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Published on: October 25, 2019
The Chlamydia trachomatis IncM Protein Interferes with Host Cell Cytokinesis, Centrosome Positioning, and Golgi
Maria Pequito Luís1,2, Inês Serrano Pereira1,2, Joana N Bugalhão1,2
1Associate Laboratory i4HB, Institute for Health and Bioeconomy, NOVA School of Science and Technology, NOVA University Lisbon, Caparica, Portugal.
Abstract:
Chlamydia trachomatis is an obligate intracellular bacterial pathogen that causes ocular and urogenital infections in humans. The ability of C. trachomatis to grow intracellularly in a pathogen-containing vacuole (known as an inclusion) depends on chlamydial effector proteins transported into the host cell by a type III secretion system. Among these effectors, several inclusion membrane proteins (Incs) insert in the vacuolar membrane. Here, we show that human cell lines infected by a C. trachomatis strain deficient for Inc CT288/CTL0540 (renamed IncM) displayed less multinucleation than when infected by IncM-producing strains (wild type or complemented). This indicated that IncM is involved in the ability of Chlamydia to inhibit host cell cytokinesis. The capacity of IncM to induce multinucleation in infected cells was shown to be conserved among its chlamydial homologues and appeared to require its two larger regions predicted to be exposed to the host cell cytosol. C. trachomatis-infected cells also displayed IncM-dependent defects in centrosome positioning, Golgi distribution around the inclusion, and morphology and stability of the inclusion. The altered morphology of inclusions containing IncM-deficient C. trachomatis was further affected by depolymerization of host cell microtubules. This was not observed after depolymerization of microfilaments, and inclusions containing wild-type C. trachomatis did not alter their morphology upon depolymerization of microtubules. Overall, these findings suggest that IncM may exert its effector function by acting directly or indirectly on host cell microtubules.
Insights
The bacterial protein IncM from Chlamydia trachomatis inhibits host cell cytokinesis and alters cell structure. IncM impacts microtubule dynamics, affecting bacterial inclusion morphology and stability within host cells.
Area of Science:
- Microbiology
- Cell Biology
- Infectious Diseases
Background:
- Chlamydia trachomatis is an obligate intracellular bacterium causing human infections.
- Type III secretion systems deliver effector proteins, including inclusion membrane proteins (Incs), into host cells.
- Incs are crucial for pathogen survival and manipulation of host cell processes.
Purpose of the Study:
- To investigate the role of the Chlamydia trachomatis IncM effector protein in host cell manipulation.
- To determine the impact of IncM on host cell cytokinesis, centrosome positioning, and inclusion morphology.
- To elucidate the mechanism by which IncM influences host cell microtubules.
Main Methods:
- Infection of human cell lines with wild-type and IncM-deficient Chlamydia trachomatis strains.
- Analysis of host cell multinucleation, centrosome positioning, and Golgi distribution.
- Assessment of inclusion morphology and stability under conditions of microtubule or microfilament depolymerization.
Main Results:
- Chlamydia trachomatis strains lacking IncM exhibited reduced multinucleation compared to wild-type strains.
- IncM is conserved among Chlamydia species and requires specific cytosolic regions for function.
- IncM-deficient infections led to defects in centrosome positioning and Golgi organization.
- Inclusion morphology and stability were compromised in IncM-deficient infections, particularly upon microtubule depolymerization.
Conclusions:
- IncM is a key Chlamydia trachomatis effector that inhibits host cell cytokinesis.
- IncM influences host cell microtubule dynamics, directly or indirectly affecting inclusion structure.
- Understanding IncM's function provides insights into Chlamydia's pathogenesis and host-pathogen interactions.
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