Research

Living cells generate mechanical forces to perform their physiological functions, and most of that force originates in the actin cytoskeleton. Myosin motor proteins walk along actin filaments, consuming chemical energy stored in ATP to produce tensile force — a mechanism called actomyosin contractility that operates in both muscle and non-muscle cells. Because of this activity, the actin cytoskeleton is driven out of thermal equilibrium, which shapes its mechanical behavior in ways that passive polymer networks don't show. We study how this force generation and contraction emerge from the properties of the underlying motors and filaments.

Actin structures inside cells play a role in nearly every biological function, and depending on conditions, they can behave like an elastic solid or a viscous fluid. Understanding this viscoelastic behavior is essential for explaining both cell mechanics and the broader cellular processes that depend on it. We investigate how the mechanical and dynamic properties of microscopic components — filaments, crosslinkers, and motors — determine the macroscopic viscoelastic behavior and moduli of the actin cytoskeleton.

Intracellular forces generated by actomyosin contractility don't stay inside the cell — they transmit outward and can substantially remodel the extracellular matrix (ECM) that surrounds it, though the mechanisms behind that remodeling remain unclear. We're interested in how cells modulate their contractility to biophysically interact with and deform extracellular environments that vary widely in mechanical character, including viscoelasticity and viscoplasticity. Our computational models trace how forces from actomyosin contractility are transmitted to and reshape the ECM under different conditions.

Cell migration underlies diverse biological processes, from wound healing to tumor cell invasion to the formation of neural crest and vasculature, and it can be directed by biophysical cues such as chemotactic gradients, electric fields, substrate geometry, and substrate stiffness. Experimental study of migration has real limitations, so we've developed a computational biomechanical model that captures phenomena in mesenchymal cell migration on two-dimensional substrates — including durotaxis, contact inhibition of locomotion, and contact guidance.