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

Area of Science:

• Biophysics
• Developmental Biology
• Cell Biology

Background:

• Cell intercalation is vital for morphogenesis and wound healing, involving complex cell behaviors.
• Existing biophysical models lack the resolution to capture continuous cell neighbor exchange and cortex uncoupling.

Purpose of the Study:

• To develop a novel biophysical model, the Apposed-Cortex Adhesion Model (ACAM), for studying active cell intercalation in 2D epithelial tissues.
• To elucidate the physical roles of molecular players in cell intercalation and tissue deformation.

Main Methods:

• Developed the Apposed-Cortex Adhesion Model (ACAM) representing cell cortices as continuous viscoelastic rope-loops.
• Explicitly modeled bicellular junctions, apposed cortices, and adhesion molecules.
• Simulated active cell intercalation dynamics in a 2D epithelial context.

Main Results:

• Demonstrated that active cell neighbor exchanges can be driven by junctional mechanisms, specifically active contractility and cortical turnover.
• Showed that junction shrinkage and removal by active contractility precede passive extension of new junctions.
• Revealed that adhesion molecule turnover regulates tension transmission and junction deformation by controlling cortex slippage.

Conclusions:

• The ACAM provides a multi-scale understanding of cell intercalation, linking molecular properties to tissue-level behaviors.
• Active contractility and adhesion dynamics at bicellular junctions are sufficient to drive intercalation.
• The model predicts increased rosette formation in actively intercalating tissues with high adhesion friction.