Evidence map›Paper›PMID 27430273›Full record

ArticleInfection and immunity2016

Beyond Tryptophan Synthase: Identification of Genes That Contribute to Chlamydia trachomatis Survival during Gamma Interferon-Induced Persistence and Reactivation.

Matthew K Muramatsu, Julie A Brothwell, Barry D Stein, Timothy E Putman, Daniel D Rockey, David E Nelson

Open access · bronzeAbstract read
In one paragraph

Article in Infection and immunity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.

0numbers the graph read from it
0cells of the map it votes in
28citing papers in PubMed
2.6field-weighted citation impact, top 12% 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

28 citing papers in PubMed, 32 citations in OpenAlex.

  1. Article
  2. Article
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  4. Tail-specific protease is an essentialInfection and immunity · 2024
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  5. Recognition ofInfection and immunity · 2024
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  6. Expression activation of over 70% ofInfection and immunity · 2024
    Article
  7. Review
  8. Article
  9. Review
  10. Review
  11. Article
  12. Review
  13. The role of tryptophan inFrontiers in cellular and infection microbiology · 2022
    Review
  14. Article
  15. Article
  16. Article
  17. Article
  18. Akt Phosphorylation Influences Persistent Chlamydial Infection andFrontiers in cellular and infection microbiology · 2021
    Article
  19. Review
  20. Article
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

6 authors at 4 institutions in 1 country.

Matthew K MuramatsuDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Julie A BrothwellDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA.
Barry D SteinDepartment of Biology, Indiana University, Bloomington, Indiana, USA.
Timothy E PutmanDepartment of Biomedical Sciences, Oregon State University, Corvallis, Oregon, USA.
Daniel D RockeyDepartment of Biomedical Sciences, Oregon State University, Corvallis, Oregon, USA.
David E NelsonDepartment of Microbiology and Immunology, Indiana University School of Medicine, Indianapolis, Indiana, USA nelsonde@indiana.edu.
Indiana University School of MedicineOregon State University · USIndiana University Bloomington · USIndiana University – Purdue University Indianapolis · US

Funding

Genetic analysis of mechanisms of chlamydial immune evasionR01AI099278 · NIAID · INDIANA UNIVERSITY INDIANAPOLIS · PI NELSON, DAVID EMMET · 2012 to 2023
$4.6M
Genetic analysis of mechanisms of chlamydial immune evasionR56AI099278 · NIAID · INDIANA UNIVERSITY INDIANAPOLIS · PI NELSON, DAVID EMMET · 2017 to 2017
$579k
NIAID NIH HHS R01 AI099278NIAID NIH HHS R56 AI099278
6 · The paper itself

Abstract

Chlamydia trachomatis can enter a viable but nonculturable state in vitro termed persistence. A common feature of C. trachomatis persistence models is that reticulate bodies fail to divide and make few infectious progeny until the persistence-inducing stressor is removed. One model of persistence that has relevance to human disease involves tryptophan limitation mediated by the host enzyme indoleamine 2,3-dioxygenase, which converts l-tryptophan to N-formylkynurenine. Genital C. trachomatis strains can counter tryptophan limitation because they encode a tryptophan-synthesizing enzyme. Tryptophan synthase is the only enzyme that has been confirmed to play a role in interferon gamma (IFN-γ)-induced persistence, although profound changes in chlamydial physiology and gene expression occur in the presence of persistence-inducing stressors. Thus, we screened a population of mutagenized C. trachomatis strains for mutants that failed to reactivate from IFN-γ-induced persistence. Six mutants were identified, and the mutations linked to the persistence phenotype in three of these were successfully mapped. One mutant had a missense mutation in tryptophan synthase; however, this mutant behaved differently from previously described synthase null mutants. Two hypothetical genes of unknown function, ctl0225 and ctl0694, were also identified and may be involved in amino acid transport and DNA damage repair, respectively. Our results indicate that C. trachomatis utilizes functionally diverse genes to mediate survival during and reactivation from persistence in HeLa cells.

Indexed as

Amino Acid Transport SystemsCell ProliferationChlamydia trachomatisDNA RepairHeLa CellsHumansInterferon-gammaMutationSequence Analysis, DNATryptophan SynthaseAmino Acid Transport SystemsInterferon-gammaTryptophan Synthase

Identifiers

PMID27430273
PMCPMC5038056
OpenAlexW2503092171

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.