First, motile cells collide and touch via their respective lamellae, whose actin exhibit high retrograde flow. A cellular adhesion forms between the lamellae, reducing the actins' retrograde flow rate in the area immediately surrounding the adhesion. Consequently, the cells' velocity and motility are reduced. This then allows actin stress fibers and microtubules to form and align with each other in both colliding partners. The alignment of these stress fibers locally accumulates elastic tension in the lamellae. Eventually, the tension buildup becomes too great, and the cell adhesion complex dissociates, collapses the lamellae protrusions, and releases the cells in different directions in an effort to alleviate the elastic tension. A possible alternate event that also leads to the assembly dissociation is that upon stress fiber alignment, the cells' leading edges repolarize away from the contiguous lamellae. This produces significant elastic tension across the entire cell bodies, "not only at the local site of contact", and likewise causes the adhesion complex's disassembly. Elastic tension has been thought to be the primary driving force of the protrusion collapse, complex disassembly, and the cells' dispersion. Though this hypothetical tension has been characterized and visualized, how tension builds in lamellae and how cell repolarization contributes to tension buildup remain open to investigation.