UCSF

Like any successful intracellular pathogen, Chlamydia trachomatis must overcome several host defenses to complete its developmental cycle. Chlamydia is thought to accomplish this through the employment of effector proteins, particularly a unique class of effectors which are inserted in the Chlamydial inclusion membrane. To test the hypothesis that these inclusion membrane proteins (Incs) target host cell proteins, our lab conducted an affinity purification-mass spectrometry screen (AP-MS) in which cells were transfected with individually tagged Incs. The predicted interaction between the Inc Tri1 and the host ubiquitin ligase TRAF7 is the subject of this work.In this dissertation, we characterize the Tri:TRAF7 complex during infection and reveal that Tri1 can disrupt native TRAF7 protein-protein interactions (PPIs, Chapter 2). Through additional analysis of this TRAF7 interactome dataset, we revealed that Tri1 can also promote novel TRAF7 PPIs (Chapter 3). Finally, we conducted RNAseq analysis to determine the role of Tri1 during infection and determined that it may play a modest role in altering signaling pathways. Overall, this work contributes to the growing literature on C. trachomatis Incs and highlights the important roles they may play during infection.