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Updated: Jun 29, 2025

Analyzing Cell Surface Adhesion Remodeling in Response to Mechanical Tension Using Magnetic Beads
Published on: March 8, 2017
Reverse Mechanotransduction: Driving Chromatin Compaction to Decompaction Increases Cell Adhesion Strength and
Julie Buisson1, Xinyu Zhang2, Tomaso Zambelli2
1Inserm UMR_S 1121, CNRS EMR 7003, Université de Strasbourg, Biomaterials and Bioengineering, Centre de Recherche en Biomédecine de Strasbourg, Strasbourg F-67000, France.
Chromatin remodeling impacts cell adhesion strength by altering nuclear volume and cytoskeleton. This study reveals a reverse mechanotransduction pathway from the nucleus to the cell surface, regulating cell shape and adhesion.
Area of Science:
- Cell Biology
- Biophysics
- Mechanobiology
Background:
- Mechanical signals influence cell function through mechanotransduction.
- The role of chromatin remodeling in regulating cell adhesion strength is largely unexplored.
Purpose of the Study:
- To investigate whether chromatin remodeling influences cell adhesion strength.
- To elucidate the pathway by which nuclear changes affect cell surface properties.
Main Methods:
- Fluidic force microscopy was employed to measure epithelial cell adhesion strength.
- Chromatin compaction was induced via histone acetyltransferase inhibition and ATP depletion.
- Chromatin decompaction was achieved by removing chromatin remodelers.
Main Results:
- Chromatin compaction reduced nuclear volume, disrupted the actin cytoskeleton and focal adhesions, and decreased cell adhesion strength and traction force.
- Chromatin decompaction restored cell shape, adhesion strength, and traction force.
- Cells utilized depolymerized proteins to restore focal adhesions during decompaction.
Conclusions:
- Chromatin remodeling shapes cells and regulates adhesion strength via a reverse mechanotransduction pathway.
- This pathway involves the nucleus communicating with the cell surface, including RhoA activation.
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