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  • The EMBO Journal (2005) 24, 1287 - 1300
  • doi:10.1038/sj.emboj.7600595

Published online: 24 February 2005

Listeria monocytogenes exploits ERM protein functions to efficiently spread from cell to cell

Sascha Pust1,4,a, Helen Morrison2,3,a, Jürgen Wehland1, Antonio S Sechi1,5 and Peter Herrlich2,3

  1. Department of Cell Biology, Gesellschaft für Biotechnologische Forschung (GBF), Braunschweig, Germany
  2. Forschungszentrum Karlsruhe, Institute of Toxicology and Genetics, Karlsruhe, Germany
  3. Institute of Molecular Biotechnology, Jena, Germany
  4. Present address: Albert-Ludwigs Universität Freiburg, Institut für Experimentelle und Klinische Pharmakologie und Toxikologie I, Albertstras zlige 25, 79104 Freiburg, Germany
  5. Present address: Institut für Biomedizinische Technologien—Zellbiologie, Universitätsklinikum Aachen, Rheinisch-Westfälische Technische Hochschule (RWTH), Pauwelsstrasse 30, 52057 Aachen, Germany

Correspondence to:

Antonio S Sechi, Department of Cell Biology, Gesellschaft für Biotechnologische Forschung (GBF), Mascheroder Weg 1, 38124 Braunschweig, Germany. Tel.: +49 531 6181241; Fax: +49 531 6181444; E-mail: antonio.sechi@rwth-aachen.de

aThese two authors contributed equally to this work

Received 31 August 2004; Accepted 2 February 2005

Cell-to-cell spread is a fundamental step in the infection cycle of Listeria monocytogenes that strictly depends on the formation of bacteria-induced protrusions. Since Listeria actin tails in the protrusions are tightly associated with the plasma membrane, we hypothesised that membrane–cytoskeleton linkers would be required for initiating and sustaining their formation and the subsequent cell-to-cell spread. We have found that ezrin, a member of the ezrin, radixin and moesin (ERM) family that functions as a key membrane–cytoskeleton linker, accumulates at Listeria protrusions. The ability of Listeria to induce protrusions and effectively spread between adjacent cells depends on the interaction of ERM proteins with both a membrane component such as CD44 and actin filaments. Interfering with either of these interactions or with ERM proteins phosphorylation not only reduces the number of protrusions but also alters their morphology, resulting in the formation of short and collapsed protrusions. As a consequence, Listeria cell-to-cell spread is severely impaired. Thus, ERM proteins are exploited by Listeria to escape the host immune response and to succeed in the development of the infection.

  • Keywords:

    • actin cytoskeleton,
    • ERM proteins,
    • infection,
    • Listeria monocytogenes,
    • protrusion