Anthrax toxins cooperatively inhibit endocytic recycling by the Rab11/Sec15 exocyst

Annabel Guichard, Shauna M. McGillivray, Beatriz Cruz-Moreno, Nina M. van Sorge, Victor Nizet and Ethan Bier ()
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Annabel Guichard: Section of Cell and Developmental Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0349, USA
Shauna M. McGillivray: University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0687, USA
Beatriz Cruz-Moreno: Section of Cell and Developmental Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0349, USA
Nina M. van Sorge: University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0687, USA
Victor Nizet: University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0687, USA
Ethan Bier: Section of Cell and Developmental Biology, University of California, San Diego, 9500 Gilman Drive, La Jolla, California 92093-0349, USA

Nature, 2010, vol. 467, issue 7317, 854-858

Abstract: Mechanism of action of anthrax toxins The pathogen Bacillus anthracis secretes two potent toxins during anthrax infection, known as lethal factor (LF) and oedema factor (EF). Using transgenic Drosophila as a model system for the identification of pathways that might be involved in anthrax pathogenesis, Ethan Bier and colleagues show that these two toxins interact synergistically to block Rab11/Sec15 exocyst-dependent endocytic recycling, resulting in reduced Notch signalling and cadherin-dependent adhesion at the adherens junction. Tests in human endothelial cells indicate that the toxins have a similar effect on Rab11/Sec15 activity and Notch signalling.

Date: 2010
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DOI: 10.1038/nature09446

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