Evidence map›Paper›PMID 39779702›Full record

ArticleNature communications2025

Dynamic transitions of initiator binding coordinate the replication of the two chromosomes in Vibrio cholerae.

Théophile Niault, Ariel Talavera, Eric Le Cam, Sonia Baconnais, Ole Skovgaard, Florian Fournes, Léa Wagner, Hedvig Tamman, Andrew Thompson, Dannele Echemendia-Blanco and 4 more

Abstract read
In one paragraph

Article in Nature communications, 2025. 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
–field-weighted citation impact
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. 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

14 authors.

Théophile NiaultInstitut Pasteur, Université Paris Cité, CNRS UMR3525, Unité Plasticité du Génome Bactérien, Département Génomes et Génétique, Paris, France.
Ariel TalaveraCellular and Molecular Microbiology, Faculté des Sciences, Université libre de Bruxelles (ULB), Boulevard du Triomphe, Brussels, Belgium.ORCID http://orcid.org/0000-0002-1865-5959
Eric Le CamGenome Integrity and Cancer UMR 9019 CNRS, Université Paris Saclay, Gustave Roussy, Villejuif, France.ORCID http://orcid.org/0000-0002-6832-6117
Sonia BaconnaisGenome Integrity and Cancer UMR 9019 CNRS, Université Paris Saclay, Gustave Roussy, Villejuif, France.
Ole SkovgaardDepartment of Science and Environment, Systems and Models, Roskilde University, Roskilde, Denmark.ORCID http://orcid.org/0000-0002-4860-1847
Florian FournesInstitut Pasteur, Université Paris Cité, CNRS UMR3525, Unité Plasticité du Génome Bactérien, Département Génomes et Génétique, Paris, France.ORCID http://orcid.org/0000-0002-7763-7478
Léa WagnerInstitut Pasteur, Université Paris Cité, CNRS UMR3525, Unité Plasticité du Génome Bactérien, Département Génomes et Génétique, Paris, France.ORCID http://orcid.org/0000-0001-8315-3376
Hedvig TammanCellular and Molecular Microbiology, Faculté des Sciences, Université libre de Bruxelles (ULB), Boulevard du Triomphe, Brussels, Belgium.ORCID http://orcid.org/0000-0003-4453-7814
Andrew ThompsonSOLEIL Synchrotron, Saint-Aubin - BP48, Gif sur Yvette, France.
Dannele Echemendia-BlancoCellular and Molecular Microbiology, Faculté des Sciences, Université libre de Bruxelles (ULB), Boulevard du Triomphe, Brussels, Belgium.
Noa GuzziInstitut Pasteur, Université Paris Cité, CNRS UMR3525, Unité Plasticité du Génome Bactérien, Département Génomes et Génétique, Paris, France.
Abel Garcia-PinoCellular and Molecular Microbiology, Faculté des Sciences, Université libre de Bruxelles (ULB), Boulevard du Triomphe, Brussels, Belgium. abel.garcia.pino@ulb.be.ORCID http://orcid.org/0000-0002-0634-0300
Didier MazelInstitut Pasteur, Université Paris Cité, CNRS UMR3525, Unité Plasticité du Génome Bactérien, Département Génomes et Génétique, Paris, France. didier.mazel@pasteur.fr.ORCID http://orcid.org/0000-0001-6482-6002
Marie-Eve ValInstitut Pasteur, Université Paris Cité, CNRS UMR3525, Unité Plasticité du Génome Bactérien, Département Génomes et Génétique, Paris, France. marie-eve.kennedy-val@pasteur.fr.ORCID http://orcid.org/0000-0001-7097-9072

Funding

Agence Nationale de la Recherche (French National Research Agency) ANR-10-LABX62-IBEIDAgence Nationale de la Recherche (French National Research Agency) ANR-19CE12-0001Fondation pour la Recherche Médicale (Foundation for Medical Research in France) EQU202103012569
6 · The paper itself

Abstract

The replication of the two chromosomes in the pathogenic bacterium Vibrio cholerae is coordinated by the binding of initiator protein RctB to a checkpoint sequence, crtS. Replication of crtS on the primary chromosome (Chr1) triggers replication of the secondary chromosome (Chr2), but the details are poorly understood. Here, we analyze RctB binding patterns in the V. cholerae genome across various cell cycle stages. We find that RctB primarily binds to sites inhibiting replication initiation at the Chr2 origin (ori2). This inhibitory effect is counteracted when crtS is replicated on Chr1, causing a shift in RctB binding to sites that activate replication at ori2. Structural analyzes indicate the formation of diverse oligomeric states of RctB, coupled to the allosteric effect of DNA, which determine ori2 accessibility. We propose a synchronization model where, upon replication, crtS locally destabilizes the RctB inhibition complex, releasing the Chr2 replication origin.

Indexed as

Bacterial ProteinsChromosomes, BacterialDNA ReplicationReplication OriginVibrio choleraeBinding SitesCell CycleDNA, BacterialDNA-Binding ProteinsProtein BindingBacterial ProteinsDNA, BacterialDNA-Binding Proteins

Identifiers

PMID39779702
PMCPMC11711613

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.