Evidence map›Paper›PMID 41419483›Full record

ArticleNature communications2025

A metabolism-chromatin axis promotes differential ribosomal RNA transcription in the human malaria parasite.

Justine E Couble, Tiziano Vignolini, Grégory Doré, Selina Mussgnug, Bérangère Lombard, Michael Richard, Damarys Loew, Michael Büttner, Rafael Dueñas-Sánchez, Gernot Poschet and 2 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

12 authors.

Justine E CoubleInstitut Pasteur, Université Paris Cité, INSERM U1347, G5 Parasite RNA Biology Group, F-75015, Paris, France.ORCID http://orcid.org/0009-0001-2545-8822
Tiziano VignoliniInstitut Pasteur, Université Paris Cité, INSERM U1347, G5 Parasite RNA Biology Group, F-75015, Paris, France.
Grégory DoréInstitut Pasteur, Université Paris Cité, INSERM U1347, G5 Parasite RNA Biology Group, F-75015, Paris, France.
Selina MussgnugInstitut Pasteur, Université Paris Cité, INSERM U1347, G5 Parasite RNA Biology Group, F-75015, Paris, France.
Bérangère LombardInstitut Curie, PSL Research University, CurieCoreTech Mass Spectrometry Proteomics, Paris, France.ORCID http://orcid.org/0000-0001-9044-3662
Michael RichardInstitut Curie, PSL Research University, CurieCoreTech Mass Spectrometry Proteomics, Paris, France.ORCID http://orcid.org/0000-0002-9907-9702
Damarys LoewInstitut Curie, PSL Research University, CurieCoreTech Mass Spectrometry Proteomics, Paris, France.ORCID http://orcid.org/0000-0002-9111-8842
Michael BüttnerMetabolomics Core Technology Platform, Centre for Organismal Studies, Heidelberg University, 69120, Heidelberg, Germany.
Rafael Dueñas-SánchezMetabolomics Core Technology Platform, Centre for Organismal Studies, Heidelberg University, 69120, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-5497-0825
Gernot PoschetMetabolomics Core Technology Platform, Centre for Organismal Studies, Heidelberg University, 69120, Heidelberg, Germany.ORCID http://orcid.org/0000-0002-5344-0865
Jessica M BryantInstitut Pasteur, Université Paris Cité, INSERM U1201, CNRS EMR9195, Biology of Host-Parasite Interactions Unit, F-75015, Paris, France.ORCID http://orcid.org/0000-0002-2349-8353
Sebastian BaumgartenInstitut Pasteur, Université Paris Cité, INSERM U1347, G5 Parasite RNA Biology Group, F-75015, Paris, France. sebastian.baumgarten@pasteur.fr.ORCID http://orcid.org/0000-0003-2646-7699

Funding

Agence Nationale de la Recherche (French National Research Agency) ANR-21-CE15-0002-02Agence Nationale de la Recherche (French National Research Agency) ANR-21-CE15-0010-01EC | EU Framework Programme for Research and Innovation H2020 | H2020 Priority Excellent Science | H2020 European Research Council (H2020 Excellent Science - European Research Council) ERC Starting Grant 947819
6 · The paper itself

Abstract

The transmission of the most virulent human malaria parasite, Plasmodium falciparum, relies on its survival in the contrasting environments of the human host and mosquito vector. One of the most fascinating adaptations to this lifestyle is the specific silencing of individual rDNA genes in the human host that are de-repressed following host-to-vector transmission. In this study, we define the epigenetic signatures of rRNA transcription and find that rDNA silencing relies on aerobic glycolysis, the sole energy-generating pathway in the human host. We show that disruption of NAD

Indexed as

ChromatinMalaria, FalciparumPlasmodium falciparumRNA, RibosomalTranscription, GeneticAnimalsDNA, RibosomalEpigenesis, GeneticGlycolysisHost-Parasite InteractionsHumansMitochondriaNADProtozoan ProteinsSirtuin 2SirtuinsChromatinDNA, RibosomalNADProtozoan ProteinsRNA, RibosomalSirtuin 2Sirtuins

Identifiers

PMID41419483
PMCPMC12824157

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.