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@ARTICLE{Rbsam:1007690,
      author       = {Rübsam, Matthias and Püllen, Robin and Tellkamp, Frederik
                      and Bianco, Alessandra and Peskoller, Marc and Bloch,
                      Wilhelm and Green, Kathleen J. and Merkel, Rudolf and
                      Hoffmann, Bernd and Wickström, Sara A. and Niessen, Carien
                      M.},
      title        = {{P}olarity signaling balances epithelial contractility and
                      mechanical resistance},
      journal      = {Scientific reports},
      volume       = {13},
      number       = {1},
      issn         = {2045-2322},
      address      = {[London]},
      publisher    = {Macmillan Publishers Limited, part of Springer Nature},
      reportid     = {FZJ-2023-02164},
      pages        = {7743},
      year         = {2023},
      abstract     = {Epithelia maintain a functional barrier during tissue
                      turnover while facing varying mechanical stress. This
                      maintenance requires both dynamic cell rearrangements driven
                      by actomyosin-linked intercellular adherens junctions and
                      ability to adapt to and resist extrinsic mechanical forces
                      enabled by keratin filament-linked desmosomes. How these two
                      systems crosstalk to coordinate cellular movement and
                      mechanical resilience is not known. Here we show that in
                      stratifying epithelia the polarity protein aPKCλ controls
                      the reorganization from stress fibers to cortical actomyosin
                      during differentiation and upward movement of cells. Without
                      aPKC, stress fibers are retained resulting in increased
                      contractile prestress. This aberrant stress is
                      counterbalanced by reorganization and bundling of keratins,
                      thereby increasing mechanical resilience. Inhibiting
                      contractility in aPKCλ−/− cells restores normal
                      cortical keratin networks but also normalizes resilience.
                      Consistently, increasing contractile stress is sufficient to
                      induce keratin bundling and enhance resilience, mimicking
                      aPKC loss. In conclusion, our data indicate that keratins
                      sense the contractile stress state of stratified epithelia
                      and balance increased contractility by mounting a protective
                      response to maintain tissue integrity.},
      cin          = {IBI-2},
      ddc          = {600},
      cid          = {I:(DE-Juel1)IBI-2-20200312},
      pnm          = {5243 - Information Processing in Distributed Systems
                      (POF4-524) / DFG project 273723265 - Mechanosensation und
                      Mechanoreaktion in epidermalen Systemen},
      pid          = {G:(DE-HGF)POF4-5243 / G:(GEPRIS)273723265},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {37173371},
      UT           = {WOS:000992578000016},
      doi          = {10.1038/s41598-023-33485-5},
      url          = {https://juser.fz-juelich.de/record/1007690},
}