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

Aaron S Dhanda, Connie Yu, Katarina T Lulic, Valentina Rausch, Diana Yang, Benjamin J Nichols, Sung Hyun Kim, Simona Polo, Carsten Hansen, Julian A Guttman

Research output: Contribution to journalArticlepeer-review

Abstract / Description of output

Listeria monocytogenes move from one cell to another using actin-rich membrane protrusions that propel the bacteria 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 demonstrate 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 usurped by these bacterial pathogens.

Original languageEnglish
Publication statusPublished - 21 Jan 2020


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