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16. Control of epithelial cell structure and developmental fate: lessons from Helicobacter pylori.

Author

Mimuro H, Berg DE, and Sasakawa C

Subjects
Adhesins, Bacterial physiology, Antigens, Bacterial physiology, Bacterial Adhesion physiology, Bacterial Proteins physiology, Cell Polarity, Epithelial Cells metabolism, Epithelial Cells microbiology, Epithelial Cells pathology, Gastric Mucosa metabolism, Gastric Mucosa microbiology, Gastric Mucosa pathology, Gastritis etiology, Helicobacter Infections etiology, Helicobacter pylori physiology, Humans, Integrins metabolism, Models, Biological, Phosphorylation, Signal Transduction, Virulence physiology, Helicobacter pylori pathogenicity, Host-Pathogen Interactions physiology
Abstract

Valuable insights into eukaryotic regulatory circuits can emerge from studying interactions of bacterial pathogens such as Helicobacter pylori with host tissues. H. pylori uses a type IV secretion system (T4SS) to deliver its CagA virulence protein to epithelial cells, where much of it becomes phosphorylated. CagA's phosphorylated and non-phosphorylated forms each interact with host regulatory proteins to alter cell structure and cell fate. Kwok and colleagues showed that CagA destined for phosphorylation is delivered using host integrin as receptor and H. pylori's CagL protein as an integrin-specific adhesin, and that CagL-integrin-binding activates the kinase cascade responsible for CagA phosphorylation. This research contributes to understanding infectious disease and the control of cell fates.

Published
2008
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