2019 journal article
Nuclear envelope deformation controls cell cycle progression in response to mechanical force
EMBO REPORTS, 20(9).
author keywords: AP1; c-Jun; mechanotransduction; nuclear envelope; TEAD
MeSH headings : Cell Cycle / genetics; Cell Cycle / physiology; Cell Division / genetics; Cell Division / physiology; Cell Line; Cell Nucleus / genetics; Cell Nucleus / metabolism; Flow Cytometry; G1 Phase / genetics; G1 Phase / physiology; HeLa Cells; Humans; Mechanotransduction, Cellular / genetics; Mechanotransduction, Cellular / physiology; Microscopy, Atomic Force; Nuclear Envelope / genetics; Nuclear Envelope / metabolism; Plasmids / genetics; RNA, Small Interfering / genetics; RNA, Small Interfering / metabolism; S Phase / genetics; S Phase / physiology; Transcription Factors / genetics; Transcription Factors / metabolism
TL;DR:
It is shown that applying compressive force on the nucleus in the absence of myosin II‐mediated tension is sufficient to restore G1 to S transition and reveal that the nuclear envelope can operate as a mechanical sensor whose deformation controls cell growth in response to tension.
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UN Sustainable Development Goal Categories
3. Good Health and Well-being
(Web of Science)
Source: Web Of Science
Added: August 19, 2019
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.