Over the last ten years, a peculiar behavior of living cells is revealed: their modulus increases weakly with loading frequency (the so-called weak power law behavior) (for a pure elastic solid, the slope is 0; for a viscous fluid, the slope is 1).  The underlying mechanism is not clear at all; although a phenomenological soft glass rheology model (a model based on a disordered structure system) has been proposed, it cannot explain the multi-power laws at different loading frequencies (see Stamenovic et al, Biophys J Letter, 2007). 

We recently find that podosomes, very dynamic, self-organized structures, can function as mechanosensors.  For details, see the recent issue of Current Biology.

http://www.mechse.uiuc.edu/content/news/article.php?article_id=226

It is generally believed that similar to soluble ligand-induced signal transduction, mechanotransduction initiates at the local force-membrane interface (e.g., at focal adhesions) by inducing local conformational changes or unfolding of membrane-bound proteins, followed by a cascade of diffusion-based or translocation-based signaling in the cytoplasm. However, all published reports, including past studies with the reporter type of construct extended here, were limited in timescale to address this fundamental issue.

What might be the differences, if there is any, between mechanical signaling and chemical signaling in a living cell?

Some argue that since a local applied force decays rapidly at the cell surface, it causes only local deformation that, in turn, can activate only local biochemical activities (e.g., protein phosphorylation), followed by diffusion and/or tranlocation based signaling, similar to soluble ligand induced chemical signaling. However, recent experiments have shown that a force of a physiological magnitude, applied via a focal adhesion, can propagate a long distance into the cell to deform cytoplasmic structures and nuclear structures at remote sites.