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Main Menu - Block
- Overview
- Anatomy and Histology
- Cryo-Electron Microscopy
- Electron Microscopy
- Flow Cytometry
- Gene Targeting and Transgenics
- Immortalized Cell Line Culture
- Integrative Imaging
- Invertebrate Shared Resource
- Janelia Experimental Technology
- Mass Spectrometry
- Media Prep
- Molecular Genomics
- Primary & iPS Cell Culture
- Project Pipeline Support
- Project Technical Resources
- Quantitative Genomics
- Scientific Computing Software
- Scientific Computing Systems
- Viral Tools
- Vivarium
Abstract
Bacterial infection of mucosal epithelial cells triggers cell exfoliation to limit the dissemination of infection within the tissue. Therefore, mucosal pathogens must possess strategies to counteract cell extrusion in response to infection. Chlamydia trachomatis spends most of its intracellular development in the non-infectious form. Thus, premature host cell extrusion is detrimental to the pathogen. We demonstrate that C. trachomatis alters the dynamics of focal adhesions. Live-cell microscopy showed that focal adhesions in C. trachomatis-infected cells displayed increased stability. In contrast, focal adhesions in mock-infected cells readily disassembled upon inhibition of myosin II by blebbisttin. Super-resolution microscopy revealed a reorganization of paxillin and FAK in infected cells. Ectopically expressed type III effector TarP localized to focal adhesions, leading to their stabilization and reorganization in a vinculin-dependent manner. Overall, the results indicate that C. trachomatis possesses a dedicated mechanism to regulate host cell focal adhesion dynamics.
