Evidence map›Paper›PMID 33846410›Full record

ArticleScientific reports2021

CD25890, a conserved protein that modulates sporulation initiation in Clostridioides difficile.

Diogo Martins, Michael A DiCandia, Aristides L Mendes, Daniela Wetzel, Shonna M McBride, Adriano O Henriques, Mónica Serrano

Open access · goldAbstract read
In one paragraph

Article in Scientific reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.

0numbers the graph read from it
0cells of the map it votes in
11citing papers in PubMed
0.6field-weighted citation impact, top 30% 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

11 citing papers in PubMed, 11 citations in OpenAlex.

  1. Structural and biophysical insights into the unique RNase YicC.bioRxiv : the preprint server for biology · 2026
    Article
  2. Clostridioides difficile pathogenesis and control.Nature reviews. Microbiology · 2026
    Review
  3. Article
  4. Article
  5. Article
  6. Clostridioides difficile Sporulation.Advances in experimental medicine and biology · 2024
    Review
  7. Article
  8. Review
  9. Article
  10. Review
  11. 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

7 authors at 2 institutions in 2 countries.

Diogo MartinsInstituto de Tecnologia Química E Biológica António Xavier, Avenida da República, 2780-157, Oeiras, Portugal.
Michael A DiCandiaDepartment of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA.
Aristides L MendesInstituto de Tecnologia Química E Biológica António Xavier, Avenida da República, 2780-157, Oeiras, Portugal.
Daniela WetzelDepartment of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA.
Shonna M McBrideDepartment of Microbiology and Immunology, Emory University School of Medicine, Atlanta, GA, USA.
Adriano O HenriquesInstituto de Tecnologia Química E Biológica António Xavier, Avenida da República, 2780-157, Oeiras, Portugal.
Mónica SerranoInstituto de Tecnologia Química E Biológica António Xavier, Avenida da República, 2780-157, Oeiras, Portugal. serrano@itqb.unl.pt.
Instituto de Biologia Experimental e Tecnológica · PTEmory University · US

Funding

PREDOCTORAL TRAINING PROGRAM IN GENETICST32GM008490 · NIGMS · EMORY UNIVERSITY · PI BOSS, JEREMY M. · 1993 to 2022
$8.0M
Decoding Antibiotic-induced Susceptibility to Clostridium difficile InfectionU01AI124290 · NIAID · BAYLOR COLLEGE OF MEDICINE · PI BRITTON, ROBERT A, GAREY, KEVIN W · 2016 to 2020
$7.9M
Host-induced Initiation of Clostridium difficile SporulationR01AI116933 · NIAID · EMORY UNIVERSITY · PI SHONNA M. MCBRIDE · 2015 to 2026
$4.8M
Mechanisms of Clostridium difficile spore germinationR01AI116895 · NIAID · TEXAS A&M UNIVERSITY · PI SORG, JOE · 2015 to 2024
$3.9M
Polymeric Agents for the Treatment of Clostridium difficile InfectionsR33AI121684 · NIAID · EMORY UNIVERSITY · PI GELLMAN, SAMUEL H., MCBRIDE, SHONNA M. · 2018 to 2020
$1.4M
Polymeric Agents for the Treatment of Clostridium difficile InfectionsR21AI121684 · NIAID · EMORY UNIVERSITY · PI GELLMAN, SAMUEL H., MCBRIDE, SHONNA M. · 2016 to 2017
$415k
NIAID NIH HHS R01 AI116895NIAID NIH HHS R01 AI116933NIAID NIH HHS R21 AI121684NIAID NIH HHS R33 AI121684NIAID NIH HHS U01 AI124290NIGMS NIH HHS T32 GM008490
6 · The paper itself

Abstract

Bacteria that reside in the gastrointestinal tract of healthy humans are essential for our health, sustenance and well-being. About 50-60% of those bacteria have the ability to produce resilient spores that are important for the life cycle in the gut and for host-to-host transmission. A genomic signature for sporulation in the human intestine was recently described, which spans both commensals and pathogens such as Clostridioides difficile and contains several genes of unknown function. We report on the characterization of a signature gene, CD25890, which, as we show is involved in the control of sporulation initiation in C. difficile under certain nutritional conditions. Spo0A is the main regulatory protein controlling entry into sporulation and we show that an in-frame deletion of CD25890 results in increased expression of spo0A per cell and increased sporulation. The effect of CD25890 on spo0A is likely indirect and mediated through repression of the sinRR´ operon. Deletion of the CD25890 gene, however, does not alter the expression of the genes coding for the cytotoxins or the genes involved in biofilm formation. Our results suggest that CD25890 acts to modulate sporulation in response to the nutrients present in the environment.

Indexed as

Genes, BacterialAnimalsBacterial ProteinsClostridioides difficileClostridium InfectionsGene Expression Regulation, BacterialHumansMesocricetusSpores, BacterialBacterial Proteins

Identifiers

PMID33846410
PMCPMC8041843
OpenAlexW3155163945

What OpenQuestion holds

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LicenceCC BY
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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.