Final Abstract for URS Program
Salmonella is a well-known pathogen that is linked to food born illnesses common around the world. This pathogen can cause symptoms such as fever, diarrhea, and chills in the host. One of the mechanisms Salmonella uses to infect its host’s epithelial cells deals with the S. typhimurium pathogenicity island 1 (SPI-1). Expression of SPI-1 is activated in response to environmental signals that correlate with the ileum of the small intestine (low oxygen, high osmolarity, and neutral pH). HilA is the central activator of the SPI-1 complex, and when the transcription factor, MarA, is over-expressed in Salmonella, hilA transcription is repressed. It seems, though, that MarA does not directly cause hilA repression, and the proteins and/or other components that MarA interacts with to aid in repression of hilA are unknown. Here, I show several gene candidates that possibly interact with MarA and how I found them. These candidates include narP, csgA, and nfi. Through transposon mutagenesis, we were able to sequence different portions of the Salmonella genome that were interrupted in several different mutants. These sequences were then compared to the known genes in the Salmonella genome using the National Center for Biotechnology Information database. These results bring us a step closer to narrowing down a possible gene that is responsible for interacting with and aiding MarA-dependent in repression of hilA. These findings open a whole new horizon of possibilities in testing how different conditions and different drugs can target these multiple pieces to the puzzle that is Salmonella pathogenesis and antibiotic resistance.