We develop a multi-scale computational model for adhesion complexes mechanics. We extend the classical clutch hypothesis to model individual adhesion chains made of a contractile actin network, a talin rod, and an integrin molecule that binds at individual adhesion sites on the extracellular matrix.
Here, we used a pull-and-hold model of molecular clutch–based cell mechanosensing, which also recapitulates opposite cellular response at low rigidities.
Here, we used stochastic clutch models for cell adhesion to show that positive and negative durotaxis found across cell types are explained by asymmetries in the cell adhesion dynamics. We rationalize durotaxis by asymmetric mechanotransduction in the cell adhesion behavior that further polarizes the intracellular retrograde flow and the protruding velocity at the cell membrane.