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A surprising sweetener from enteropathogenic Escherichia coli
Jaclyn S Pearson1, Elizabeth L Hartland
1a Department of Microbiology and Immunology ; University of Melbourne at the Peter Doherty Institute for Infection and Immunity ; Melbourne , Australia.
Gut Microbes
|December 24, 2014
Summary
Enteropathogenic Escherichia coli (EPEC) uses a unique mechanism to prevent gut inflammation. The type III secretion system (T3SS) effector NleB attaches N-acetylglucosamine to arginine, blocking cell death and promoting bacterial attachment.
Area of Science:
- Microbiology
- Cell Biology
- Pathogen-Host Interactions
Background:
- Enteropathogenic Escherichia coli (EPEC) infections cause minimal gut inflammation compared to invasive pathogens.
- EPEC utilizes the type III secretion system (T3SS) to deliver effector proteins into host cells.
- Cell death pathways are crucial in host defense against bacterial infections.
Purpose of the Study:
- To investigate the mechanism by which EPEC blocks host cell death.
- To elucidate the role of the T3SS effector NleB in preventing inflammation and damage.
- To characterize the novel post-translational modification mediated by NleB.
Main Methods:
- Investigated the function of the T3SS effector NleB in EPEC infections.
- Analyzed the post-translational modification of death domain-containing adaptor proteins.
- Utilized biochemical assays to define the N-acetylglucosamine (GlcNAc) attachment to arginine.
Main Results:
- EPEC's NleB effector prevents host cell death by modifying adaptor proteins.
- NleB covalently attaches N-acetylglucosamine (GlcNAc) to a conserved arginine in death domains.
- This arginine modification, a novel N-linked glycosylation of arginine, inhibits apoptosis and promotes enterocyte survival.
Conclusions:
- NleB-mediated arginine glycosylation is a key virulence mechanism for EPEC.
- Blocking host cell death allows for prolonged bacterial attachment and colonization of the gut epithelium.
- This finding reveals a previously unreported modification in mammalian cell biology with significant implications for understanding host-pathogen interactions.
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