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Chlamydiae assemble a pathogen synapse to hijack the host endoplasmic reticulum

Maud Dumoux1, Daniel K Clare, Helen R Saibil

  • 1Institute of Structural and Molecular Biology, Birkbeck & University College London, Malet Street, London, WC1E 7HX, UK.

Traffic (Copenhagen, Denmark)
|August 21, 2012
PubMed

Insights

Chlamydia bacteria hijack the host endoplasmic reticulum (ER) to form their protective inclusion. This pathogen-controlled process is essential for bacterial survival and replication, involving direct ER-bacteria connections.

Area of Science:

  • Microbiology
  • Cell Biology
  • Pathogen-Host Interactions

Background:

  • Chlamydiae are obligate intracellular bacteria residing in a membrane-bound inclusion.
  • The inclusion membrane's interaction with host organelles and its origin are poorly understood.
  • Understanding these interactions is key to deciphering Chlamydia pathogenesis.

Purpose of the Study:

  • To investigate the relationship between the Chlamydia inclusion membrane and host cellular organelles.
  • To determine the role of the endoplasmic reticulum (ER) in Chlamydia infection.
  • To elucidate the mechanism of inclusion biogenesis and its dependence on host factors.

Main Methods:

  • Immunofluorescence microscopy and electron tomography to visualize host-pathogen interactions.
  • Analysis of protein localization and translocation between the ER and inclusion.
  • Functional assays assessing the impact of ER manipulation on Chlamydia development.

Main Results:

  • The host endoplasmic reticulum (ER), particularly rough ER (rER), is specifically recruited to the Chlamydia inclusion.
  • Key rER proteins are enriched on and translocated into the inclusion membrane.
  • ER recruitment is orchestrated by Chlamydia and occurs independently of host trafficking.
  • ER integrity is crucial for inclusion development; ER vacuolation stalls growth, while disruption causes inclusion bursting.
  • Pathogen synapses' form at rER contact sites, linking chlamydial secretion complexes to the inclusion membrane.

Conclusions:

  • Chlamydia actively hijacks the host ER to establish and maintain its inclusion.
  • The ER provides essential components and structural support for the inclusion membrane.
  • This study reveals a sophisticated supramolecular assembly for pathogen manipulation of a host organelle.

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