Keywords

Chlamydia trachomatis; Protein tyrosine phosphatase 1B; TepP

Abstract

Chlamydia trachomatis is well known to be reliant upon eukaryotic host cells for replication and the continuation of its developmental cycle, but many pathways it exploits in order to gain access to the eukaryotic host are still not fully understood. The bacterial type III-secreted (T3SS) translocated actin-recruiting phosphoprotein (TarP) has been extensively studied in its relationship to the rearrangement of the actin cytoskeleton of chlamydial infected cells. TarP is documented as being phosphorylated on its tyrosine residues by Src family kinases and has recently been confirmed to interact with host protein tyrosine phosphatase 1B (PTP1B) that is crucial to chlamydial growth. Another T3SS protein, translocated early-phosphoprotein (TepP), is released after TarP as another effector molecule, and has also been theorized to also follow similar Src kinase phosphorylation on its tyrosine residues, though there is less support in the literature for this claim. An investigation was designed to gain concrete evidence of TepP's phosphorylation with either Src kinase, HeLa lysate, or a mixture of the two, and to then extrapolate upon this relationship to determine whether this phosphorylation of TepP's tyrosine residues is compatible with dephosphorylation via PTP1B in a similar pathway to TarP. Both GST-tagged TepP and untagged TepP were originally confirmed with a kinase assay to be phosphorylated via Src kinase, though there were much fainter signals for phosphorylation with the HeLa lysate or HeLa and Src together, potentially indicating an agent within HeLa lysate capable of counteracting phosphorylation. GST-tagged TepP was then shown to be successfully dephosphorylated by PTP1B. These data suggest that similar to other early chlamydial effectors, the temporal phosphorylation and dephosphorylation of TepP likely plays an important role in controlling host cell signaling needed to facilitate completion of the chlamydial developmental cycle.

Thesis Completion Year

2026

Thesis Completion Semester

Spring

Thesis Chair

Jewett, Travis

College

College of Medicine

Thesis Discipline

Biomedical Sciences

Language

English

Access Status

Campus Access

Length of Campus Access

5 years

Campus Location

Orlando (Main) Campus

Restricted to the UCF community until 5-15-2031; it will then be open access.

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Rights Statement

In Copyright