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Imaging InlC Secretion to Investigate Cellular Infection by the Bacterial Pathogen Listeria monocytogenes
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Imaging InlC Secretion to Investigate Cellular Infection by the Bacterial Pathogen Listeria monocytogenes

Published on: September 19, 2013

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Host endoplasmic reticulum COPII proteins control cell-to-cell spread of the bacterial pathogen Listeria

Antonella Gianfelice1, Phuong H B Le1, Luciano A Rigano1

  • 1Department of Microbiology and Immunology, University of Otago, Dunedin, New Zealand.

Cellular Microbiology
|December 23, 2014
PubMed

Insights

Listeria monocytogenes uses COPII proteins to spread between cells. The bacterial protein InlC inhibits this host process, revealing a new target for controlling Listeria infections.

Area of Science:

  • Cell biology
  • Microbiology
  • Infectious diseases

Background:

  • Listeria monocytogenes spreads between human cells via actin-dependent motility and plasma membrane protrusions.
  • The bacterial protein InlC promotes protrusion formation by inhibiting the host protein Tuba in enterocytes.

Purpose of the Study:

  • To investigate the role of host cell machinery in Listeria monocytogenes cell-to-cell spread.
  • To elucidate the mechanism by which the bacterial protein InlC influences host cell structures during infection.

Main Methods:

  • Co-precipitation assays to identify protein interactions between bacterial factors and host machinery.
  • Depletion studies of specific host proteins (Sec31A, Sec13) and genetic impairment of COPII components (Sar1).
  • Cell treatment with brefeldin A to disrupt COPII trafficking and observation of protrusion formation and cell-cell junction integrity.

Main Results:

  • COPII (Coat Protein Complex II) components Sec31A and Sec13 directly interact with the host scaffolding protein Tuba.
  • The bacterial protein InlC antagonizes the interaction between Tuba and COPII components.
  • Depletion of Sec31A or Sec13, or impairment of Sar1, restored normal protrusion formation in inlC-deficient Listeria mutants.
  • Inhibition of COPII components or brefeldin A treatment disrupted cell-cell junctions and affected protrusion formation.

Conclusions:

  • Host COPII machinery plays a crucial role in restricting Listeria monocytogenes cell-to-cell spread.
  • The bacterial protein InlC overcomes this host restriction by antagonizing Tuba-COPII interactions.
  • COPII may facilitate Listeria spread by delivering host proteins that induce tension at cell junctions, suggesting potential therapeutic targets.

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