Nexilin is a dynamic component of Listeria monocytogenes and enteropathogenic Escherichia coli actin-rich structures

Authors

  • H. T. Law,

    1. Simon Fraser University, Department of Biological Sciences, Shrum Science Centre, Room B8276, Burnaby, BC, V5A 1S6, Canada.
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    • These authors contributed equally to this work.

  • Matteo Bonazzi,

    1. Institut Pasteur, Unité des Interactions Bactéries-Cellules, Paris F-75015, France.
    2. INSERM, U604, Paris F-75015, France.
    3. INRA, USC2020, Paris F-75015, France.
    4. CPBS – UMR 5236/CNRS – UM1/UM21919 route de Mende 34 293 MONTPELLIER, France, Cedex 5.
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    • These authors contributed equally to this work.

  • Jeremy Jackson,

    1. Simon Fraser University, Department of Biological Sciences, Shrum Science Centre, Room B8276, Burnaby, BC, V5A 1S6, Canada.
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  • Pascale Cossart,

    1. Institut Pasteur, Unité des Interactions Bactéries-Cellules, Paris F-75015, France.
    2. INSERM, U604, Paris F-75015, France.
    3. INRA, USC2020, Paris F-75015, France.
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  • Julian Andrew Guttman

    Corresponding author
    1. Simon Fraser University, Department of Biological Sciences, Shrum Science Centre, Room B8276, Burnaby, BC, V5A 1S6, Canada.
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E-mail jguttman@sfu.ca; Tel. (+1) 778 782 4459; Fax (+1) 778 782 3496.

Summary

The bacterial pathogens Listeria monocytogenes and enteropathogenic Escherichia coli (EPEC) generate motile actin-rich structures (comet tails and pedestals) as part of their infectious processes. Nexilin, an actin-associated protein and a component of focal adhesions, has been suggested to be involved in actin-based motility. To determine whether nexilin is commandeered during L. monocytogenes and EPEC infections, we infected cultured cells and found that nexilin is crucial for L. monocytogenes invasion as levels of internalized bacteria were significantly decreased in nexilin-targeted siRNA-treated cells. In addition, nexilin is a component of the machinery that drives the formation of L. monocytogenes comet tails and EPEC pedestals. Nexilin colocalizes with stationary bacteria and accumulates at the distal portion of comet tails and pedestals of motile bacteria. We also show that nexilin is crucial for efficient comet tail formation as cells pre-treated with nexilin siRNA generate malformed comet tails, whereas nexilin is dispensable during EPEC pedestal generation. These findings demonstrate that nexilin is required for efficient infection with invasive and adherent bacteria and is key to the actin-rich structures these microbes generate.

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