Microfilament-coordinated adhesion dynamics drives single cell migration and shapes whole tissues

Cell adhesion is a foundational process in both individual and collective cell migration. It plays a critical role in immune cell function and in the coordinated movement of cell sheets during tissue development. While the importance of adhesion in solitary migration is well established, its role in collective migration remains less fully understood. Research has shown that maintaining contact between neighboring cells is essential for directional movement in these cases. However, the mechanisms by which adhesion is regulated across multiple cells are not yet clear. This uncertainty has driven recent efforts to understand how intracellular structures like the actin cytoskeleton coordinate adhesion. The need for a more detailed understanding of this coordination is especially relevant in both normal development and disease progression. These gaps in knowledge highlight the value of revisiting existing models of adhesion regulation in light of new findings.

This review aims to clarify the mechanisms by which cell-cell and cell-matrix adhesions are coordinated during collective cell migration. It focuses on the role of the actin cytoskeleton in integrating signals from both cadherin and integrin adhesions. The study addresses the need to better understand how these adhesions are regulated in a synchronized manner. It also explores the influence of mechanical forces on the stability and turnover of adhesive contacts. The authors propose that recent findings in this area can help refine existing models of adhesion dynamics. Their goal is to provide a more comprehensive view of how adhesion is controlled in both single and collective migration. This includes examining how these processes are affected in three-dimensional environments. The review also highlights how these insights might inform future research on tissue development and cancer progression.

The authors synthesize findings from recent studies on adhesion dynamics and actin regulation. They focus on the role of the actin cytoskeleton in linking cadherin and integrin adhesions. The review integrates data from both in vitro and in vivo models of cell migration. It examines how mechanical forces influence the formation and disassembly of adhesive contacts. The authors analyze the adhesive clutch hypothesis in light of new evidence. They consider how this model explains the balance between adhesion and movement. The review also incorporates findings from three-dimensional migration models. These models provide a more realistic context for understanding adhesion coordination.

The actin cytoskeleton is shown to act as a central coordinator of both cell-cell and cell-matrix adhesions. Mechanical forces are found to play a key role in the reinforcement and turnover of adhesive contacts. The adhesive clutch model is revisited in light of recent discoveries about adhesion regulation. This model suggests that adhesion strength is modulated during cell protrusion. The review highlights how this mechanism may be influenced by the actin cytoskeleton. Evidence from three-dimensional models supports the importance of mechanical regulation in migration. These findings suggest that adhesion dynamics are more complex than previously thought. The results also indicate that adhesion coordination is critical in both normal and pathological contexts.

The authors conclude that coordinated adhesion regulation is essential for both single and collective cell migration. They emphasize the role of the actin cytoskeleton in integrating signals from cadherin and integrin adhesions. The review suggests that mechanical forces are a key factor in maintaining and modulating adhesive contacts. The adhesive clutch hypothesis is presented as a useful framework for understanding adhesion dynamics. The authors note that recent findings support a more nuanced view of this model. They propose that three-dimensional models provide a more accurate representation of adhesion coordination. The study highlights the importance of these findings in both developmental and pathological contexts. The conclusions are based on the synthesis of current evidence and do not extend beyond what is supported by the literature.