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High-resolution Imaging of Nuclear Dynamics in Live Cells under Uniaxial Tensile Strain
Published on: June 2, 2019
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Rupture Dynamics and Chromatin Herniation in Deformed Nuclei
Dan Deviri1, Dennis E Discher2, Sam A Safran1
1Department of Materials and Interfaces, Weizmann Institute of Science, Rehovot, Israel.
Biophysical Journal
|September 7, 2017
Summary
Cell nuclei can rupture when squeezed through tight spaces, potentially causing cell death. This study models nuclear envelope healing and chromatin leakage, linking it to lamin protein levels.
Area of Science:
- Cell biology
- Biophysics
- Mechanobiology
Background:
- Cell migration through confined environments is crucial for physiological and pathological processes.
- Nuclear envelope rupture during migration can lead to cell death if not repaired.
- The nuclear envelope's mechanical properties, influenced by lamin composition, are key to its integrity.
Purpose of the Study:
- To develop a viscoelastic model for nuclear envelope hole evolution after deformation.
- To investigate chromatin herniation through nuclear envelope defects.
- To explore the relationship between lamin expression and nuclear envelope self-healing.
Main Methods:
- Development of a viscoelastic mechanical model for the nuclear lamina.
- Simulation of hole nucleation and evolution in the nuclear envelope.
- Estimation of chromatin herniation dynamics.
Main Results:
- The model describes the self-healing mechanism of the nuclear envelope after mechanical stress.
- Chromatin herniation is predicted to occur through mechanically induced holes.
- Lamin expression levels are correlated with the extent of chromatin herniation.
Conclusions:
- The nuclear envelope possesses self-healing capabilities crucial for cell survival during migration.
- Lamin composition plays a significant role in regulating nuclear envelope integrity and preventing chromatin loss.
- This model provides insights into the biomechanics of the nucleus and its response to mechanical stress.
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