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PMID:21320697

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Citation

Los, FC, Kao, CY, Smitham, J, McDonald, KL, Ha, C, Peixoto, CA and Aroian, RV (2011) RAB-5- and RAB-11-dependent vesicle-trafficking pathways are required for plasma membrane repair after attack by bacterial pore-forming toxin. Cell Host Microbe 9:147-57

Abstract

Pore-forming toxins (PFTs) secreted by pathogenic bacteria are the most common bacterial protein toxins and are important virulence factors for infection. PFTs punch holes in host cell plasma membranes, and although cells can counteract the resulting membrane damage, the underlying mechanisms at play remain unclear. Using Caenorhabditis elegans as a model, we demonstrate in vivo and in an intact epithelium that intestinal cells respond to PFTs by increasing levels of endocytosis, dependent upon RAB-5 and RAB-11, which are master regulators of endocytic and exocytic events. Furthermore, we find that RAB-5 and RAB-11 are required for protection against PFT and to restore integrity to the plasma membrane. One physical mechanism involved is the RAB-11-dependent expulsion of microvilli from the apical side of the intestinal epithelial cells. Specific vesicle-trafficking pathways thus protect cells against an attack by PFTs on plasma membrane integrity, via altered plasma membrane dynamics.

Links

PubMed PMC3057397 Online version:10.1016/j.chom.2011.01.005

Keywords

Animals; Bacteria/metabolism; Bacterial Physiological Phenomena; Bacterial Toxins/metabolism; Caenorhabditis elegans/genetics; Caenorhabditis elegans/metabolism; Caenorhabditis elegans/microbiology; Caenorhabditis elegans Proteins/genetics; Caenorhabditis elegans Proteins/metabolism; Cell Membrane/genetics; Cell Membrane/metabolism; Cell Membrane/microbiology; Cytoplasmic Vesicles/genetics; Cytoplasmic Vesicles/metabolism; Endocytosis; Epithelial Cells/metabolism; Epithelial Cells/microbiology; Vesicular Transport Proteins/genetics; Vesicular Transport Proteins/metabolism

Significance

Annotations

Gene product Qualifier GO Term Evidence Code with/from Aspect Extension Notes Status


See also

References

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