Evidence map›Paper›PMID 39372762›Full record

ArticlebioRxiv : the preprint server for biology2024

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 7 more

Abstract readPreprint
In one paragraph

Article in bioRxiv : the preprint server for biology, 2024. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Not yet cited in PubMed.

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

0 citing papers in PubMed.

No citing paper in PubMed yet.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

17 authors.

Kaitlin P McCreeryDepartment of Cell and Tissue Dynamics, Max Planck Institute for Molecular Biomedicine, 48149 Münster, Germany.
Aki StubbDepartment of Cell and Tissue Dynamics, Max Planck Institute for Molecular Biomedicine, 48149 Münster, Germany.
Rebecca StephensLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Nadezda A FursovaSystem Biology of Gene Expression, National Cancer Institute, National Institute of Health, Bethesda, MD 20892.
Andrew CookLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Kai KruseBioinformatics Service Unit, Max Planck Institute for Molecular Biomedicine, 48149 Münster, Germany.
Anja MichelbachDepartment of Cell and Tissue Dynamics, Max Planck Institute for Molecular Biomedicine, 48149 Münster, Germany.
Leah C BiggsDepartment of Cell and Tissue Dynamics, Max Planck Institute for Molecular Biomedicine, 48149 Münster, Germany.
Adib KeikhosraviHigh-Throughput Imaging Facility, National Cancer Institute, National Institute of Health, Bethesda, MD 20892.
Sonja NykänenStem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, 00290 Helsinki Finland.
Christel Hydén-GranskogHelsinki University Hospital, Reproductive Medicine Unit, P.O. Box 150, 00029 HUS, Helsinki, Finland.
Jizhong ZouiPSC Core, National Heart, Lung, and Blood Institute, National Institutes of Health, Bethesda, MD 20892, USA.
Jan-Wilm LackmannCECAD Research Center, University of Cologne, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
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, Joseph-Stelzmann-Str. 26, 50931 Cologne, Germany.
Sanna VuoristoStem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, 00290 Helsinki Finland.
Yekaterina A MiroshnikovaLaboratory of Molecular Biology, National Institute of Diabetes and Digestive and Kidney Diseases, National Institutes of Health, Bethesda, MD, 20892, USA.
Sara A WickströmDepartment of Cell and Tissue Dynamics, Max Planck Institute for Molecular Biomedicine, 48149 Münster, Germany.

Funding

No grant is acknowledged in the PubMed record.

6 · The paper itself

Abstract

Acquisition of specific cell shapes and morphologies is a central component of cell fate transitions. Although signaling 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 transitions and mechanical deformations to control state transitions remains a fundamental open question. Here, we focus on two distinct models of pluripotency, primed pluripotent stem cells and pre-implantation inner cell mass cells of human embryos to discover that cell fate transitions associate with rapid changes in nuclear shape and volume which collectively alter the nuclear mechanophenotype. Mechanistic studies in human induced pluripotent stem cells further reveal that these phenotypical changes and the associated active fluctuations of the nuclear envelope arise from growth factor signaling-controlled changes in chromatin mechanics and cytoskeletal confinement. These collective mechano-osmotic changes trigger global transcriptional repression and a condensation-prone environment that primes 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 signaling and chromatin state to control cell fate transition dynamics.

Identifiers

PMID39372762
PMCPMC11451594

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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.