@article {65694,
	title = {A post-invasion role for  type III effector TarP in modulating the dynamics and organization of host cell focal adhesions.},
	journal = {Journal of Biological Chemistry},
	volume = {295},
	year = {2020},
	month = {2020 Oct 23},
	pages = {14763-14779},
	abstract = {<p>The human pathogen targets epithelial cells lining the genital mucosa. We observed that infection of various cell types, including fibroblasts and epithelial cells resulted in the formation of unusually stable and mature focal adhesions that resisted disassembly induced by the myosin II inhibitor, blebbistatin. Super-resolution microscopy revealed in infected cells the vertical displacement of paxillin and FAK from the signaling layer of focal adhesions; while vinculin remained in its normal position within the force transduction layer. The candidate type III effector TarP which localized to focal adhesions during infection and when expressed ectopically, was sufficient to mimic both the reorganization and blebbistatin-resistant phenotypes. These effects of TarP, including its localization to focal adhesions, required a post-invasion interaction with the host protein vinculin through a specific domain at the C-terminus of TarP. This interaction is repurposed from an actin-recruiting and -remodeling complex to one that mediates nano-architectural and dynamic changes of focal adhesions. The consequence of -stabilized focal adhesions was restricted cell motility and enhanced attachment to the extracellular matrix. Thus, via a novel mechanism, inserts TarP within focal adhesions to alter their organization and stability.</p>
},
	issn = {1083-351X},
	doi = {10.1074/jbc.RA120.015219},
	author = {Pedrosa, Antonio T and Murphy, Korinn N and Nogueira, Ana T and Brinkworth, Amanda J and Thwaites, Tristan R and Aaron, Jesse and Chew, Teng-Leong and Carabeo, Rey A}
}
@article {49021,
	title = {The Chlamydia type III effector TarP alters the dynamics and organization of host focal adhesions.},
	journal = {bioRxiv},
	year = {2018},
	month = {2018 Jan 23},
	abstract = {<p>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.</p>
},
	doi = {10.1101/250563},
	author = {Pedrosa, Antonio T and Nogueira, Ana T and Thwaites, Tristan R and Aaron, Jesse and Chew, Teng-Leong and Carabeo, Rey A}
}
