Most adherent cells are capable of sensing the external forces and probing the mechanical properties of their surroundings. These are classical hallmarks of what is termed mechanotransduction. Mechanotransduction is generally attributed to the sensory functions of focal adhesion (FA) proteins upon activation by mechanical stimuli. A striking feature of cell mechanosensing is the growth of FAs in response to increased cytoskeletal or extracellular tension. Despite growing knowledge about the molecular structures of cell focal adhesions, it has remained elusive as to how these anchorage points grow and how their sensory function operates. The aim of this contribution is to show that force-dependent enlargement of FAs could be driven by spontaneous clustering of transmembrane receptors, independent from active sensory mechanisms. The elasticity of bonds is the key regulator of this process. The mechanical work associated with the cytoskeletal tension alters the free energy landscape and facilitates the recruitment of free receptors to establish new bonds with ligands. Therefore, mechanotransduction could be the manifestation of a thermodynamic process in cell FAs to achieve the state of minimum free energy, independent from the sensory function of molecular sensors in FAs, as postulated in available models.

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