SpiC Is Required for Translocation ofSalmonellaPathogenicity Island 2 Effectors and Secretion of Translocon Proteins SseB and SseC

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Abstract
TheSalmonellapathogenicity island 2 (SPI2) type III secretion system (TTSS) promotesSalmonella entericaserovar Typhimurium virulence for mice and increased survival and replication within eukaryotic cells. After phagocytosis,Salmonellaserovar Typhimurium assembles the SPI2 TTSS to translocate over a dozen effector proteins across the phagosome membrane. SpiC has been previously shown to be a translocated effector with a large contribution to virulence (K. Uchiya, M. A. Barbieri, K. Funato, A. H. Shah, P. D. Stahl, and E. A. Groisman, EMBO J. 18:3924-3933, 1999). This report demonstrates by competitive index that the virulence phenotype of aspiCmutant is equivalent to that of a secretion component mutant. In addition, translocation of SPI2 effector proteins was shown to require SpiC. Thus, the severe virulence phenotype resulting from deletion ofspiCis likely due to the inability to translocate all SPI2 effectors. SpiC was also required to secrete translocon proteins SseB and SseC but not translocated effector SseJ, indicating that lack of assembly of the translocon explains thespiCmutant phenotype.