Postdoctoral Research

Characterization of the molecular mechanisms that allow the pathogenic bacterium Shigella flexneri to sense and survive numerous environments.

My postdoctoral research was carried out in the laboratory of Dr. Shelley Payne at the University of Texas.  As a postdoctoral fellow in the Section of Molecular Genetics and Microbiology at the University of Texas at Austin, I worked to understand how bacterial pathogens respond to changes in their environment.  The model system that I used  was the facultative intracellular bacterium Shigella flexneri, which encounters many stressful environments during its journey through the external environment and human host.  The conditions in the external environment, including nutrient and ion availability, temperature, moisture, pH, aerobicity, and the presence of other microorganisms, are extremely variable.  After ingestion by the human host, Shigella must evade the host immune response, survive the acidic stomach, successfully transverse the small intestine to arrive in the colon and infect the colonic epithelial cells, which presents yet another set of distinct environmental conditions.  Each of these potentially stressful environments that Shigella encounters may induce the expression of a particular set of genes that results in phenotypic changes.  Thus, one of the approaches that I used in my research wasidentification and characterization of Shigella genes that are induced when Shigella encounters stressful environments, specifically those that are induced when Shigella is in the colonic epithelial cells.

Papers from my post-doctoral research:

Wei J, Goldberg MB, Burland V, Venkatesan MM, Deng W, Fournier G, Mayhew GF, Plunkett G 3rd, Rose DJ, Darling A, Mau B, Perna NT, Payne SM, Runyen-JaneckyLJ, Zhou S, Schwartz DC, Blattner FR. 2003. Complete genome sequence and comparative genomics of Shigella flexneri serotype 2a strain 2457T.  Infect Immun. May;71(5):2775-86.

Runyen-Janecky LJ, Reeves SA, Gonzales EG, Payne SM. 2003. Contribution of the Shigella flexneri Sit, Iuc, and Feo iron acquisition systems to iron acquisition in vitro and in cultured cells. Infect Immun. Apr;71(4):1919-28.

Mogull SA, Runyen-Janecky LJ, Hong M, Payne SM. 2001. dksA is required for intercellular spread of Shigella flexneri via an RpoS-independent mechanism. Infect Immun. Sep;69(9):5742-51.