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Moving Cell Boundaries Drive Nuclear Shaping during Cell Spreading.

Yuan Li1, David Lovett1, Qiao Zhang1

  • 1Department of Chemical Engineering, University of Florida, Gainesville, Florida.

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|August 20, 2015
PubMed
Summary

Cell spreading drives nuclear shape changes. This study reveals cell spreading is necessary and sufficient for nuclear flattening, independent of myosin activity, using a mechanical model.

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Area of Science:

  • Cell biology
  • Biophysics
  • Mechanobiology

Background:

  • Nuclear shape is altered in pathologies, but mechanisms of nuclear shaping are unclear.
  • Understanding nuclear shape regulation is crucial for cell biology and disease research.

Purpose of the Study:

  • To investigate the dynamics of nuclear shaping during cell spreading.
  • To determine the mechanical factors driving nuclear shape changes in NIH3T3 fibroblasts.

Main Methods:

  • Live-cell imaging of NIH3T3 fibroblasts during cell spreading.
  • Pharmacological inhibition of cytoskeletal components (actin, myosin).
  • Computational modeling of cell and nuclear mechanics.

Main Results:

  • Nuclear flattening correlated with cell spreading, reaching steady-state values.
  • Actomyosin, microtubules, intermediate filaments, and LINC complex were dispensable for flattening if cell spreading occurred.
  • Inhibition of actin polymerization or myosin activity affected cell spreading and nuclear flattening.

Conclusions:

  • Cell spreading is the primary driver for nuclear flattening under various conditions.
  • A simple mechanical model explains nuclear shape establishment via frictional stress transmission.
  • Cell spreading is necessary and sufficient for nuclear shape regulation.