cAMP signaling by anthrax edema toxin induces transendothelial cell tunnels, which are resealed by MIM via Arp2/3-driven actin polymerization

RhoA-inhibitory bacterial toxins, such as Staphylococcus aureus EDIN toxin, induce large transendothelial cell macroaperture (TEM) tunnels that rupture the host endothelium barrier and promote bacterial dissemination. Host cells repair these tunnels by extending actin-rich membrane waves from the TE...

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Veröffentlicht in:Cell host & microbe Jg. 10; H. 5; S. 464
Hauptverfasser: Maddugoda, Madhavi P, Stefani, Caroline, Gonzalez-Rodriguez, David, Saarikangas, Juha, Torrino, Stéphanie, Janel, Sebastien, Munro, Patrick, Doye, Anne, Prodon, François, Aurrand-Lions, Michel, Goossens, Pierre L, Lafont, Frank, Bassereau, Patricia, Lappalainen, Pekka, Brochard, Françoise, Lemichez, Emmanuel
Format: Journal Article
Sprache:Englisch
Veröffentlicht: United States 17.11.2011
Schlagworte:
Actin-Related Protein 2-3 Complex - chemistry
Actin-Related Protein 2-3 Complex - genetics
Actin-Related Protein 2-3 Complex - metabolism
Animals
Anthrax - metabolism
Anthrax - microbiology
Antigens, Bacterial - metabolism
Bacillus anthracis - genetics
Bacillus anthracis - metabolism
Bacterial Toxins - metabolism
Cyclic AMP - metabolism
Human Umbilical Vein Endothelial Cells - metabolism
Human Umbilical Vein Endothelial Cells - microbiology
Humans
Mice
Mice, Inbred BALB C
Microfilament Proteins - genetics
Microfilament Proteins - metabolism
Neoplasm Proteins - genetics
Neoplasm Proteins - metabolism
Polymerization
Signal Transduction
ISSN:1934-6069, 1934-6069
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Zusammenfassung:RhoA-inhibitory bacterial toxins, such as Staphylococcus aureus EDIN toxin, induce large transendothelial cell macroaperture (TEM) tunnels that rupture the host endothelium barrier and promote bacterial dissemination. Host cells repair these tunnels by extending actin-rich membrane waves from the TEM edges. We reveal that cyclic-AMP signaling produced by Bacillus anthracis edema toxin (ET) also induces TEM formation, which correlates with increased vascular permeability. We show that ET-induced TEM formation resembles liquid dewetting, a physical process of nucleation and growth of holes within a thin liquid film. We also identify the cellular mechanisms of tunnel closure and reveal that the I-BAR domain protein Missing in Metastasis (MIM) senses de novo membrane curvature generated by the TEM, accumulates at the TEM edge, and triggers Arp2/3-dependent actin polymerization, which induces actin-rich membrane waves that close the TEM. Thus, the balance between ET-induced TEM formation and resealing likely determines the integrity of the host endothelium barrier.
Bibliographie:ObjectType-Article-1
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ISSN:1934-6069
1934-6069
DOI:10.1016/j.chom.2011.09.014