Evidence map›Paper›PMID 32302590›Full record

ArticleCell2020

Heterochromatin-Driven Nuclear Softening Protects the Genome against Mechanical Stress-Induced Damage.

Michele M Nava, Yekaterina A Miroshnikova, Leah C Biggs, Daniel B Whitefield, Franziska Metge, Jorge Boucas, Helena Vihinen, Eija Jokitalo, Xinping Li, Juan Manuel García Arcos and 5 more

Abstract read
In one paragraph

Article in Cell, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 360 papers.

0numbers the graph read from it
0cells of the map it votes in
360citing 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

360 citing papers in PubMed.

  1. Review
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  4. Article
  5. Review
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  7. Article
  8. Mechanical regulation of cell memory.Nature structural & molecular biology · 2026
    Review
  9. Article
  10. Article
  11. Article
  12. Review
  13. Article
  14. Article
  15. Mechanics of compression-driven morphogenesis.Development (Cambridge, England) · 2026
    Review
  16. Article
  17. Article
  18. Article
  19. Article
  20. Review

300 more citing papers are in PubMed but not listed here.

4 · The record

Corrections and comments

5 · Who and what money

Authors and funding

15 authors.

Michele M NavaHelsinki Institute of Life Science, Biomedicum Helsinki, University of Helsinki, 00290 Helsinki, Finland; Wihuri Research Institute, Biomedicum Helsinki, University of Helsinki, 00290 Helsinki, Finland; Stem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, 00290 Helsinki, Finland; Max Planck Institute for Biology of Ageing, 50931 Cologne, Germany; Cologne Excellence Cluster for Stress Responses in Ageing-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany.
Yekaterina A MiroshnikovaHelsinki Institute of Life Science, Biomedicum Helsinki, University of Helsinki, 00290 Helsinki, Finland; Wihuri Research Institute, Biomedicum Helsinki, University of Helsinki, 00290 Helsinki, Finland; Stem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, 00290 Helsinki, Finland; Max Planck Institute for Biology of Ageing, 50931 Cologne, Germany; Cologne Excellence Cluster for Stress Responses in Ageing-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany.
Leah C BiggsHelsinki Institute of Life Science, Biomedicum Helsinki, University of Helsinki, 00290 Helsinki, Finland; Wihuri Research Institute, Biomedicum Helsinki, University of Helsinki, 00290 Helsinki, Finland; Stem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, 00290 Helsinki, Finland.
Daniel B WhitefieldDepartment of Biomedical Engineering, Carnegie Mellon University, Pittsburgh, PA 15213, USA.
Franziska MetgeMax Planck Institute for Biology of Ageing, 50931 Cologne, Germany.
Jorge BoucasMax Planck Institute for Biology of Ageing, 50931 Cologne, Germany.
Helena VihinenElectron Microscopy Unit, Institute of Biotechnology, HiLIFE, University of Helsinki, 00014 Helsinki, Finland.
Eija JokitaloElectron Microscopy Unit, Institute of Biotechnology, HiLIFE, University of Helsinki, 00014 Helsinki, Finland.
Xinping LiMax Planck Institute for Biology of Ageing, 50931 Cologne, Germany.
Juan Manuel García ArcosInstitut Curie, PSL Research University, CNRS, UMR 144 and Institut Pierre-Gilles de Gennes, PSL Research University, 75005 Paris, France.
Bernd HoffmannForschungszentrum Jülich, Institute of Biological Information Processing-2: Mechanobiology, 52428 Jülich, Germany.
Rudolf MerkelForschungszentrum Jülich, Institute of Biological Information Processing-2: Mechanobiology, 52428 Jülich, Germany.
Carien M NiessenCologne Excellence Cluster for Stress Responses in Ageing-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany; Department of Dermatology, Center for Molecular Medicine, University of Cologne, 50931 Cologne, Germany.
Kris Noel DahlDepartment of Biomedical Engineering, Carnegie Mellon University, Pittsburgh, PA 15213, USA; Department of Chemical Engineering, Carnegie Mellon University, Pittsburgh, PA 15213, USA.
Sara A WickströmHelsinki Institute of Life Science, Biomedicum Helsinki, University of Helsinki, 00290 Helsinki, Finland; Wihuri Research Institute, Biomedicum Helsinki, University of Helsinki, 00290 Helsinki, Finland; Stem Cells and Metabolism Research Program, Faculty of Medicine, University of Helsinki, 00290 Helsinki, Finland; Max Planck Institute for Biology of Ageing, 50931 Cologne, Germany; Cologne Excellence Cluster for Stress Responses in Ageing-Associated Diseases (CECAD), University of Cologne, 50931 Cologne, Germany. Electronic address: sara.wickstrom@helsinki.fi.

Funding

Training in Biomechanics in Regenerative MedicineT32EB003392 · NIBIB · UNIVERSITY OF PITTSBURGH AT PITTSBURGH · PI WOO, SAVIO L-Y. · 2005 to 2020
$4.0M
NIBIB NIH HHS T32 EB003392
6 · The paper itself

Abstract

Tissue homeostasis requires maintenance of functional integrity under stress. A central source of stress is mechanical force that acts on cells, their nuclei, and chromatin, but how the genome is protected against mechanical stress is unclear. We show that mechanical stretch deforms the nucleus, which cells initially counteract via a calcium-dependent nuclear softening driven by loss of H3K9me3-marked heterochromatin. The resulting changes in chromatin rheology and architecture are required to insulate genetic material from mechanical force. Failure to mount this nuclear mechanoresponse results in DNA damage. Persistent, high-amplitude stretch induces supracellular alignment of tissue to redistribute mechanical energy before it reaches the nucleus. This tissue-scale mechanoadaptation functions through a separate pathway mediated by cell-cell contacts and allows cells/tissues to switch off nuclear mechanotransduction to restore initial chromatin state. Our work identifies an unconventional role of chromatin in altering its own mechanical state to maintain genome integrity in response to deformation.

Indexed as

AnimalsCell LineCell NucleusChromatinHeterochromatinHumansMaleMechanoreceptorsMechanotransduction, CellularMesenchymal Stem CellsMiceStress, MechanicalChromatinHeterochromatinchromatinDNA damageheterochromatinmechanoprotectionmechanotransductionnuclear architecturenuclear laminanuclear mechanicsstem cells

Identifiers

PMID32302590
PMCPMC7237863

What OpenQuestion holds

Textmetadata
LicenceCC BY-NC-ND
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.