Evidence map›Paper›PMID 39969508›Full record

ArticleeLife2025

SMARCAD1 and TOPBP1 contribute to heterochromatin maintenance at the transition from the 2C-like to the pluripotent state.

Ruben Sebastian-Perez, Shoma Nakagawa, Xiaochuan Tu, Sergi Aranda, Martina Pesaresi, Pablo Aurelio Gomez-Garcia, Marc Alcoverro-Bertran, Jose Luis Gomez-Vazquez, Davide Carnevali, Eva Borràs and 7 more

Abstract read
In one paragraph

Article in eLife, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.

0numbers the graph read from it
0cells of the map it votes in
2citing 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

2 citing papers in PubMed.

  1. Article
  2. 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

17 authors.

Ruben Sebastian-Perez *Centre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.ORCID https://orcid.org/0000-0001-7209-7612
Shoma Nakagawa *Centre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Xiaochuan Tu *Centre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Sergi ArandaCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.ORCID https://orcid.org/0000-0003-3853-430X
Martina PesaresiCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Pablo Aurelio Gomez-GarciaCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Marc Alcoverro-BertranCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Jose Luis Gomez-VazquezCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Davide CarnevaliCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Eva BorràsCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Eduard SabidóCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Laura MartinCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Malka Nissim-RafiniaDepartment of Genetics, The Alexander Silberman Institute of Life Sciences, Edmond J. Safra Campus, The Hebrew University of Jerusalem, Jerusalem, Israel.
Eran MeshorerDepartment of Genetics, The Alexander Silberman Institute of Life Sciences, Edmond J. Safra Campus, The Hebrew University of Jerusalem, Jerusalem, Israel.
Maria Victoria NeguemborCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Luciano Di CroceCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.
Maria Pia CosmaCentre for Genomic Regulation (CRG), The Barcelona Institute of Science and Technology, Barcelona, Spain.ORCID https://orcid.org/0000-0003-4207-5097

Funding

Agència de Gestió d'Ajuts Universitaris i de Recerca 2021-SGR2021-01300Departament d'Empresa i Coneixement, Generalitat de Catalunya 2018FI_B_00637FP7 People: Marie-Curie Actions 608959Fundació la Marató de TV3 202027-10Horizon 2020 Framework Programme 686637Horizon 2020 Framework Programme 964342Instituto de Salud Carlos III PI19/01814Instituto de Salud Carlos III PT17/0019'la Caixa' Foundation LCF/BQ/DR20/11790016Ministerio de Ciencia e Innovación 2014ES05SFOP007Ministerio de Ciencia e Innovación BFU2017-86760-P/AEI/FEDERMinisterio de Ciencia e Innovación Juan de la Cierva-Incorporación 2017Ministerio de Ciencia e Innovación PID2020-114080GB I00/AEI/10.13039/501100011033Ministerio de Ciencia e Innovación PRE2018-085107Ministerio de Ciencia, Innovación y Universidades RYC-2018-025002-IMinisterio de Economía y Competitividad BES-2015-072802Ministerio de Economía y Competitividad PID2019-108322GB-100National Natural Science Foundation of China 31971177
6 · The paper itself

Abstract

Chromocenters are established after the 2-cell (2C) stage during mouse embryonic development, but the factors that mediate chromocenter formation remain largely unknown. To identify regulators of 2C heterochromatin establishment in mice, we generated an inducible system to convert embryonic stem cells (ESCs) to 2C-like cells. This conversion is marked by a global reorganization and dispersion of H3K9me3-heterochromatin foci, which are then reversibly formed upon re-entry into pluripotency. By profiling the chromatin-bound proteome (chromatome) through genome capture of ESCs transitioning to 2C-like cells, we uncover chromatin regulators involved in de novo heterochromatin formation. We identified TOPBP1 and investigated its binding partner SMARCAD1. SMARCAD1 and TOPBP1 associate with H3K9me3-heterochromatin in ESCs. Interestingly, the nuclear localization of SMARCAD1 is lost in 2C-like cells. SMARCAD1 or TOPBP1 depletion in mouse embryos leads to developmental arrest, reduction of H3K9me3, and remodeling of heterochromatin foci. Collectively, our findings contribute to comprehending the maintenance of chromocenters during early development.

Indexed as

Carrier ProteinsDNA-Binding ProteinsDNA HelicasesEmbryonic Stem CellsHeterochromatinNuclear ProteinsPluripotent Stem CellsAnimalsEmbryonic DevelopmentHistonesMiceCarrier ProteinsDNA-Binding ProteinsDNA HelicasesHeterochromatinHistonesNuclear Proteins2C-like cellschromatindevelopmental biologyembryonic stem cellsmouseproteomicsregenerative medicinestem cells

Identifiers

PMID39969508
PMCPMC11839162

What OpenQuestion holds

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Registered trials

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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.