A Role for Phosphoinositide 3-Kinase in Bacterial Invasion

Listeria monocytogenes is a bacterial pathogen that invades cultured nonphagocytic cells. Inhibitors and a dominant negative mutation were used to demonstrate that efficient entry requires the phosphoinositide (PI) 3-kinase p85α-p110. Infection with L. monocytogenes caused rapid increases in cellular amounts of PI(3,4)P2 and PI(3,4,5)P3, indicating that invading bacteria stimulated PI 3-kinase activity. This stimulation required the bacterial protein InlB, host cell tyrosine phosphorylation, and association of p85α with one or more tyrosine-phosphorylated proteins. This role for PI 3-kinase in bacterial entry may have parallels in some endocytic events.

[1]  David Baltimore,et al.  An Essential Role for NF-κB in Preventing TNF-α-Induced Cell Death , 1996, Science.

[2]  P. Cossart,et al.  E-Cadherin Is the Receptor for Internalin, a Surface Protein Required for Entry of L. monocytogenes into Epithelial Cells , 1996, Cell.

[3]  Barbara J. Reaves,et al.  Phosphoinositide 3-kinases and membrane traffic. , 1996, Trends in cell biology.

[4]  P. Cossart,et al.  Molecular and genetic determinants involved in invasion of mammalian cells by Listeria monocytogenes. , 1996, Current topics in microbiology and immunology.

[5]  L. Cantley,et al.  Phosphatidylinositol (3,4,5)P3 interacts with SH2 domains and modulates PI 3-kinase association with tyrosine-phosphorylated proteins , 1995, Cell.

[6]  O. Hazeki,et al.  Wortmannin as a unique probe for an intracellular signalling protein, phosphoinositide 3-kinase. , 1995, Trends in biochemical sciences.

[7]  B. Payrastre,et al.  Integrin-dependent translocation of phosphoinositide 3-kinase to the cytoskeleton of thrombin-activated platelets involves specific interactions of p85 alpha with actin filaments and focal adhesion kinase , 1995, The Journal of cell biology.

[8]  P. Cossart,et al.  Entry of Listeria monocytogenes into hepatocytes requires expression of InIB, a surface protein of the internalin multigene family , 1995, Molecular microbiology.

[9]  T. Kitamura,et al.  1-Phosphatidylinositol 3-kinase activity is required for insulin-stimulated glucose transport but not for RAS activation in CHO cells. , 1994, Proceedings of the National Academy of Sciences of the United States of America.

[10]  B. Finlay,et al.  Listeria monocytogenes, an invasive bacterium, stimulates MAP kinase upon attachment to epithelial cells. , 1994, Molecular biology of the cell.

[11]  K Y Hui,et al.  A specific inhibitor of phosphatidylinositol 3-kinase, 2-(4-morpholinyl)-8-phenyl-4H-1-benzopyran-4-one (LY294002). , 1994, The Journal of biological chemistry.

[12]  K. Hara.  Phosphoinositide 3-kinase activity is required for insulin-stimulated glucose transport but not for ras activation in CHO cells , 1994 .

[13]  I. Campbell,et al.  The GTPase dynamin binds to and is activated by a subset of SH3 domains , 1993, Cell.

[14]  P. Cossart,et al.  Entry of L. monocytogenes into cells is mediated by internalin, a repeat protein reminiscent of surface antigens from gram-positive cocci , 1991, Cell.

[15]  M. Hansen,et al.  Re-examination and further development of a precise and rapid dye method for measuring cell growth/cell kill. , 1989, Journal of immunological methods.