SseA is required for translocation of Salmonella pathogenicity island-2 effectors into host cells

Microbes and Infection
Brian K CoombesB Brett Finlay

Abstract

The Salmonella pathogenicity island-2 (SPI2) is a virulence locus on the bacterial chromosome required for intracellular proliferation and systemic infection in mice. Cell culture models and a murine model of systemic infection were used to address the role of an uncharacterized SPI2 open reading frame, designated as sseA, in Salmonella virulence. A Salmonella strain with an unmarked internal deletion of sseA displayed a phenotype that was similar to an SPI2-encoded type III secretion system apparatus mutant. Moreover, SseA was required for survival and replication within epithelial cells and macrophages. Murine infection studies confirmed that the DeltasseA strain was severely attenuated for virulence. Using immunofluorescence microscopy, the virulence defect in the DeltasseA strain was attributed to an inability to translocate SPI2 effector proteins into host cells. These data demonstrate that SseA is essential for SPI2-mediated translocation of effector proteins.

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Citations

Aug 24, 2004·Infection and Immunity·Sonya L Kujat ChoyB Brett Finlay
Jul 21, 2004·Journal of Bacteriology·Shipan Dai, Daoguo Zhou
Nov 22, 2005·PLoS Genetics·William W L HsiaoFiona S L Brinkman
Nov 23, 2005·Proceedings of the National Academy of Sciences of the United States of America·Brian K CoombesB Brett Finlay
Jun 14, 2005·Molecular Microbiology·Jetta J E Bijlsma, Eduardo A Groisman
Apr 15, 2016·Proceedings of the National Academy of Sciences of the United States of America·Juan DuCammie F Lesser
Jul 19, 2014·The Journal of Biological Chemistry·Sarah E AllisonBrian K Coombes
Mar 24, 2017·Nucleic Acids Research·Michael J EllisDavid B Haniford

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