| Structural highlights
Function
SOPB_SALTY Converts phosphatidylinositol 3,4,5-trisphosphate (PtdIns 3,4,5-P3) to PtdIns 3-P and prevents the transition of PtdIns 3-P to PtdIns 3,5-P2. It is one of the known effectors injected by Salmonella into the host cell and is required for invasion and for an efficient generation and maintenance of Salmonella-containing vacuole (SVC). Alteration of the phosphoinositide composition of the plasma membrane causes membrane ruffling and actin cytoskeleton rearrangements. The persistence of PtdIns 3-P diverts the SCV from the endocytic pathway resulting in enlarged vesicles, which are essential to create a favorable environment where Salmonella can replicate and avoid immune defenses of the host cell.[1] [2] [3] [4]
References
- ↑ Mirold S, Ehrbar K, Weissmuller A, Prager R, Tschape H, Russmann H, Hardt WD. Salmonella host cell invasion emerged by acquisition of a mosaic of separate genetic elements, including Salmonella pathogenicity island 1 (SPI1), SPI5, and sopE2. J Bacteriol. 2001 Apr;183(7):2348-58. PMID:11244077 doi:https://dx.doi.org/10.1128/JB.183.7.2348-2358.2001
- ↑ Zhou D, Chen LM, Hernandez L, Shears SB, Galan JE. A Salmonella inositol polyphosphatase acts in conjunction with other bacterial effectors to promote host cell actin cytoskeleton rearrangements and bacterial internalization. Mol Microbiol. 2001 Jan;39(2):248-59. PMID:11136447
- ↑ Terebiznik MR, Vieira OV, Marcus SL, Slade A, Yip CM, Trimble WS, Meyer T, Finlay BB, Grinstein S. Elimination of host cell PtdIns(4,5)P(2) by bacterial SigD promotes membrane fission during invasion by Salmonella. Nat Cell Biol. 2002 Oct;4(10):766-73. PMID:12360287 doi:https://dx.doi.org/10.1038/ncb854
- ↑ Hernandez LD, Hueffer K, Wenk MR, Galan JE. Salmonella modulates vesicular traffic by altering phosphoinositide metabolism. Science. 2004 Jun 18;304(5678):1805-7. PMID:15205533 doi:https://dx.doi.org/10.1126/science.1098188
|
