Both intercellular and cell-matrix adhesions coordinately regulate a host of crucial tissue functions, including barrier integrity, cell shape, and tissue organization. It is now widely accepted that mechanical forces can play a critical role in these functions. Focal adhesions are tension-sensing complexes that link the actomyosin network to the mechanics of the extracellular matrix. Cadherins are crucial mechanical and signalling hubs at intercellular junctions in tissues. Yet, the mechanisms of propagating mechanical information through tissues via intercellular contacts have only recently become a focus of research.

Our work investigates the mechanical properties of cadherin-based intercellular junctions and the propagation of mechanical information across cell-cell junctions. We recently demonstrated that cadherin-based complexes, which are critical cell-to-cell adhesion proteins in all soft tissues, constitute a new class of force sensing elements in the mechanical and signalling networks of tissues. My lab uses micro- and micromechanical methods, in conjunction with biochemical approaches, to interrogate the adhesive properties of cadherin bonds and the mechanisms of mechanotransduction. Biophysical studies of cadherin binding from single proteins to live cells quantified differences in cadherin properties thought to govern intercellular cohesion and tissue patterning during tissue patterning. Recent approaches further interrogated how mechanical information is transduced between cells to the cytoskeleton. Our findings show that cadherin complexes are tension sensors that probe the tissue environment to proportionally regulate cell mechanics. Studies are beginning to reveal the rudiments of the mechanosensing mechanism. We also recently demonstrated the reciprocal modulation of cadherin and focal adhesions through mechanical pathways. These exciting new findings are relevant to a wide range of biological processes that include tissue regeneration, wound healing, development and disease.