ArticlePLoS pathogens2016
Polarized Cell Division of Chlamydia trachomatis.
Article in PLoS pathogens, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. An erratum has been issued. Cited by 69 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
69 citing papers in PubMed, 113 citations in OpenAlex.
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- Pathogenicity and virulence ofVirulence · 2025Review
- Distinct modes of cell division drivemBio · 2025Article
- The second messenger signaling molecule cyclic di-AMP drives developmental cycle progression ineLife · 2025Article
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- Recruitment of the cellular lipid transport protein CERT to C. psittaci inclusions regulates the timing of bacterial egress.Scientific reports · 2025Article
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- Altering the redox status ofeLife · 2025Article
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- The T3SS structural and effector genes ofFrontiers in cellular and infection microbiology · 2025Article
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- The MraY Inhibitor Muraymycin D2 and Its Derivatives Induce Enlarged Cells in Obligate IntracellularAntibiotics (Basel, Switzerland) · 2024Article
- Aberrant Bodies: An Alternative Metabolic Homeostasis Allowing Survivability?Microorganisms · 2024Review
- Insights into innate immune cell evasion byFrontiers in immunology · 2024Review
- Article
9 more citing papers are in PubMed but not listed here.
Corrections and comments
- Commented on by
- Erratum issued
Authors and funding
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Bacterial cell division predominantly occurs by a highly conserved process, termed binary fission, that requires the bacterial homologue of tubulin, FtsZ. Other mechanisms of bacterial cell division that are independent of FtsZ are rare. Although the obligate intracellular human pathogen Chlamydia trachomatis, the leading bacterial cause of sexually transmitted infections and trachoma, lacks FtsZ, it has been assumed to divide by binary fission. We show here that Chlamydia divides by a polarized cell division process similar to the budding process of a subset of the Planctomycetes that also lack FtsZ. Prior to cell division, the major outer-membrane protein of Chlamydia is restricted to one pole of the cell, and the nascent daughter cell emerges from this pole by an asymmetric expansion of the membrane. Components of the chlamydial cell division machinery accumulate at the site of polar growth prior to the initiation of asymmetric membrane expansion and inhibitors that disrupt the polarity of C. trachomatis prevent cell division. The polarized cell division of C. trachomatis is the result of the unipolar growth and FtsZ-independent fission of this coccoid organism. This mechanism of cell division has not been documented in other human bacterial pathogens suggesting the potential for developing Chlamydia-specific therapeutic treatments.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.