Evidence map›Paper›PMID 41023488›Full record

ArticleNature cell biology2025

Mechano-osmotic signals control chromatin state and fate transitions in pluripotent stem cells.

Kaitlin P McCreery, Aki Stubb, Rebecca Stephens, Nadezda A Fursova, Andrew Cook, Kai Kruse, Anja Michelbach, Leah C Biggs, Adib Keikhosravi, Sonja Nykänen and 8 more

Abstract read
In one paragraph

Article in Nature cell biology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.

0numbers the graph read from it
0cells of the map it votes in
22citing 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

22 citing papers in PubMed.

  1. Review
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  11. Morphogenic colloids.Nature communications · 2026
    Article
  12. Article
  13. Review
  14. Review
  15. Article
  16. Review
  17. Article
  18. Stress transmission towards the nucleus of the cell.Frontiers in cell and developmental biology · 2026
    Review
  19. Forcing cell fate.Nature cell biology · 2025
    Article
  20. Article
4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

18 authors.

Kaitlin P McCreery *Department of Cell and Tissue Dynamics, Max Planck Institute for Molecular Biomedicine, Münster, Germany.ORCID http://orcid.org/0000-0002-0420-2828
Aki Stubb *Department of Cell and Tissue Dynamics, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
Rebecca StephensLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
Nadezda A FursovaSystems Biology of Gene Expression, National Cancer Institute, National Institute of Health, Bethesda, MD, USA.
Andrew CookLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA.
Kai KruseBioinformatics Service Unit, Max Planck Institute for Molecular Biomedicine, Münster, Germany.ORCID http://orcid.org/0000-0002-7951-7357
Anja MichelbachDepartment of Cell and Tissue Dynamics, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
Leah C BiggsDepartment of Cell and Tissue Dynamics, Max Planck Institute for Molecular Biomedicine, Münster, Germany.
Adib KeikhosraviHigh-Throughput Imaging Facility, National Cancer Institute, National Institute of Health, Bethesda, MD, USA.
Sonja NykänenStem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Roosa PulkkanenStem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Christel Hydén-GranskogHelsinki University Hospital, Reproductive Medicine Unit, Helsinki, Finland.
Jizhong ZouiPSC Core, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD, USA.
Jan-Wilm LackmannCECAD Research Center, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0001-8182-8034
Carien M NiessenDepartment Cell Biology of the Skin, Cologne Excellence Cluster on Cellular Stress Responses in Aging Associated Diseases (CECAD), Center for Molecular Medicine Cologne, University Hospital Cologne, University of Cologne, Cologne, Germany.ORCID http://orcid.org/0000-0002-4892-9391
Sanna VuoristoStem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, Helsinki, Finland.
Yekaterina A MiroshnikovaLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, USA. kate@mpi-muenster.mpg.de.
Sara A WickströmDepartment of Cell and Tissue Dynamics, Max Planck Institute for Molecular Biomedicine, Münster, Germany. sara.wickstrom@mpi-muenster.mpg.de.ORCID http://orcid.org/0000-0001-6383-6292

Funding

Academy of Finland (Suomen Akatemia) Center of Excellence BarrierForceAcademy of Finland (Suomen Akatemia) Postdoctoral FellowshipAcademy of Finland (Suomen Akatemia) Research Fellowship 353549Academy of Finland (Suomen Akatemia) R'Life Programme consortium NucleoMechDeutsche Forschungsgemeinschaft (German Research Foundation) FOR 5504
6 · The paper itself

Abstract

Acquisition of specific cell shapes and morphologies is a central component of cell fate transitions. Although signalling circuits and gene regulatory networks that regulate pluripotent stem cell differentiation have been intensely studied, how these networks are integrated in space and time with morphological changes and mechanical deformations to control state transitions remains a fundamental open question. Here we focus on two distinct models of pluripotency, preimplantation inner cell mass cells of human embryos and primed pluripotent stem cells, to discover that cell fate transitions associate with rapid, compaction-triggered changes in nuclear shape and volume. These phenotypical changes and the associated active deformation of the nuclear envelope arise from growth factor signalling-controlled changes in cytoskeletal confinement and chromatin mechanics. The resulting osmotic stress state triggers global transcriptional repression, macromolecular crowding and remodelling of nuclear condensates that prime chromatin for a cell fate transition by attenuating repression of differentiation genes. However, while this mechano-osmotic chromatin priming has the potential to accelerate fate transitions and differentiation, sustained biochemical signals are required for robust induction of specific lineages. Our findings uncover a critical mechanochemical feedback mechanism that integrates nuclear mechanics, shape and volume with biochemical signalling and chromatin state to control cell fate transition dynamics.

Indexed as

Biomolecular CondensatesBlastocystCell LineageChromatinMechanotransduction, CellularOsmotic PressurePluripotent Stem CellsCell Cycle ProteinsCell DifferentiationCell NucleusCell Nucleus ShapeChromatin Assembly and DisassemblyFeedback, PhysiologicalGene Expression Regulation, DevelopmentalHumansPolycomb Repressive Complex 1CBX2 protein, humanCell Cycle ProteinsChromatinPolycomb Repressive Complex 1PRC1 protein, human

Identifiers

PMID41023488
PMCPMC12527910

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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.