Single cell

On Single cell mechanotransduction

The laminin–keratin link shields the nucleus from mechanical deformation and signalling

Here we show that laminin hinders the mechanoresponses of breast epithelial cells by shielding the nucleus from mechanical deformation. By combining mechanical perturbations and mathematical modelling, we show that β4 integrins establish a mechanical linkage between the substrate and keratin cytoskeleton, which stiffens the network and shields the nucleus from actomyosin-mediated mechanical deformation.

Cell response to extracellular matrix viscous energy dissipation outweighs high- rigidity sensing

Here, we have exploited engineered stiff viscoelastic protein hydrogels to show that, contrary to current models of cell-ECM interaction, substrate viscous energy dissipation attenuates mechanosensing even when cells are exposed to higher effective rigidity. This behavior is however readily captured by a pull-and-hold model of molecular clutch–based cell mechanosensing, which also recapitulates opposite cellular response at low rigidities.

Mechanotransmission of haemodynamic forces by the endothelial glycocalyx in a full-scale arterial model

Here we apply a multiscale approach to elucidate how haemodynamic shear forces are transmitted to the transmembrane anchors of endothelial cells.

On Single cell migration

A computational model for early cell spreading, migration, and competing taxis

Here, we derived a computational model of cell motility that incorporates the most important mechanisms towards cell motility: cell protrusion, polarization, and retrograde flow.

Positive, negative and controlled durotaxis

Here, we provide a mechanistic rationale for durotaxis by integrating stochastic clutch models for cell adhesion with an active gel theory of cell migration. We 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.

Competing elastic and viscous gradients determine directional cell migration

Here, we integrate clutch models for cell adhesions with an active gel theory of cell migration to reveal the mechanisms that govern viscotaxis. We show that viscotaxis is enabled by an asymmetric expression of cell adhesions that further polarize the intracellular motility forces to establish the cell front, similar to durotaxis. More importantly, when both relaxation and elastic gradients coexist, durotaxis appears more efficient in controlling directed cell migration.

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