[5] The disruption of the membrane-actin cortex interactions[4] are dependent on the activity of myosin-ATPase[6] Bleb initiation is affected by three main factors: high intracellular pressure, decreased amounts of cortex-membrane linker proteins, and deterioration of the actin cortex.
[7][8] When this integrity is compromised, the addition of pressure is able to make the membrane bulge out from the rest of the cell.
[8] Bleb formation has been artificially induced in multiple lab cell models using different methods.
[11] Breakage of cortex-membrane bonds has also been caused by laser ablation and injection of an actin depolymerizing drug, which in both cases eventually led to blebbing of the cell membrane.
[11] Artificially increased levels of myosin contractility were also shown to induce blebbing in cells.
[11] Some viruses, such as the poxvirus Vaccinia, have been shown to induce blebbing in cells as they bind to surface proteins.
[12] Although the exact mechanism is not yet fully understood, this process is crucial to endocytosing the virion and subsequent infection.
[7][11] A 2D moving cell is able to use adhesive molecules to gain traction in its environment while blebs form at the leading edge.
[7][11] By forming a bleb, the center of mass of the cell shifts forward and an overall movement of cytoplasm is accomplished.
[18][19][20][21] By interfering with myosin function, blebbistatin alters the contractile forces that impinge on the cytoskeleton-membrane interface and prevents the build up of intracellular pressure needed for blebbing.