Evidence map›Paper›PMID 37804183›Full record

ArticlePathogens and disease2023

TargeTron inactivation of plasmid-regulated Chlamydia trachomatis CT084 results in a nonlytic phenotype.

Una Karanovic, Lei Lei, Craig A Martens, Kent Barbian, Grant McClarty, Harlan D Caldwell, Chunfu Yang

Open access · bronzeAbstract read
PubMed Full text at PMC Publisher
In one paragraph

Article in Pathogens and disease, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.

0numbers the graph read from it
0cells of the map it votes in
1citing papers in PubMed
0.2field-weighted citation impact, top 46% of its field
1 · What the graph read from it

What it found

Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.

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.

2 · The registry

The trial behind it

Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.

Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.

3 · Its place in the literature

Who cites it

1 citing paper in PubMed, 1 citations in OpenAlex.

  1. Review
4 · The record

Corrections and comments

PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.

5 · Who and what money

Authors and funding

7 authors at 4 institutions in 3 countries.

Una KaranovicLaboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, 208952, United States.
Lei LeiLaboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, 208952, United States.
Craig A MartensRocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana, 59840, United States.
Kent BarbianRocky Mountain Laboratories, National Institute of Allergy and Infectious Diseases, Hamilton, Montana, 59840, United States.
Grant McClartyDepartment of Medical Microbiology and Infectious Diseases, University of Manitoba, Winnipeg, Manitoba R3T 2N2, Canada.
Harlan D CaldwellLaboratory of Clinical Immunology and Microbiology, National Institute of Allergy and Infectious Disease, National Institutes of Health, Bethesda, Maryland, 208952, United States.
Chunfu YangSchool of Public Health and Emergency Management, Southern University of Science and Technology, Shenzhen 518055, China.ORCID 0000-0001-7116-0501
National Institutes of Health · USNational Institute of Allergy and Infectious Diseases · USSouthern University of Science and Technology · CNUniversity of Manitoba · CA

Funding

NIAID NIH HHSNIH HHS
6 · The paper itself

Abstract

Chlamydia trachomatis is an obligate intracellular bacterium that causes blinding trachoma and sexually transmitted disease. The chlamydial plasmid is a critical virulence factor in the pathogenesis of these diseases. Plasmid gene protein 4 (Pgp4) plays a major role in chlamydial virulence by regulating the expression of both chromosomal genes and Pgp3. Despite the importance of Pgp4 in mediating lytic exit from host cells the pathogenic mechanism by which it functions is unknown. CT084 is a highly conserved chromosomal gene with homology to phospholipase D. We showed CT084 expression is regulated by Pgp4 and expressed late in the chlamydial developmental cycle. To investigate the function of CT084 in chlamydial lytic exit from infected cells, we made a CT084 null strain (ct084::bla) by using Targetron. The ct084::bla strain grew normally in vitro compared to wild-type strain; however, the strain did not lyse infected cells and produced significantly less and smaller plaques. Collectively, our finding shows Pgp4-regulated CT084-mediated chlamydia lytic exit from infected host cells.

Indexed as

Chlamydia InfectionsTrachomaBacterial ProteinsChlamydia trachomatisHumansPhenotypePlasmidsBacterial ProteinsChlamydia trachomatisCT084lytic exitphospholipaseplasmid

Identifiers

PMID37804183
PMCPMC10589100
OpenAlexW4387431855

What OpenQuestion holds

Textmetadata
Read underepoch 390

Registered trials

None linked

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.