Salmonella species are responsible for causing typhoid fever and other diseases in humans. Because Salmonella species are responsible for causing a variety of illnesses, it is important to determine the underlying mechanism behind their virulence. In order to successfully invade the host, Salmonella use two type three secretion systems to inject bacterial effector proteins into the host cell. These effector proteins are responsible for a variety of functions during infection including: hijacking the host cell machiner to allow for bacterial uptake and formation and maintenance of an intracellular niche that allows for bacterial replication within the host cell. While some effector proteins have been well characterized, the role of most effector proteins in promoting Salmonella infection is still unknown. The goal of this project is to characterize a particular effector protein called SteA, which has been shown to be important for increased Salmonella virulence but its actual mechanism is unknown. This proposal has three specific aims examining: 1) the role of SteA in the Salmonella infection process, 2) the role SteA plays in altering host cell physiology during Salmonella infection, and 3) the host cell proteins SteA interacts with to accomplish its role.
Aims 1 and 2 will be completed using fluorescence microscopy and Aim 3 will be completed using immunoprecipitation and mass spectrometry. Completion of these aims will aid in understanding how SteA causes increased virulence in Salmonella infection and provide new insight on healthy cell biology.
Salmonella species are responsible for causing a variety of diseases, ranging from typhoid fever to enteritis. This goal of this project is to study certain Salmonella proteins in the context of the cell biology of Salmonella infection in order to better understand the mechanism behind these diseases. Once we understand the mechanism of Salmonella infection, we can develop better antibiotics to target Salmonella and prevent the devastating effects caused by these diseases.