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EMBO Rep. 2019 Sep;20(9):e48084. doi: 10.15252/embr.201948084. Epub 2019 Aug 1.

Nuclear envelope deformation controls cell cycle progression in response to mechanical force.

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Institute for Advanced Biosciences, Centre de recherche UGA - INSERM U1209 - CNRS UMR 5309, Grenoble, France.
Laboratoire Interdisciplinaire de Physique, UMR CNRS 5588, Université Grenoble Alpes, Grenoble, France.
Department of Molecular Biomedical Sciences, College of Veterinary Medicine, North Carolina State University, Raleigh, NC, USA.


The shape of the cell nucleus can vary considerably during developmental and pathological processes; however, the impact of nuclear morphology on cell behavior is not known. Here, we observed that the nuclear envelope flattens as cells transit from G1 to S phase and inhibition of myosin II prevents nuclear flattening and impedes progression to S phase. Strikingly, we show that applying compressive force on the nucleus in the absence of myosin II-mediated tension is sufficient to restore G1 to S transition. Using a combination of tools to manipulate nuclear morphology, we observed that nuclear flattening activates a subset of transcription factors, including TEAD and AP1, leading to transcriptional induction of target genes that promote G1 to S transition. In addition, we found that nuclear flattening mediates TEAD and AP1 activation in response to ROCK-generated contractility or cell spreading. Our results reveal that the nuclear envelope can operate as a mechanical sensor whose deformation controls cell growth in response to tension.


TEAD ; AP1; c-Jun; mechanotransduction; nuclear envelope

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