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Journal Article

Metavinculin modulates force transduction in cell adhesion sites

MPS-Authors
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Kanoldt,  Verena
Grashoff, Carsten / Molecular Mechanotransduction, Max Planck Institute of Biochemistry, Max Planck Society;

/persons/resource/persons127892

Kluger,  Carleen
Grashoff, Carsten / Molecular Mechanotransduction, Max Planck Institute of Biochemistry, Max Planck Society;

/persons/resource/persons145330

Barz,  Christiane
Grashoff, Carsten / Molecular Mechanotransduction, Max Planck Institute of Biochemistry, Max Planck Society;

/persons/resource/persons256161

Schweizer,  Anna-Lena
Grashoff, Carsten / Molecular Mechanotransduction, Max Planck Institute of Biochemistry, Max Planck Society;

/persons/resource/persons127896

Chrostek-Grashoff,  Anna
Grashoff, Carsten / Molecular Mechanotransduction, Max Planck Institute of Biochemistry, Max Planck Society;

/persons/resource/persons78025

Grashoff,  Carsten
Grashoff, Carsten / Molecular Mechanotransduction, Max Planck Institute of Biochemistry, Max Planck Society;

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Fulltext (public)

s41467-020-20125-z.pdf
(Publisher version), 2MB

Supplementary Material (public)

41467_2020_20125_MOESM1_ESM.pdf
(Supplementary material), 9MB

Citation

Kanoldt, V., Kluger, C., Barz, C., Schweizer, A.-L., Ramanujam, D., Windgasse, L., et al. (2020). Metavinculin modulates force transduction in cell adhesion sites. Nature Communications, 11(1): 6403. doi:10.1038/s41467-020-20125-z.


Cite as: http://hdl.handle.net/21.11116/0000-0007-D407-2
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. Muscle cells express an adhesion molecule called metavinculin, which has been associated with cardiomyopathies. Here, the authors employed molecular tension sensors to reveal that metavinculin expression modulates cell adhesion mechanics and they develop a mouse model to demonstrate that the presence of metavinculin is not as critical for heart muscle function as previously thought.