Cell Motility through Blebbing

The cell is internally lined with an actomyosin network that forms the cortex, and is linked to the cell membrane via linker proteins such as ezrin.

In response to appropriate signals, the cortical actin network destabilizes and ruptures, leading to localized detachment of the membrane from the cortex.

The internal hydrostatic pressure causes the detached membrane to swell outwards and rapidly fill with the cytoplasm, forming a rounded protrusion called a bleb.

Inside the bleb, a cytoskeletal regulator, Rnd3, prevents RhoA activation and inhibits the reassembly of the actin cortex, allowing further expansion of the bleb.

As the bleb expands, the Rnd3 concentration decreases, resulting in RhoA activation.

Activated RhoA promotes reassembly of actin and ezrin, thus re-establishing the cortex in the bleb.

Finally, myosin-II associates with and contracts the actin bundles, generating the force to retract the bleb and push the cell forward through the extracellular matrix.