Lab Members


Principal Investigator

Shelley M. Payne, Ph.D.

Shelley Payne

UT-CNS Profile
PubMed Record

Google Scholar Record


B.A. Rice University, 1972
Ph.D. Texas Health Science Center (Dallas), 1977
POSTDOC: University of California at Berkeley

Our studies focus on the genetics and regulation of iron acquisition systems and other virulence factors of Shigella and Vibrio species. The iron transport systems are of interest because the ability of potential pathogens to acquire iron from the host is an important determinant of microbial virulence. Iron is required for growth of bacteria, but little free iron is available in mammalian hosts. Many bacteria have been found to secrete high affinity iron-binding compounds, or siderophores, which may function to remove iron from host proteins and make it available to the microorganism for growth in vivo.

Vibrio species produce a variety of siderophores and iron-regulated outer membrane proteins. In response to iron deprivation, Vibrio cholerae synthesizes a norspermadine containing siderophore, and five cell surface proteins, including receptors for the siderophore and for heme. The Shigella species, a group of enteric pathogens, have at least three distinct iron transport systems. Two of these, the aerobactin and enterobactin systems, consist of siderophores and their associated outer membrane receptor proteins. Expression of these systems is regulated at the level of transcription by the concentration of iron within the cell. A third pathway is required for the transport and utilization of iron in the form of heme. Virulence assays of mutants defective in one or more of these systems suggest that siderophores provide iron in the extracellular environment while heme transport is utilized by Shigella growing intracellularly within epithelial cells. A heme-binding protein is found on the surface of wild-type Shigellae. Although this protein is not required for heme transport, it is required for invasion of intestinal epithelial cells by S. flexneri. The protein allows the bacteria to bind large amounts of heme on the surface of the bacteria and promotes the attachment of the bacteria to the host cells. This protein is encoded on a large 220 kilobase plasmid, and its synthesis is regulated by both temperature and pH. Analysis of regulatory mutants indicates that at least two loci, one chromosomal and one plasmid encoded, are responsible for the regulation of the structural gene for this cell surface protein. Genetic and recombinant DNA techniques are being used to characterize chromosomal and plasmid sequences involved in iron transport and invasion in these enteric pathogens. The genes have been cloned and gene fusions have been constructed to measure the expression of these genes under different environmental conditions. Techniques have been developed also to measure gene expression and synthesis of virulence-associated proteins by S. flexneri growing within host cells. These studies will allow us to determine the molecular mechanisms of iron acquisition and ultimately to assess the roles of these systems in bacterial infections.


Senior Scientists

Alex R. Mey, Ph.D.  

Alex MeyPubMed Record
Google Scholar Record


B.A. Biology, University of Texas at Austin, 1994
Ph.D. Molecular Biology, University of Texas at Austin, 2002

I am interested in how V. cholerae senses and responds to environmental signals, and how these signals are integrated into the regulation of virulence gene expression and pathogenesis in the host. My most recent studies have focused on the role of amino acids in the expression of the virulence gene regulator ToxR. Through this work, I have uncovered a previously unknown link between ToxR and the global regulator CsrA, which is involved in controlling various cellular processes including carbon metabolism, quorum sensing, and virulence in response to extracellular signals. By linking environmental sensing to the ToxR regulon, CsrA may effectively act as a switch that controls pathogenesis in response environmental stimuli. We are currently working to understand more completely the role of CsrA in V. cholerae cellular metabolism and virulence.

In my spare time, I enjoy reading, playing piano, baking, hiking, traveling, and spending time with my family.


Research Technicians

Carolyn Fisher  
Carolyn Fisher


B.S. Texas A&M University, Biomedical Science, 1979

In my 10+ years in the Payne lab I have worked on various projects studying both Vibrio cholerae and Shigella flexneri. My current project involves the study of manganese homeostasis in Vibrio cholerae. In addition to research, I help keep the lab running by purchasing supplies and equipment. Outside the lab, I enjoy taking care of my animals which include chickens, a horse, cattle, and two dogs and spending time with family.



Postdoctoral Fellow

Camilo Gómez, Ph.D.



Google Scholar Profile


B.S. Universidad de los Andes (Bogotá, Colombia), Chemistry, 2014
B.S. Universidad de los Andes (Bogotá, Colombia), Microbiology, 2015
M.S. Universidad de los Andes (Bogotá, Colombia), Biological Sciences, 2017
Ph.D. The University of Texas at Austin (Austin, TX), Cell and Molecular Biology, 2022

Iron is an indispensable nutrient for most organisms, and pathogens are not an exception. I use the gastrointestinal human pathogen Vibrio cholerae as a model organism to study ferrous iron acquisition in bacteria. V. cholerae utilizes the FeoABC operon as a system for ferrous iron transport and, although this system is widespread among bacteria, its mechanism remains largely unknown. My research in Payne’s lab is focused on the interaction between the Feo proteins and the role that they play in iron transport. Besides, I am starting to explore the Feo system through an evolutionary approach to understand how this system works in other species. In the lab, we are start using Helicobacter pylori as a secondary model organism.

Outside of lab, my favorite hobbies include cooking, swimming, and reading.


 Graduate Students


Grace Kago  


B.A. McDaniel College, Biology, 2010
When bacteria encounter environments that are stressful, they implement a global reprogramming of their genetic expression that allows them to switch their metabolism from "growth" mode to "survival" mode. For pathogenic bacteria whose function includes invading and spreading in a host, these response processes are tightly regulated especially in the context of infection. My research interests are focused on characterizing the way that Shigella spp. response to certain environments intersects with their virulence.
Outside of the lab, I can be found brainstorming ways to translate science concepts into different vernacular languages and spending time with friends and family.

Google Scholar Profile


Jennifer E. Poo  


Transformed cell lines and animal models are widely used to study enteric pathogens; however, these models do not adequately recapitulate the environment of the human intestinal epithelium. Human intestinal enteroids, on the other hand, are derived from intestinal stem cells isolated directly from patients, and can be differentiated to form the intestinal epithelium ex vivo, which provides a model for Shigella pathogenesis that mimics in vivo infections. My research focuses on how Shigella interacts with the human innate immune system using intestinal enteroids as a more biologically relevant model for disease.

Undergraduate Students

Austin D. Pham