Journal article
The Chlamydia trachomatis type III-secreted effector protein CteG induces centrosome amplification through interactions with centrin-2
Proceedings of the National Academy of Sciences - PNAS, Vol.120(20), e2303487120
05/16/2023
DOI: 10.1073/pnas.2303487120
PMCID: PMC10193975
PMID: 37155906
Abstract
The centrosome is the main microtubule organizing center of the cell and is crucial for mitotic spindle assembly, chromosome segregation, and cell division. Centrosome duplication is tightly controlled, yet several pathogens, most notably oncogenic viruses, perturb this process leading to increased centrosome numbers. Infection by the obligate intracellular bacterium
(
) correlates with blocked cytokinesis, supernumerary centrosomes, and multipolar spindles; however, the mechanisms behind how
induces these cellular abnormalities remain largely unknown. Here we show that the secreted effector protein, CteG, binds to centrin-2 (CETN2), a key structural component of centrosomes and regulator of centriole duplication. Our data indicate that both CteG and CETN2 are necessary for infection-induced centrosome amplification, in a manner that requires the C-terminus of CteG. Strikingly, CteG is important for in vivo infection and growth in primary cervical cells but is dispensable for growth in immortalized cells, highlighting the importance of this effector protein to chlamydial infection. These findings begin to provide mechanistic insight into how
induces cellular abnormalities during infection, but also indicate that obligate intracellular bacteria may contribute to cellular transformation events. Centrosome amplification mediated by CteG-CETN2 interactions may explain why chlamydial infection leads to an increased risk of cervical or ovarian cancer.
Details
- Title: Subtitle
- The Chlamydia trachomatis type III-secreted effector protein CteG induces centrosome amplification through interactions with centrin-2
- Creators
- Brianna Steiert - University of IowaCarolina M Icardi - University of IowaRobert Faris - University of IowaPaige N McCaslin - University of IowaParker Smith - University of IowaAloysius J Klingelhutz - University of IowaPeter M Yau - University of Illinois Urbana-ChampaignMary M Weber - University of Iowa
- Resource Type
- Journal article
- Publication Details
- Proceedings of the National Academy of Sciences - PNAS, Vol.120(20), e2303487120
- DOI
- 10.1073/pnas.2303487120
- PMID
- 37155906
- PMCID
- PMC10193975
- NLM abbreviation
- Proc Natl Acad Sci U S A
- eISSN
- 1091-6490
- Grant note
- R01 AI155434 / NIAID NIH HHS T32 AI007511 / NIAID NIH HHS R01 AI150812 / NIAID NIH HHS
- Language
- English
- Date published
- 05/16/2023
- Academic Unit
- Molecular Physiology and Biophysics; Microbiology and Immunology; Radiation Oncology
- Record Identifier
- 9984406605102771
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