Intracellular Salmonella enterica redirect exocytic transport processes in a Salmonella pathogenicity island 2-dependent manner.

During intracellular life, Salmonella enterica proliferate within a specialized membrane compartment, the Salmonella-containing vacuole (SCV), and interfere with the microtubule cytoskeleton and cellular transport. To characterize the interaction of intracellular Salmonella with host cell transport processes, we utilized various model systems to follow microtubule-dependent transport. The vesicular stomatitis virus glycoprotein (VSVG) is a commonly used marker to follow protein transport from the Golgi to the plasma membrane.

The Shiga toxin 1-converting bacteriophage BP-4795 encodes an NleA-like type III effector protein.

In this study, the complete DNA sequence of Shiga toxin 1-converting bacteriophage BP-4795 was determined. The genome of BP-4795 consists of 85 open reading frames, including two complete IS629 elements and three morons at the end of its late regulatory region. One of these morons encodes a type III effector that is translocated by the locus of enterocyte effacement-encoded type III secretion system into HeLa cells, where it localizes with the Golgi apparatus.

Effector proteins encoded by Salmonella pathogenicity island 2 interfere with the microtubule cytoskeleton after translocation into host cells.

The facultative intracellular pathogen Salmonella enterica has evolved strategies to modify its fate inside host cells. One key virulence factor for the intracellular pathogenesis is the type III secretion system encoded by Salmonella Pathogenicity Island 2 (SPI2). We have previously described SPI2-encoded SseF and SseG as effector proteins that are translocated by intracellular Salmonella.

SseF and SseG are translocated effectors of the type III secretion system of Salmonella pathogenicity island 2 that modulate aggregation of endosomal compartments.

The type III secretion system encoded by Salmonella pathogenicity island 2 (SPI 2) is important for intracellular proliferation in infected host cells. Intracellular Salmonella use this system to translocate a set of effector proteins into the host cell. We studied the role of SseF and SseG, two SPI 2-encoded proteins.

SpiC is required for translocation of Salmonella pathogenicity island 2 effectors and secretion of translocon proteins SseB and SseC.

The Salmonella pathogenicity island 2 (SPI2) type III secretion system (TTSS) promotes Salmonella enterica serovar Typhimurium virulence for mice and increased survival and replication within eukaryotic cells. After phagocytosis, Salmonella serovar 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.