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Dynamin-dependent entry of Chlamydia trachomatis is sequentially regulated by the effectors TarP and TmeA

Matthew D Romero1, Rey A Carabeo1

  • 1Department of Pathology and Microbiology, College of Medicine, University of Nebraska Medical Center, Omaha, NE.

Research Square
|October 16, 2023
PubMed

Insights

Chlamydia invasion relies on TarP and TmeA effectors, which recruit and activate host dynamin 2 (Dyn2) for pathogen uptake. Dyn2 regulates actin dynamics, crucial for efficient Chlamydia epithelial cell entry.

Area of Science:

  • Microbiology
  • Cell Biology
  • Molecular Biology

Background:

  • Chlamydia employs effectors TarP and TmeA to manipulate host cell actin dynamics during epithelial cell invasion.
  • Understanding the precise molecular mechanisms governing pathogen uptake is essential for developing targeted interventions.

Approach:

  • Investigated the role of host dynamin 2 (Dyn2) in Chlamydia epithelial cell invasion.
  • Elucidated the interplay between Chlamydia effectors TarP, TmeA, and host Dyn2 function.
  • Utilized small molecule Dyn2 activator Ryngo 1-23 to probe TmeA's role in Dyn2 oligomerization.

Key Points:

  • TarP recruits Dyn2 via phosphatidylinositol 3-kinase and Rac1.
  • TmeA facilitates Dyn2 activation through oligomerization, a process bypassed by Ryngo 1-23.
  • Dyn2 regulates the turnover of TarP- and TmeA-associated actin networks.

Conclusions:

  • Dynamin 2 is a critical host factor for completing Chlamydia invasion.
  • TarP and TmeA functionally interact with Dyn2 to modulate actin dynamics and pathogen uptake.
  • This study reveals an interdependent relationship between host Dyn2 and Chlamydia effectors during invasion.

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