Evidence map›Paper›PMID 39191776›Full record

ArticleNature communications2024

Developmental signals control chromosome segregation fidelity during pluripotency and neurogenesis by modulating replicative stress.

Anchel de Jaime-Soguero, Janina Hattemer, Anja Bufe, Alexander Haas, Jeroen van den Berg, Vincent van Batenburg, Biswajit Das, Barbara di Marco, Stefania Androulaki, Nicolas Böhly and 18 more

Abstract read
In one paragraph

Article in Nature communications, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.

0numbers the graph read from it
0cells of the map it votes in
6citing 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

6 citing papers in PubMed.

  1. Article
  2. Article
  3. Article
  4. Morphogen Gradients as Drivers of Mosaicism During Early Human Development.BioEssays : news and reviews in molecular, cellular and developmental biology · 2026
    Review
  5. Article
  6. 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

28 authors.

Anchel de Jaime-Soguero *Centre for Organismal Studies (COS), Heidelberg University, Heidelberg, Germany.ORCID 0000-0002-9358-3676
Janina Hattemer *Centre for Organismal Studies (COS), Heidelberg University, Heidelberg, Germany.
Anja BufeCentre for Organismal Studies (COS), Heidelberg University, Heidelberg, Germany.ORCID 0000-0003-3427-3413
Alexander HaasDepartment of Molecular Oncology, Section for Cellular Oncology, University Medical Center Göttingen (UMG), Göttingen, Germany.
Jeroen van den BergOncode Institute, Utrecht, The Netherlands.
Vincent van BatenburgOncode Institute, Utrecht, The Netherlands.
Biswajit DasDepartment of Medical Biochemistry and Biophysics, Umeå University, Umeå, Sweden.
Barbara di MarcoDepartment of Clinical Neurobiology, University Hospital Heidelberg and German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID 0000-0003-1751-7455
Stefania AndroulakiCentre for Organismal Studies (COS), Heidelberg University, Heidelberg, Germany.
Nicolas BöhlyDepartment of Molecular Oncology, Section for Cellular Oncology, University Medical Center Göttingen (UMG), Göttingen, Germany.ORCID 0000-0003-0988-7720
Jonathan J M LandryGenomics Core Facility, European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.
Brigitte SchoellInstitute of Human Genetics, Heidelberg University, Heidelberg, Germany.
Viviane S RosaMRC Laboratory of Molecular Biology, Cambridge, UK.
Laura VillacortaGenomics Core Facility, European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.
Yagmur BaskanCentre for Organismal Studies (COS), Heidelberg University, Heidelberg, Germany.
Marleen TrappSchaller Research Group, German Cancer Research Center (DKFZ), Heidelberg, Germany.
Vladimir BenesGenomics Core Facility, European Molecular Biology Laboratory (EMBL), Heidelberg, Germany.ORCID 0000-0002-0352-2547
Andrei ChabesDepartment of Medical Biochemistry and Biophysics, Umeå University, Umeå, Sweden.ORCID 0000-0003-1708-8259
Marta ShahbaziMRC Laboratory of Molecular Biology, Cambridge, UK.ORCID 0000-0002-1599-5747
Anna JauchInstitute of Human Genetics, Heidelberg University, Heidelberg, Germany.
Ulrike EngelNikon Imaging Center at the University of Heidelberg, Bioquant, Heidelberg, Germany.ORCID 0000-0002-6953-6845
Annarita PatriziSchaller Research Group, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID 0000-0002-7004-5664
Rocio SotilloDivision of Molecular Thoracic Oncology, German Cancer Research Center (DKFZ), Heidelberg, Germany.ORCID 0000-0002-0855-7917
Alexander van OudenaardenOncode Institute, Utrecht, The Netherlands.ORCID 0000-0002-9442-3551
Josephine BageritzCentre for Organismal Studies (COS), Heidelberg University, Heidelberg, Germany.ORCID 0000-0002-9531-0452
Julieta AlfonsoDepartment of Clinical Neurobiology, University Hospital Heidelberg and German Cancer Research Center (DKFZ), Heidelberg, Germany.
Holger BastiansDepartment of Molecular Oncology, Section for Cellular Oncology, University Medical Center Göttingen (UMG), Göttingen, Germany.ORCID 0000-0001-7915-3648
Sergio P AcebrónCentre for Organismal Studies (COS), Heidelberg University, Heidelberg, Germany. sergio.acebron@cos.uni-heidelberg.de.ORCID 0000-0002-7694-2497

Funding

Medical Research Council MC_UP_1201/24
6 · The paper itself

Abstract

Human development relies on the correct replication, maintenance and segregation of our genetic blueprints. How these processes are monitored across embryonic lineages, and why genomic mosaicism varies during development remain unknown. Using pluripotent stem cells, we identify that several patterning signals-including WNT, BMP, and FGF-converge into the modulation of DNA replication stress and damage during S-phase, which in turn controls chromosome segregation fidelity in mitosis. We show that the WNT and BMP signals protect from excessive origin firing, DNA damage and chromosome missegregation derived from stalled forks in pluripotency. Cell signalling control of chromosome segregation declines during lineage specification into the three germ layers, but re-emerges in neural progenitors. In particular, we find that the neurogenic factor FGF2 induces DNA replication stress-mediated chromosome missegregation during the onset of neurogenesis, which could provide a rationale for the elevated chromosomal mosaicism of the developing brain. Our results highlight roles for morphogens and cellular identity in genome maintenance that contribute to somatic mosaicism during mammalian development.

Indexed as

Chromosome SegregationDNA ReplicationNeurogenesisAnimalsBone Morphogenetic ProteinsDNA DamageFibroblast Growth Factor 2HumansMiceMitosisMosaicismPluripotent Stem CellsSignal TransductionBone Morphogenetic ProteinsFibroblast Growth Factor 2

Identifiers

PMID39191776
PMCPMC11350214

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.