between motile free-living and sessile biofilm lifestyles. These behavioral switches are modulated by multiple interacting signal transduction pathways and global regulators.
The objective of Dr. Benitez' research is to identify critical regulators controlling bacterial behavior in the cholera bacterium. To this end, his laboratory combines multiple approaches such as bacterial genetics, functional genomics, and animal models. Emphasis is placed on conserved regulatory proteins or pathways that regulate virulence, motility, and biofilm formation in the broadest range of bacterial pathogens. The ultimate goal of his research is to identify bacterial targets for small molecules capable of modifying bacterial behavior to prevent them from causing disease.
Mechanism of Phagosomal Escape by Francisella tularensis, Rexford Asare, Ph.D.
There is no vaccine against Francisella tularensis, the causative agent of tularemia, and very limited therapeutic intervention to treat the disease. Dr. Asare’s research is focused on elucidating the contribution of Francisella type VI secretion effectors to phagosome biogenesis, escape mechanism, and cytosolic replication within host cells in order to develop therapeutic intervention or a vaccination for tularemia. He has successfully identified and characterized genes involved in intracellular replication and escape of Francisella in macrophages and S2 cells. Many of the gene products are designated as either hypothetical proteins or proteins of unknown function. He is currently investigating the relationship between these genes and the type VI secretion system. Dr. Asare is also investigating the role of these proteins in the escape and intracellular replication of Francisella in human macrophages.
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