Intermediate filaments enable pathogen docking to trigger type 3 effector translocation
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Author
Stamm, Luisa M.
Raaben, Matthijs
Kim, Caleb M.
Kahoud, Emily
Queiroz, Ana L.
Herrera, Bobby Brooke
Mor-Vaknin, Nirit
Markovitz, David M.
Note: Order does not necessarily reflect citation order of authors.
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https://doi.org/10.1038/nmicrobiol.2016.25Metadata
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Russo, B. C., L. M. Stamm, M. Raaben, C. M. Kim, E. Kahoud, L. R. Robinson, S. Bose, et al. 2016. “Intermediate filaments enable pathogen docking to trigger type 3 effector translocation.” Nature microbiology 1 (1): 16025. doi:10.1038/nmicrobiol.2016.25. http://dx.doi.org/10.1038/nmicrobiol.2016.25.Abstract
Type 3 secretion systems (T3SSs) of bacterial pathogens translocate bacterial effector proteins that mediate disease into the eukaryotic cytosol. Effectors traverse the plasma membrane through a translocon pore formed by T3SS proteins. In a genome-wide selection, we identified the intermediate filament vimentin as required for infection by the T3SS-dependent pathogen Shigella flexneri. We found that vimentin is required for efficient T3SS translocation of effectors by S. flexneri and other pathogens that use T3SS, Salmonella Typhimurium and Yersinia pseudotuberculosis. Vimentin and the intestinal epithelial intermediate filament keratin 18 interact with the C-terminus of the Shigella translocon pore protein IpaC. Vimentin and its interaction with IpaC are dispensable for pore formation, but are required for stable docking of S. flexneri to cells; moreover, stable docking triggers effector secretion. These findings establish that stable docking of the bacterium specifically requires intermediate filaments, is a process distinct from pore formation, and is a prerequisite for effector secretion.Other Sources
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC5006386/pdf/Terms of Use
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