Our goal is to gain a quantitative, molecular-level understanding of how cells and tissues sense, transmit and respond to mechanical information from their environment to regulate critical physiological functions. 

Cells in our body exist not only in a rich biochemical environment but also in a highly complex and dynamic mechanical environment. Whether it is blood flow, lung expansion, heart contraction or the matrix that surrounds cells everywhere, this environment is  critical for most important functions in life. Starting from embryogenesis,  tissue development and differentiation to immune, cardiovascular, musculoskeletal and brain function, the mechanical environment plays an important role in all these processes through regulatory interactions with cellular function. Not surprisingly, breakdown or mis-regulation of the interactions between cellular functions and the mechanical environment results in developmental defects, immune disorders, cardiomyopathies and cancer.

We are primarily but not exclusively interested in the cellular function  of directed cell migration and role of integrin-based adhesions as sensors, transmitters and transducers of mechanical information.

Whether it be the sweeping eagle in his flight, or the open apple-blossom, the toiling work-horse, the blithe swan, the branching oak, the winding stream at its base, the drifting clouds, over all the coursing sun, form ever follows function, and this is the law. – Louis Sullivan

Our central hypothesis is that multi-molecular structures  such as adhesions allow a cell to sense and respond to mechanical cues such as matrix stiffness, fluid flow by encoding that information and cellular response in its dynamic architecture and composition.  We test our hypothesis by  utilizing a wide array of quantitative microscopy-based approaches and tools from engineering, physics and cell biology and investigate the relationship between forces/mechanics and molecular, sub-cellular and cellular organization, signaling and dynamics.

Our ultimate aim is to extend our fundamental and mechanistic knowledge to 3D-cancer models where changes in the microenvironment leads to tumor growth and metastasis through breakdown of homeostasis between cells and their mechanical environment. By identifying pathways that go awry in cancer, we hope to contribute in developing novel therapeutics and targeting strategies.