University of Wisconsin – Madison (Sept. 2015 – Current)
Graduate student in the Chemistry Ph.D. program
University of Minnesota - Twin Cities (Sept. 2011- Dec. 2014)
BS in Chemistry and a minor in Biochemistry
Many common bacterial pathogens use chemical signals to coordinate group behaviors. In the canonical quorum sensing (QS) system of V. fischeri, a synthase, LuxI, produces an N-acyl homoserine lactone (AHL) that is recognized by a receptor, LuxR, at high signal density. LuxR is a transcription factor that regulates bioluminescence and other group behaviors at high population density in an AHL dependent manner. SdiA is a LuxR homolog found in Escherichia coli and Salmonella enterica serovar typhimurium. SdiA does not have a corresponding synthase, however, and these species do not produce AHL signals. SdiA does not respond to population density, but rather has been shown to respond to AHLs produced by other bacterial species in its environment. SdiA regulates many aspects of pathogenesis including directing the location of the infection, survival in the mammalian digestive system, and the production of virulence factors. Accordingly, modulation of SdiA activity might be a useful anti-virulence strategy. I am working to identify and characterize the structure-activity-relationships (SAR) of potent agonists and antagonists of SdiA in E. coli and S. typhimurium and determine the molecular mechanisms of ligand mediated SdiA activity.