Mahurin Honors College Capstone Experience/Thesis Projects



Additional Departmental Affiliation


Document Type



Legionella pneumophila an intracellular, opportunistic pathogen that is the causative agent of Legionnaires’ disease and Pontiac fever. A key component of Legionella’s pathogenicity is a series of effector proteins, which aid in the establishment of the Legionella-containing vacuole (LCV). The abundant library of effector proteins L. pneumophila has within its arsenal gives L. pneumophila the ability to infect several different hosts. The pathogenesis of L. pneumophila within various hosts depends on its ability to modulate the activity of its effector proteins through protein-protein interactions within effectors and eukaryotic host cell proteins. By understanding how L. pneumophila regulates its effectors, a better understanding of L. pneumophila’s pathogenicity in humans can be established. Meta-effectors are effectors that regulate the activity of other effectors. To be classified as a meta-effector, an effector protein must bind to and regulate other effector proteins. The Banga lab discovered that several effector proteins migrated to the nucleus of the cell. Due to their migration, we hypothesized that these effectors may be regulating each other’s function. In this study, the effectors RavQ, RavO, Ceg10, MavA, LegAS4, LneA, and LneB were tested for protein-protein interactions to analyze potential meta-effector pairings by utilizing the bacterial adenylate cyclase two-hybrid system. Our results did not show any interactions within these effectors and suggest that none of the effectors tested may regulate each other. However, these findings are limited by the experimental constraints of the bacterial two-hybrid system.

Advisor(s) or Committee Chair

Simran Banga, Ph.D.


Biology | Microbiology | Molecular Biology

Available for download on Thursday, June 26, 2025