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Infect Immun. 2012 Mar;80(3):1252-66. doi: 10.1128/IAI.06082-11. Epub 2011 Dec 12.

Identification of components of the host type IA phosphoinositide 3-kinase pathway that promote internalization of Listeria monocytogenes.

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  • 1Department of Molecular Biology and Microbiology, College of Medicine, Burnett School of Biomedical Sciences, University of Central Florida, Orlando, Florida, USA.

Abstract

The bacterial pathogen Listeria monocytogenes causes food-borne illnesses resulting in gastroenteritis, meningitis, or abortion. Listeria promotes its internalization into some human cells through binding of the bacterial surface protein InlB to the host receptor tyrosine kinase Met. The interaction of InlB with the Met receptor stimulates host signaling pathways that promote cell surface changes driving bacterial uptake. One human signaling protein that plays a critical role in Listeria entry is type IA phosphoinositide 3-kinase (PI 3-kinase). The molecular mechanism by which PI 3-kinase promotes bacterial internalization is not understood. Here we perform an RNA interference (RNAi)-based screen to identify components of the type IA PI 3-kinase pathway that control the entry of Listeria into the human cell line HeLa. The 64 genes targeted encode known upstream regulators or downstream effectors of type IA PI 3-kinase. The results of this screen indicate that at least 9 members of the PI 3-kinase pathway play important roles in Listeria uptake. These 9 human proteins include a Rab5 GTPase, several regulators of Arf or Rac1 GTPases, and the serine/threonine kinases phosphoinositide-dependent kinase 1 (PDK1), mammalian target of rapamycin (mTor), and protein kinase C-ζ. These findings represent a key first step toward understanding the mechanism by which type IA PI 3-kinase controls bacterial internalization.

PMID:
22158742
[PubMed - indexed for MEDLINE]
PMCID:
PMC3294670
Free PMC Article
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