Among the various cell types found in the bodies of humans and other mammals, immune cells are characterised by their rapid movement. Key components of these cells are thread-like protein structures known as actin filaments, which form a network along the inner side of the cell membrane – the cell's surface. This network is dynamic and constantly being remodelled, as actin building blocks are either added to or removed from the ends of filaments. According to the classical model, the generation of cell movement also requires the molecular motor myosin. These motors shift filaments against each other and thereby contract the network at the rear of the cell, creating a flow of actin filaments from front to back. This flow enables the cell to move forwards. However, experiments in which myosin activity was biochemically suppressed have shown that cells are also capable of moving independently of this molecular motor.
Now, researchers at the Universities of Bayreuth and Grenoble have discovered a mechanism by which cells can achieve this myosin-independent movement. To do so, they developed a model demonstrating that the addition and removal of actin building blocks at the filaments is sufficient to generate cell movement – provided that this process occurs rapidly enough. Above this critical speed threshold, the distribution of actin filaments within the originally spherical cell changes, leading to the formation of a front and rear that differ in tension: at the front of the cell, where filaments lie less densely beneath the membrane, greater tensions arise than at the rear, where more filaments are present over the same surface area. This difference causes further actin filaments to flow from the front to the rear, setting up a self-sustaining cycle. In the end, a flow of actin – and thus cell movement – arises even in the absence of molecular motors.
