Cellular junctions are strongly dynamic biopolymeric assemblies of the bulky adhesion receptors, like the E-cadherin, Selectin etc. E-cadherin, the most abundant adhesion protein in human cells, engage in trans-interactions to constitute an array of mechanical links between adjacent cells. Remodeling of these links depends on tensile forces and inherent stochastic fluctuations in the cytoplasm. The usual tight regulation of this remodeling dynamics gets disturbed during abnormal conditions, such as defective morphogenesis or cancer metastasis. We develop computational models of the dynamical states of cell-cell junctions to understand the key molecular interactions that are responsible for this regulation process. 

Actomyosin cortex is one of the most dynamic subcellular ‘organelle’ capable of adopting various shape and architecture. Cell uses actin filaments to perform a variety of mechanical functions, ranging from maintenance of shape to controlling forces at peripheral regions to forming the cytokinetic ring during division. We build polymer physics models of actomyosin networks to decipher how they adapt to various geometric constraints and controls the functional positioning of different actin associated proteins during specific biomechanical events involving the cell cortex.