Keywords

Chlamydia TARP Drosophila Apoptosis Effector

Subject Categories

Cell Biology | Microbiology

Abstract

As the most prevalent bacterial STI in the United States and leading cause of infection-related blindness worldwide, the obligate intracellular bacteria, Chlamydia trachomatis (Ct), poses a significant threat to public health. As an obligate intracellular bacteria, invasion of the host cell is a crucial step in Chlamydia’s developmental cycle. To drive invasion, Ct injects prepackaged effectors into the host cell using a T3SS. An early Chlamydial effector, translocated actin recruiting phosphoprotein, or Tarp, interacts with host cell actin to promote invasion, mediated via Tarp’s C-terminal region. Although the function of Tarp’s C-terminus is well defined, the Tarp’s N-terminus (N-Tarp) is relatively uncharacterized. Here, we utilize Drosophila melanogaster as an in vivo cell biology platform to study N-Tarp’s function. Using this method, we discovered that the N-terminal region of Tarp has a novel function – altering host Hippo signaling. The Hippo pathway is a conserved signaling pathway that controls cell proliferation and survival. Interestingly, it has been observed that Chlamydia infected cells are resistant to apoptotic stimuli, though the mechanism remains unclear. We hypothesize that Chlamydia promotes host cell survival via the influence of the N-terminal region of Tarp on Hippo signaling. We found that expression of N-Tarp upregulated Hippo pathway target Diap1, but not CycE. We successfully created a Drosophila model of induced cell death; however, expression of N-Tarp was unable to alleviate the pro-apoptotic phenotype. Additionally, we successfully created a SBP-tagged N-Tarp Drosophila S2 cell line and performed a pull-down assay to isolate and analyze N-Tarp protein interacting partners. Finally, the overgrowth phenotype observed upon expression of N-Tarp is not caused by the interaction of N-Tarp and adaptor protein dSHC, an interaction previously described as anti-apoptotic.  Collectively, our findings further characterize N-Tarp’s molecular interactions. The mechanism of N-Tarp’s anti-apoptotic role remains to be elucidated.

Completion Date

2026

Semester

Summer

Committee Chair

Aranjuez, George

Degree

Master of Science (M.S.)

College

College of Medicine

Format

PDF

Document Type

Thesis

Language

English

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