N-cadherin crosstalk with integrin weakens the molecular clutch in response to surface viscosity

Eva Barcelona-Estaje, Mariana A. G. Oliva, Finlay Cunniffe, Aleixandre Rodrigo-Navarro, Paul Genever, Matthew J. Dalby, Pere Roca-Cusachs (), Marco Cantini () and Manuel Salmeron-Sanchez ()
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Eva Barcelona-Estaje: Advanced Research Centre, University of Glasgow
Mariana A. G. Oliva: Advanced Research Centre, University of Glasgow
Finlay Cunniffe: Advanced Research Centre, University of Glasgow
Aleixandre Rodrigo-Navarro: Advanced Research Centre, University of Glasgow
Paul Genever: University of York
Matthew J. Dalby: Advanced Research Centre, University of Glasgow
Pere Roca-Cusachs: the Barcelona Institute of Technology (BIST)
Marco Cantini: Advanced Research Centre, University of Glasgow
Manuel Salmeron-Sanchez: Advanced Research Centre, University of Glasgow

Nature Communications, 2024, vol. 15, issue 1, 1-12

Abstract: Abstract Mesenchymal stem cells (MSCs) interact with their surroundings via integrins, which link to the actin cytoskeleton and translate physical cues into biochemical signals through mechanotransduction. N-cadherins enable cell-cell communication and are also linked to the cytoskeleton. This crosstalk between integrins and cadherins modulates MSC mechanotransduction and fate. Here we show the role of this crosstalk in the mechanosensing of viscosity using supported lipid bilayers as substrates of varying viscosity. We functionalize these lipid bilayers with adhesion peptides for integrins (RGD) and N-cadherins (HAVDI), to demonstrate that integrins and cadherins compete for the actin cytoskeleton, leading to an altered MSC mechanosensing response. This response is characterised by a weaker integrin adhesion to the environment when cadherin ligation occurs. We model this competition via a modified molecular clutch model, which drives the integrin/cadherin crosstalk in response to surface viscosity, ultimately controlling MSC lineage commitment.

Date: 2024
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DOI: 10.1038/s41467-024-53107-6

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