Our group is interested in understanding collective and emergent behavior in out-of-equilibrium and disordered systems. My research employs methods in theoretical and computation condensed matter physics and applies to a wide range of biological and non-biological systems.
Origin of jamming and rigidity in epithelial Tissues
Every organ in the human body is lined with epithelial cells. The cells in these tissues are normally sedentary or solidlike but become migratory or fluidlike during embryonic development, tissue repair, and cancer invasion. Researchers do not understand this striking transition from stationary to active behaviors, which could help shed light on various aspects of biology, medicine, and disease progression. We develop a theoretical model of cellular organization in these tissues that takes into account more complex junctions between cells than previous models—junctions that provide insight into this stark difference in cell behavior.
A common assumption in cellular models is that a tissue always looks like a foam network, consisting of only triple junctions where three cells meet. However, cellular rosettes, where five or more cells meet at a single point, are prevalent in nature. Our generalized theoretical framework takes into account the presence of rosettes. We find that the tissue can behave as a solid or a fluid depending on the number of rosettes present as well as the mechanical tension forces in cell junctions. We also make experimentally testable predictions regarding the strong correlations and the interplay between cellular topology and mechanical tensions in a tissue.
From a physics perspective, the transformation between fluid and solid states exhibits many hallmarks of a second-order phase transition, such as a growing correlation length and universal scaling relations near the critical point. We elucidate the nature and origin of rigidity transition in tissue with a generalized theory that offers a unifying perspective of tissue mechanics.
Mechnosensing and Mechanotransduction during wound healing
Many developmental processes involve collective cell motion, driven by migratory behaviours of individual cells and their interactions with the extracellular environment. An outstanding question is how cells regulate their internal driving forces to maintain tissue cohesiveness while promoting the requisite fluidity for collective motion. Progress has been limited by the lack of an integrative framework that couples cellular physical behavior with stochastic biochemical dynamics underlying cell motion and adhesion. Here we develop a cell-based computational model for collective cell migration during epithelial wound repair that integrates tissue mechanics with active cell motility, cell-substrate adhesions, and actomyosin dynamics. Using this model we show that an optimum balance of protrusive cell crawling and actomyosin contractility drives rapid directed motion of cohesive cell groups, robust to variations in cell and substrate physical properties. We further show that disparate modes of individual cell migration can cooperate to accelerate collective cell migration by fluidizing confluent tissues.
We design an amorphous material with a full photonic bandgap inspired by how cells pack in biological tissues. The size of the photonic bandgap can be manipulated through thermal and mechanical tuning. These directionally isotropic photonic bandgaps persist in solid and fluid phases, hence giving rise to a photonic fluid-like state that is robust with respect to fluid flow, rearrangements, and thermal fluctuations in contrast to traditional photonic crystals. This design should lead to the engineering of self-assembled nonrigid photonic structures with photonic bandgaps that can be controlled in real time via mechanical and thermal tuning.