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@ARTICLE{Nava:875202,
      author       = {Nava, Michele M. and Miroshnikova, Yekaterina A. and Biggs,
                      Leah C. and Whitefield, Daniel B. and Metge, Franziska and
                      Boucas, Jorge and Vihinen, Helena and Jokitalo, Eija and Li,
                      Xinping and García Arcos, Juan Manuel and Hoffmann, Bernd
                      and Merkel, Rudolf and Niessen, Carien M. and Dahl, Kris
                      Noel and Wickström, Sara A.},
      title        = {{H}eterochromatin-{D}riven {N}uclear {S}oftening {P}rotects
                      the {G}enome against {M}echanical {S}tress-{I}nduced
                      {D}amage},
      journal      = {Cell},
      volume       = {181},
      number       = {4},
      issn         = {0092-8674},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {FZJ-2020-01870},
      pages        = {800-817},
      year         = {2020},
      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.},
      cin          = {IBI-2},
      ddc          = {610},
      cid          = {I:(DE-Juel1)IBI-2-20200312},
      pnm          = {552 - Engineering Cell Function (POF3-552)},
      pid          = {G:(DE-HGF)POF3-552},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:32302590},
      UT           = {WOS:000533623900008},
      doi          = {10.1016/j.cell.2020.03.052},
      url          = {https://juser.fz-juelich.de/record/875202},
}