13-04-2009, 16:29
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חבר מתאריך: 12.05.06
הודעות: 13,563
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Epithelial Cell Infection by Enteropathogenic E. coli
B. Aroeti
Department of cell and developmental biology, Institute of life science, Jerusalem, Israel
Phosphatidylinositol 4,5-bisphosphate [PI(4,5)P2] and phosphatidylinositol 3,4,5-triphosphate [PI(3,4,5)P3] are phosphoinositides (PIs) present in small amounts in the inner leaflet of the plasma membrane (PM) lipid bilayer of host target cells. They are thought to modulate the activity of proteins involved in enteropathogenic Escherichia coli (EPEC) infection. However, the role of PI(4,5)P2 and PI(3,4,5)P3 in EPEC pathogenesis remains obscure. We show that EPEC induces PI(4,5)P2 accumulation in bacterial infection sites. Simultaneous actin accumulation, likely involved in the construction of the actin-rich pedestal, is also observed in these sites. Acute PI(4,5)P2 deplition partially diminishes EPEC adherence to the cell surface and actin pedestal formation. These findings are consistent with a bimodal role, whereby PI(4,5)P2 contributes to EPEC association with the cell surface and to the maximal induction of actin pedestals. Finally, we show that EPEC induces PI(3,4,5)P3 clustering at bacterial infection sites, in a translocated intimin receptor (Tir)-dependent manner. Tir phosphorilated on tyrosine 454, but not on tyrosine 474, forms compexes with an active phophatidylinositol 3-kinase (PI3K), suggesting that PI3K recruited by Tir prompts the production of PI(3,4,5)P3 beneath EPEC attachment sites. The functional significanse of this event may be related to the ability of EPEC to modulate cell death, cell polarity and innate immunity.
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