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Effector Proteins Encoded by Salmonella Pathogenicity Island 2 Interfere with the Microtubule Cytoskeleton after Translocation into Host Cells
Author(s) -
Kuhle Volker,
Jäckel Daniela,
Hensel Michael
Publication year - 2004
Publication title -
traffic
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 2.677
H-Index - 130
eISSN - 1600-0854
pISSN - 1398-9219
DOI - 10.1111/j.1398-9219.2004.00179.x
Subject(s) - biology , microbiology and biotechnology , microtubule , endosome , effector , intracellular parasite , intracellular , salmonella enterica , type three secretion system , pathogenicity island , salmonella , organelle , cytoskeleton , secretion , virulence , cell , genetics , biochemistry , gene , bacteria
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 . Detailed analysis of the subcellular localization of SseF and SseG within the host cell indicated that these effector proteins are associated with endosomal membranes as well as with microtubules. Specific association with microtubules was observed after translocation by intracellular Salmonella as well as after expression by transfection vectors. In epithelial cells infected with Salmonella , both SseF and SseG are required for the aggregation of endosomal compartments along microtubules and to induce the formation of massive bundles of microtubules. These observations demonstrate that SPI2 effectors interfere with the microtubule cytoskeleton and suggest that microtubule‐dependent host cell functions such as vesicle transport or organelle positioning are altered by intracellular Salmonella .