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Metavinculin modulates force transduction in cell adhesion sites

Author

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  • Verena Kanoldt

    (Institute of Molecular Cell Biology, University of Münster
    Max Planck Institute of Biochemistry, Group of Molecular Mechanotransduction)

  • Carleen Kluger

    (Max Planck Institute of Biochemistry, Group of Molecular Mechanotransduction)

  • Christiane Barz

    (Max Planck Institute of Biochemistry, Group of Molecular Mechanotransduction)

  • Anna-Lena Schweizer

    (Institute of Molecular Cell Biology, University of Münster
    Max Planck Institute of Biochemistry, Group of Molecular Mechanotransduction)

  • Deepak Ramanujam

    (Technical University of Munich
    DZHK (German Centre for Cardiovascular Research), Partner Site Munich Heart Alliance)

  • Lukas Windgasse

    (Institute of Molecular Cell Biology, University of Münster)

  • Stefan Engelhardt

    (Technical University of Munich
    DZHK (German Centre for Cardiovascular Research), Partner Site Munich Heart Alliance)

  • Anna Chrostek-Grashoff

    (Institute of Molecular Cell Biology, University of Münster
    Max Planck Institute of Biochemistry, Group of Molecular Mechanotransduction)

  • Carsten Grashoff

    (Institute of Molecular Cell Biology, University of Münster
    Max Planck Institute of Biochemistry, Group of Molecular Mechanotransduction)

Abstract

Vinculin is a ubiquitously expressed protein, crucial for the regulation of force transduction in cells. Muscle cells express a vinculin splice-isoform called metavinculin, which has been associated with cardiomyopathies. However, the molecular function of metavinculin has remained unclear and its role for heart muscle disorders undefined. Here, we have employed a set of piconewton-sensitive tension sensors to probe metavinculin mechanics in cells. Our experiments reveal that metavinculin bears higher molecular forces but is less frequently engaged as compared to vinculin, leading to altered force propagation in cell adhesions. In addition, we have generated knockout mice to investigate the consequences of metavinculin loss in vivo. Unexpectedly, these animals display an unaltered tissue response in a cardiac hypertrophy model. Together, the data reveal that the transduction of cell adhesion forces is modulated by expression of metavinculin, yet its role for heart muscle function seems more subtle than previously thought.

Suggested Citation

  • Verena Kanoldt & Carleen Kluger & Christiane Barz & Anna-Lena Schweizer & Deepak Ramanujam & Lukas Windgasse & Stefan Engelhardt & Anna Chrostek-Grashoff & Carsten Grashoff, 2020. "Metavinculin modulates force transduction in cell adhesion sites," Nature Communications, Nature, vol. 11(1), pages 1-10, December.
    • Handle: RePEc:nat:natcom:v:11:y:2020:i:1:d:10.1038_s41467-020-20125-z
    DOI: 10.1038/s41467-020-20125-z
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