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By this means, cells were induced to maintain the same surface area while contacting a different number of adhesion sites.

This experimental setting allowed us to finely tune FA number regardless of cell size.

On a larger scale, this condition keeps organ functionality, while changes in the mechanical balance between the cells and the surrounding milieu result in tissue malfunctioning or malignant transformation.

The ability of cells to perceive ECM mechanics and spread is associated to Hippo pathway effectors Yes-associated protein (YAP) and WW domain-containing transcription regulator protein 1 (WWTR1 or TAZ) shuttling to the nucleus to exert their co-transcriptional activity.

Graphs: quantification of the number of FAs per cell (FA number), cell area and YAP nuclear/cytoplasmic ratio in AD-MSCs cultured on ESS, fibronectin or poly- areas and coated with fibronectin.

Here we unveil the molecular mechanism by which cell spreading and Rho A GTPase activity control FA formation through YAP to stabilize the anchorage of the actin cytoskeleton to the cell membrane.

This mechanism requires YAP co-transcriptional function and involves the activation of genes encoding for integrins and FA docking proteins.

Bottom right: Quantitative RT–PCR analysis of vinculin (VCL), zyxin (ZYX), talin1 (TLN1), talin2 (TLN2), RHOA genes in AD-MSCs cultured onto 10,000 versus 1,024 μm.

The results are expressed as mean fold regulation obtained in 2 independent experiments and the bar indicates the s.d.

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