TY - JOUR
T1 - Type II phosphatidylinositol 4-kinases promote Listeria monocytogenes entry into target cells
AU - Pizarro-Cerdá, Javier
AU - Payrastre, Bernard
AU - Wang, Ying Jie
AU - Veiga, Esteban
AU - Yin, Helen L.
AU - Cossart, Pascale
N1 - Copyright:
Copyright 2008 Elsevier B.V., All rights reserved.
PY - 2007/10
Y1 - 2007/10
N2 - Interaction of the Listeria surface protein InlB with the hepatocyte growth factor receptor Met activates signalling events that trigger bacterial internalization into mammalian epithelial cells. We show here that purified phagosomes containing InlB-coated beads display type II phosphatidylinositol 4-kinase (PI4K) activity. In human epithelial HeLa cells, both PI4KIIα and PI4KIIβ isoforms are corecruited with Met around InlB-coated beads or wild-type Listeria during the early steps of internalization, and phosphatidylinositol 4-phosphate [PI(4)P]is detected at the entry site. We demonstrate that PI4KIIα or PI4KIIβ knockdown, but not type III PI4Kβ knockdown, inhibits Listeria internalization. Production of PI(4)P derivatives such as phosphatidylinositol 3,4,5-triphosphate [PI(3,4,5)P3]upon InlB stimulation is not affected by PI4KIIα or β knockdown, suggesting that these phosphoinositides are generated by a type III PI4K. Strikingly, knockdown of the PI(4)P ligand and clathrin adaptor AP-1 strongly inhibits bacterial entry. Together, our results reveal a yet non-described role for type II PI4Ks in phagocytosis.
AB - Interaction of the Listeria surface protein InlB with the hepatocyte growth factor receptor Met activates signalling events that trigger bacterial internalization into mammalian epithelial cells. We show here that purified phagosomes containing InlB-coated beads display type II phosphatidylinositol 4-kinase (PI4K) activity. In human epithelial HeLa cells, both PI4KIIα and PI4KIIβ isoforms are corecruited with Met around InlB-coated beads or wild-type Listeria during the early steps of internalization, and phosphatidylinositol 4-phosphate [PI(4)P]is detected at the entry site. We demonstrate that PI4KIIα or PI4KIIβ knockdown, but not type III PI4Kβ knockdown, inhibits Listeria internalization. Production of PI(4)P derivatives such as phosphatidylinositol 3,4,5-triphosphate [PI(3,4,5)P3]upon InlB stimulation is not affected by PI4KIIα or β knockdown, suggesting that these phosphoinositides are generated by a type III PI4K. Strikingly, knockdown of the PI(4)P ligand and clathrin adaptor AP-1 strongly inhibits bacterial entry. Together, our results reveal a yet non-described role for type II PI4Ks in phagocytosis.
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U2 - 10.1111/j.1462-5822.2007.00967.x
DO - 10.1111/j.1462-5822.2007.00967.x
M3 - Article
C2 - 17555516
AN - SCOPUS:34548444206
SN - 1462-5814
VL - 9
SP - 2381
EP - 2390
JO - Cellular Microbiology
JF - Cellular Microbiology
IS - 10
ER -