Department of Microbiology and Physiological Systems
Immunology and Infectious Disease | Microbiology
Salmonella enterica Typhimurium employs type III secreted effectors to induce cellular invasion and pathogenesis. We previously reported the secreted effector SipA is in part responsible for inducing the apical accumulation of the host membrane protein PERP, a host factor we have shown is key to the inflammatory response induced by Salmonella. We now report that the S. Typhimurium type III secreted effector SipC significantly contributes to PERP redistribution to the apical membrane surface. To our knowledge, this is the first report demonstrating a role for SipC in directing the trafficking of a host membrane protein to the cell surface. In sum, facilitation of PERP trafficking appears to be a result of type III secreted effector-mediated recruitment of vesicles to the apical surface. Our study therefore reveals a new role for SipC, and builds upon previous reports suggesting recruitment of vesicles to the cell surface is important for Salmonella invasion.
Salmonella, host pathogen interactions, inflammation, trafficking, type III secretion
Rights and Permissions
© 2016 Kelly N. Hallstrom and Beth A. McCormick.
DOI of Published Version
Gut Microbes. 2016;7(2):136-45. doi: 10.1080/19490976.2015.1128626. Link to article on publisher's site
Hallstrom KN, McCormick BA. (2016). The type three secreted effector SipC regulates the trafficking of PERP during Salmonella infection. Morningside Graduate School of Biomedical Sciences Student Publications. https://doi.org/10.1080/19490976.2015.1128626. Retrieved from https://escholarship.umassmed.edu/gsbs_sp/2030