Chlamydia psittaci inclusion membrane protein IncB associates with host protein Snapin

Selina Böcker1, Adeline Heurich1, Claudia Franke1

  • 1Department of Cell and Molecular Biology, Leibniz Institute for Natural Product Research and Infection Biology (Hans Knoell Institute), Beutenbergstrasse 11a, D-07745 Jena, Germany.

Insights

Chlamydia psittaci, a zoonotic pathogen, uses host protein Snapin to connect its inclusions to the cell's transport system. This interaction is crucial for the pathogen's early development within host cells.

Area of Science:

  • Microbiology
  • Cell Biology
  • Zoonotic Diseases

Background:

  • Chlamydia psittaci is a significant zoonotic pathogen causing psittacosis in birds and humans.
  • This obligate intracellular bacterium has a unique developmental cycle involving elementary and reticulate bodies.
  • Dynein motor proteins are essential for C. psittaci's early intracellular development, but the mediating chlamydial factors are unknown.

Purpose of the Study:

  • To identify chlamydial proteins involved in C. psittaci's interaction with host cell dynein motor proteins.
  • To investigate the role of the host protein Snapin in the intracellular trafficking of C. psittaci.

Main Methods:

  • Yeast Two-hybrid screening using C. psittaci inclusion protein IncB as bait.
  • Confocal fluorescence microscopy to visualize co-localization of IncB, Snapin, and dynein.
  • RNA interference (RNAi) to deplete Snapin and assess its effect on co-localization.
  • In vitro and in vivo interaction assays.

Main Results:

  • The host protein Snapin was identified as an IncB-interacting protein.
  • IncB, Snapin, and dynein were found to co-localize near C. psittaci inclusions in infected cells.
  • Snapin depletion using RNAi disrupted this co-localization.
  • Snapin interacts with both IncB and dynein.

Conclusions:

  • Snapin acts as a bridge, connecting C. psittaci inclusions to the host cell's microtubule network via dynein.
  • This interaction mediated by Snapin is critical for the pathogen's intracellular development.

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