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Cell Microbiol. 2002 Dec;4(12):813-24.

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

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1
Institut für Klinische Mikrobiologie, Immunologie und Hygiene, FAU Erlangen-Nürnberg, Wasserturmstr. 3-5, D-91054 Erlangen, Germany.

Abstract

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. SseF and SseG are not required for translocation of effector proteins such as SseJ, encoded by genes outside of SPI 2. Rather, both proteins are translocated and interact with phagosomal membranes after translocation. In infected epithelial cells the formation of Salmonella-induced filaments, endosomal aggregates rich in lysosomal glycoproteins, is dependent on the function of SPI 2. We observed that, in mutant strains deficient for sseF or sseG, the formation of aggregated endosomes can take place, but the composition of the structures is different from those observed in cells infected with Salmonella wild type. These observations indicate that SseF and SseG modulate the aggregation of host endosomes.

PMID:
12464012
[Indexed for MEDLINE]

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