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Replication-dependent size reduction precedes differentiation in Chlamydia trachomatis.

Jennifer K Lee1, Germán A Enciso2, Daniela Boassa3

  • 1Department of Developmental and Cell Biology, University of California, Irvine, CA, 92697-2300, USA.

Nature Communications
|January 5, 2018
PubMed
Summary
This summary is machine-generated.

Chlamydia trachomatis reticulate bodies (RBs) divide and shrink, with conversion to infectious elementary bodies (EBs) only occurring after significant replication. This size reduction controls the Chlamydia developmental cycle without external signals.

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Area of Science:

  • Microbiology
  • Cell Biology
  • Infectious Diseases

Background:

  • Chlamydia trachomatis causes common bacterial sexually transmitted infections.
  • It exhibits a unique intracellular developmental cycle involving reticulate bodies (RBs) and elementary bodies (EBs).

Purpose of the Study:

  • To investigate the mechanism controlling the conversion of RBs to EBs in Chlamydia trachomatis.
  • To elucidate the role of RB replication and size in the Chlamydia developmental cycle.

Main Methods:

  • Quantitative three-dimensional electron microscopy (3D EM) was employed to visualize and measure Chlamydia trachomatis RBs.
  • A stochastic mathematical model was developed to simulate RB replication and size dynamics.

Main Results:

  • C. trachomatis RBs divide by binary fission and reduce size sixfold during replication.
  • Conversion to EBs occurs only after at least six replication rounds and correlates with smaller RB size.
  • RB size reduction is a key factor in triggering RB-to-EB conversion.

Conclusions:

  • RB size reduction, driven by replication, controls the timing of EB conversion in Chlamydia trachomatis.
  • This intrinsic size-dependent mechanism explains the delayed and asynchronous nature of the Chlamydia developmental cycle.
  • The findings support a model where RB size, not external signals, dictates the transition to the infectious EB form.