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© Pierre Gounon
Entrée de Listeria dans une cellule épithéliale (Grossissement X 10000). Image colorisée.
Scientific Fields
Diseases
Organisms
Applications
Technique

Published in Journal of Cell Science - 15 Apr 2004

Sandra Sousa, Didier Cabanes, Aziz El-Amraoui, Christine Petit, Marc Lecuit, Pascale Cossart

Link to Pubmed [PMID] – 15090598

Link to HAL – inrae-02676456

Link to DOI – 10.1242/jcs.01066

Journal of Cell Science, 2004, 117 (Pt 10), pp.2121-2130. ⟨10.1242/jcs.01066⟩

Listeria monocytogenes is a bacterial pathogen with the capacity to invade non-phagocytic cells. This dynamic process involves coordinated membrane remodelling and actin cytoskeleton rearrangements. Although some of the molecular factors promoting these events have been identified, the driving force allowing internalization is unknown. One of the receptors for L. monocytogenes on epithelial cells is E-cadherin, a transmembrane protein normally involved in homophilic interactions that allow cell-cell contacts at the adherens junctions. E-cadherin has to be connected to the actin cytoskeleton to mediate strong cell-cell adhesion and to trigger Listeria entry; alpha- and beta-catenins play key roles in these processes. We have recently identified an unconventional myosin, myosin VIIa and its ligand vezatin, at the adherens junctions of polarized epithelial cells. Here, we demonstrate by pharmacological and genetic approaches that both myosin VIIa and vezatin are crucial for Listeria internalization. These results provide the first evidence for the role of an unconventional myosin in bacterial internalization and a novel example of the exploitation of mammalian proteins, by a pathogen, to establish a successful infection.