Wound Healing Coordinates Actin Architectures to Regulate Mechanical Work.

Area of Science:

• Cell biology
• Biophysics
• Tissue mechanics

Background:

• Understanding how cells coordinate mechanical behaviors for collective motion in tissues is crucial.
• Cellular morphologies and cytoskeletal architectures play key roles in tissue dynamics, but their precise influence on collective motion remains unclear.

Purpose of the Study:

• To investigate how diverse cellular actin network architectures modulate mechanical work during collective cell migration.
• To determine the relationship between actin network organization, wound closure rate, and mechanical power output in epithelial monolayers.

Main Methods:

• Utilized traction force microscopy to measure mechanical forces exerted by cells.
• Employed *in vitro* epithelial monolayers undergoing wound repair.
• Developed a cell-based physical model to analyze energy transformation and friction dynamics.

Main Results:

• The balance of branched and bundled actin networks optimizes wound closure rate and mechanical work magnitude.
• Monolayer effective power output is conserved and independent of specific actin architectures.
• The rate of mechanical work is limited by transitions between actin architectures and cell-substrate friction regulation.

Conclusions:

• Cellular collective motion and tissue-scale mechanical output are dynamically regulated by non-equilibrium cellular behaviors.
• A physical model elucidates how actin network transformations and differential cell-substrate friction govern the rate of mechanical work during tissue repair.