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

Julien Aureille1, Valentin Buffière-Ribot1, Ben E Harvey1

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Cell nucleus shape changes are crucial for cell cycle progression. Nuclear flattening, driven by mechanical forces, activates transcription factors, promoting cell growth and the G1 to S phase transition.

Keywords:
TEADAP1c-Junmechanotransductionnuclear envelope

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Area of Science:

  • Cell Biology
  • Mechanobiology
  • Molecular Biology

Background:

  • Nuclear morphology varies during development and disease.
  • The functional impact of nuclear shape on cell behavior remains largely unknown.

Purpose of the Study:

  • To investigate the role of nuclear morphology in cell cycle progression.
  • To elucidate the mechanisms by which nuclear shape influences cell behavior.

Main Methods:

  • Observation of nuclear envelope flattening during the G1 to S phase transition.
  • Inhibition of myosin II to study its effect on nuclear shape and cell cycle.
  • Application of compressive force to the nucleus to assess its impact on cell cycle progression.
  • Manipulation of nuclear morphology using various tools.
  • Analysis of transcription factor activation (TEAD, AP1) and target gene induction.

Main Results:

  • Nuclear envelope flattening occurs as cells transition from G1 to S phase.
  • Myosin II inhibition prevents nuclear flattening and delays G1 to S progression.
  • External compressive force can restore G1 to S transition even without myosin II.
  • Nuclear flattening activates transcription factors TEAD and AP1, inducing genes that promote G1 to S transition.
  • Nuclear flattening mediates TEAD and AP1 activation downstream of ROCK contractility and cell spreading.

Conclusions:

  • The nuclear envelope functions as a mechanical sensor.
  • Nuclear deformation regulates cell growth in response to mechanical tension.
  • Nuclear shape is a critical regulator of cell cycle progression.