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Nuclear envelope deformation controls cell cycle progression in response to mechanical force
Author(s) -
Aureille Julien,
BuffièreRibot Valentin,
Harvey Ben E,
Boyault Cyril,
Pernet Lydia,
Andersen Tomas,
Bacola Gregory,
Balland Martial,
Fraboulet Sandrine,
Van Landeghem Laurianne,
Guilluy Christophe
Publication year - 2019
Publication title -
embo reports
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 4.584
H-Index - 184
eISSN - 1469-3178
pISSN - 1469-221X
DOI - 10.15252/embr.201948084
Subject(s) - lamin , nuclear lamina , myosin , microbiology and biotechnology , cell nucleus , nucleus , nuclear protein , biology , transcription factor , flattening , nuclear transport , biophysics , gene , physics , genetics , astronomy
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 AP 1, leading to transcriptional induction of target genes that promote G1 to S transition. In addition, we found that nuclear flattening mediates TEAD and AP 1 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.