Abstract

Cell intercalation is a key cell behaviour of morphogenesis and wound healing, where local cell neighbour exchanges can cause dramatic tissue deformations such as body axis extension. While substantial experimental work has identified the key molecular players facilitating intercalation, there remains a lack of consensus and understanding of their physical roles. Existing biophysical models that represent cell-cell contacts with single edges cannot study neighbour exchange as a continuous process, where neighbouring cell cortices must uncouple. I will present an Apposed-Cortex Adhesion Model (ACAM) to understand active cell intercalation behaviours in the context of a 2D epithelial tissue. The junctional actomyosin cortex of every cell is modelled as a continuous viscoelastic rope-loop, explicitly representing cortices facing each other at bicellular junctions and the adhesion molecules that couple them. The model parameters relate directly to the physical properties of the key subcellular players that drive dynamics (actin, myosin and adhesion), providing a multi-scale understanding of cell behaviours. The ACAM predicts that active junctional contractility and cortical turnover are sufficient to shrink and remove a junction, while the growth of a new, orthogonal junction follows passively. The model reveals how the turnover of adhesion molecules specifies a friction that regulates tissue dynamics and tension transmission by controlling slippage between apposed cell cortices. Increasing the friction from adhesion in an actively intercalating tissue can lead to the formation of rosette structures, where vertices become common to many cells.