Evidence map›Paper›PMID 29529083›Full record

ArticlePLoS pathogens2018

Pleiotropic roles of Clostridium difficile sin locus.

Brintha Parasumanna Girinathan, Junjun Ou, Bruno Dupuy, Revathi Govind

Open access · goldAbstract read
In one paragraph

Article in PLoS pathogens, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers.

0numbers the graph read from it
0cells of the map it votes in
43citing papers in PubMed
4.8field-weighted citation impact, top 4% 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

43 citing papers in PubMed, 57 citations in OpenAlex.

  1. Article
  2. Article
  3. CenIR, an essential BlaIR-family regulatory system inbioRxiv : the preprint server for biology · 2026
    Article
  4. Article
  5. Article
  6. Article
  7. Review
  8. Review
  9. Article
  10. Article
  11. Article
  12. International journal of molecular sciences · 2024
    Review
  13. Clostridioides difficile Sporulation.Advances in experimental medicine and biology · 2024
    Review
  14. Review
  15. Article
  16. Article
  17. Article
  18. Regulatory transcription factors ofCritical reviews in microbiology · 2023
    Review
  19. Article
  20. Capturing the environment of the Clostridioides difficile infection cycle.Nature reviews. Gastroenterology & hepatology · 2022
    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

4 authors at 2 institutions in 2 countries.

Brintha Parasumanna GirinathanDivision of Biology, Kansas State University, Manhattan, KS, United Sates of America.ORCID 0000-0003-4920-0014
Junjun OuDepartment of Agronomy, Kansas State University, Manhattan, KS, United Sates of America.
Bruno DupuyLaboratoire Pathogénese des Bactéries Anaérobies, Institut Pasteur, Paris, France.
Revathi GovindDivision of Biology, Kansas State University, Manhattan, KS, United Sates of America.ORCID 0000-0001-6609-8600
Kansas State University · USInstitut Pasteur · FR

Funding

Synthetic Chemical Biology CoreP20GM113117 · NIGMS · UNIVERSITY OF KANSAS LAWRENCE · PI OROZCO, ROBIN C. · 2016 to 2025
$23.9M
Alternate roles of Clostridium difficile TcdRR15AI122173 · NIAID · KANSAS STATE UNIVERSITY · PI GOVIND, REVATHI · 2016 to 2016
$437k
NIAID NIH HHS R15 AI122173NIGMS NIH HHS P20 GM113117
6 · The paper itself

Abstract

Clostridium difficile is the primary cause of nosocomial diarrhea and pseudomembranous colitis. It produces dormant spores, which serve as an infectious vehicle responsible for transmission of the disease and persistence of the organism in the environment. In Bacillus subtilis, the sin locus coding SinR (113 aa) and SinI (57 aa) is responsible for sporulation inhibition. In B. subtilis, SinR mainly acts as a repressor of its target genes to control sporulation, biofilm formation, and autolysis. SinI is an inhibitor of SinR, so their interaction determines whether SinR can inhibit its target gene expression. The C. difficile genome carries two sinR homologs in the operon that we named sinR and sinR', coding for SinR (112 aa) and SinR' (105 aa), respectively. In this study, we constructed and characterized sin locus mutants in two different C. difficile strains R20291 and JIR8094, to decipher the locus's role in C. difficile physiology. Transcriptome analysis of the sinRR' mutants revealed their pleiotropic roles in controlling several pathways including sporulation, toxin production, and motility in C. difficile. Through various genetic and biochemical experiments, we have shown that SinR can regulate transcription of key regulators in these pathways, which includes sigD, spo0A, and codY. We have found that SinR' acts as an antagonist to SinR by blocking its repressor activity. Using a hamster model, we have also demonstrated that the sin locus is needed for successful C. difficile infection. This study reveals the sin locus as a central link that connects the gene regulatory networks of sporulation, toxin production, and motility; three key pathways that are important for C. difficile pathogenesis.

Indexed as

OperonAmino Acid SequenceAnimalsBacillus subtilisBacterial ProteinsBacterial ToxinsCecumCell MovementClostridioides difficileClostridium InfectionsGene Expression Regulation, BacterialMesocricetusMiceRabbitsRegulonSequence HomologyBacterial ProteinsBacterial Toxins

Identifiers

PMID29529083
PMCPMC5864091
OpenAlexW2791088953

What OpenQuestion holds

Textmetadata
LicenceCC BY
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.