Reference - Detail
|Author||Los FC, Kao CY, Smitham J, McDonald KL, Ha C, Peixoto CA, Aroian RV.|
|Title||RAB-5- and RAB-11-dependent vesicle-trafficking pathways are required for plasma membrane repair after attack by bacterial pore-forming toxin.|
|Journal||Cell Host Microbe|
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.
|MeSH||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*|
|WOS Category||PARASITOLOGY MICROBIOLOGY VIROLOGY|