Adhesion-regulated junction slippage controls cell intercalation dynamics in an Apposed-Cortex Adhesion Model

• DOI: 10.1371/journal.pcbi.1009812
• Publication Date: 2022-01-28T18:38:41Z
• Authors: Alexander Nestor-...; Guy B. Blanchard; Nathan Hervieux; Alexander G. Flet...; Jocelyn Étienne; Bénédicte Sanson
• Keywords: Slippage

Cell intercalation is a key cell behaviour of morphogenesis and wound healing, where local neighbour exchanges can cause dramatic tissue deformations such as body axis extension. Substantial experimental work has identified the molecular players facilitating intercalation, but there remains lack consensus understanding their physical roles. Existing biophysical models that represent cell-cell contacts with single edges cannot study exchange continuous process, neighbouring cortices must uncouple. Here, we develop an Apposed-Cortex Adhesion Model (ACAM) to understand active behaviours in context 2D epithelial tissue. The junctional actomyosin cortex every modelled viscoelastic rope-loop, explicitly representing facing each other at bicellular junctions adhesion molecules couple them. model parameters relate directly properties subcellular drive dynamics, providing multi-scale behaviours. We show be driven by purely mechanisms. Active contractility cortical turnover junction are sufficient shrink remove junction. Next, new, orthogonal extends passively. ACAM reveals how regulates tension transmission deformation rates controlling slippage between apposed cortices. additionally predicts rosettes, which form when vertex becomes common many cells, more likely occur actively intercalating tissues strong friction from molecules.