Related Experiment Video

Updated: Aug 6, 2026

Markerless Gene Deletion by Floxed Cassette Allelic Exchange Mutagenesis in Chlamydia trachomatis
10:35

Markerless Gene Deletion by Floxed Cassette Allelic Exchange Mutagenesis in Chlamydia trachomatis

Published on: January 30, 2020

Chlamydia trachomatis causes centrosomal defects resulting in chromosomal segregation abnormalities

Scott S Grieshaber1, Nicole A Grieshaber, Natalie Miller

  • 1Host-Parasite Interactions Section, Laboratory of Intracellular Parasites, NIAID, NIH, Rocky Mountain Laboratories, Hamilton, MT 59840, USA.

Traffic (Copenhagen, Denmark)
|August 3, 2006
PubMed

Insights

Chlamydia bacteria hijack host cell microtubules to reach the centrosome, causing genomic instability and defects in chromosome segregation after infection.

Area of Science:

  • Microbiology
  • Cell Biology
  • Genetics

Background:

  • Chlamydiae are obligate intracellular bacteria that establish a niche within host cells by trafficking along microtubules to the microtubule organizing center (MTOC).
  • This intracellular trafficking is dynein-dependent, but the precise mechanisms, particularly the role of the dynactin complex, are not fully understood and appear to be subverted by chlamydial factors.

Purpose of the Study:

  • To investigate the interaction of Chlamydiae with the host cell centrosome after trafficking to the MTOC.
  • To determine the consequences of this interaction on host cell mitosis and genomic stability.

Main Methods:

  • Live-cell imaging to track Chlamydiae localization and centrosome dynamics.
  • Immunofluorescence microscopy to assess centrosome number, spindle formation, and chromosome segregation.
  • Analysis of chromosomal instability in infected cells post-infection.

Main Results:

  • Chlamydial inclusions localize to and associate tightly with host cell centrosomes.
  • This association persists through mitosis, leading to an increase in supernumerary centrosomes.
  • Infected cells exhibit abnormal spindle poles and significant chromosomal segregation defects.

Conclusions:

  • Chlamydial infection disrupts normal centrosome function and mitotic progression.
  • The persistent association of chlamydial inclusions with centrosomes induces genomic instability in host cells.
  • Chlamydial infection can lead to lasting chromosome instability in cells that survive the infection.

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