Listeria Monocytogenes Exploits Host Caveolin for Cell-to-Cell Spreading

Resource type
Date created
2020-01-21
Authors/Contributors
Abstract
Listeria monocytogenes moves from one cell to another using actin-rich membrane protrusions that propel the bacterium toward neighboring cells. Despite cholesterol being required for this transfer process, the precise host internalization mechanism remains elusive. Here, we show that caveolin endocytosis is key to this event as bacterial cell-to-cell transfer is severely impaired when cells are depleted of caveolin-1. Only a subset of additional caveolar components (cavin-2 and EHD2) are present at sites of bacterial transfer, and although clathrin and the clathrin-associated proteins Eps15 and AP2 are absent from the bacterial invaginations, efficient L. monocytogenes spreading requires the clathrin-interacting protein epsin-1. We also directly demonstrated that isolated L. monocytogenes membrane protrusions can trigger the recruitment of caveolar proteins in a neighboring cell. The engulfment of these bacterial and cytoskeletal structures through a caveolin-based mechanism demonstrates that the classical nanometer-scale theoretical size limit for this internalization pathway is exceeded by these bacterial pathogens.
Document
Published as
Aaron S. Dhanda, Connie Yu, Katarina T. Lulic, A. Wayne Vogl, Valentina Rausch, Diana Yang, Benjamin J. Nichols, Sung Hyun Kim, Simona Polo, Carsten G. Hansen, Julian A. Guttman. mBio Jan 2020, 11 (1) e02857-19; DOI: 10.1128/mBio.02857-19.
Publication title
mBio
Document title
Listeria Monocytogenes Exploits Host Caveolin for Cell-to-Cell Spreading
Date
2020
Volume
11
Issue
1
Publisher DOI
10.1128/mBio.02857-19
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Copyright is held by the author(s).
Scholarly level
Peer reviewed?
Yes
Language
Member of collection