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Published on: October 13, 2019
Focal adhesion kinase stabilizes the cytoskeleton.
Ben Fabry1, Anna H Klemm, Sandra Kienle
1Department of Physics, Friedrich-Alexander-University Erlangen-Nuremberg, Erlangen, Germany.
Biophysical Journal
|November 10, 2011
Summary
Focal adhesion kinase (FAK) deficiency reduces cell mechanical stability by increasing cytoskeletal dynamics. Rho-kinase activation in FAK-deficient cells contributes to this instability, which can be partially restored by inhibiting rho-kinase.
Area of Science:
- Cell biology
- Biophysics
- Mechanobiology
Background:
- Focal adhesion kinase (FAK) is crucial for focal adhesion turnover.
- The role of FAK in cellular mechanical stability remains largely unexplored.
Purpose of the Study:
- To investigate the role of FAK in maintaining cell mechanical stability.
- To elucidate the mechanisms underlying FAK's influence on cytoskeletal dynamics and cell mechanics.
Main Methods:
- Utilized magnetic tweezers, atomic force microscopy, traction microscopy, and nanoscale particle tracking microrheology.
- Compared mechanical properties of wild-type, FAK-deficient (FAK-/-), and FAK-silenced (siFAK) mouse embryonic fibroblasts.
Main Results:
- FAK-deficient cells exhibited significantly lower cell stiffness and reduced adhesion strength.
- Increased cytoskeletal dynamics and reduced cell spreading were observed in FAK-deficient cells.
- Rho-kinase activation in FAK-deficient cells suppressed stress fiber formation and enhanced cortical actin distribution.
Conclusions:
- FAK plays a critical role in maintaining cell mechanical stability.
- Reduced cytoskeletal stability in FAK-deficient cells is mediated by rho-kinase activation.
- Inhibition of rho-kinase partially restores cell stiffness and cytoskeletal stability in FAK-deficient cells.
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