Initiation of Bleb Assembly2018-02-06T11:06:12+08:30

How is bleb assembly initiated?

Under normal circumstances, the plasma membrane remains tightly bound to the cell cortex. This close association is maintained by interactions with the actin cytoskeleton, myosin and other associated proteins. Hydrostatic pressure is exerted on the plasma membrane via cortical tension generated by myosin [1]. However, during blebbing myosin contracts the cortical actin cytoskeleton, detaching it from the plasma membrane. Depending on whether the cortex remains intact or ruptures during detachment, this process is referred to as local membrane detachment ([2], e.g., zebrafish primordial germ cells [3], Walker carcinoma cells [4]) or local cortex rupture ([5][6], e.g., Walker carcinosarcona [4]).

Two models of bleb formation: A. Local membrane detachment B. Local cortex rupture

Importantly, the initiation of bleb formation is a result of a local increase in hydrostatic pressure, rather than actin polymerization, as is the case for other cellular structures including lamellipodia and filopodia [7].

The frequency at which blebs are formed is determined by several factors [8], including:

Hydrostatic pressure: increased extracellular osmolarity decreases the number of blebs formed.

Membrane-cortex adhesion: increased membrane-cortex adhesion decreases the number of blebs formed, as evidenced by the overexpression of the membrane-actin crosslinker ezrin.

Membrane tension: increasing membrane tension decreases the number of blebs formed, as evidenced by treating cells with the polysaccharide crosslinker WGA (wheat germ agglutinin).

Cortex contractility: decreased cortical contractility decreases the number of blebs formed, as evidenced by treating cells with the myosin II inhibitor, blebbistatin.

View All

Latest Findings

Protein Info


  1. Dai J, and Sheetz MP. Membrane tether formation from blebbing cells. Biophys. J. 1999; 77(6):3363-70. [PMID: 10585959]
  2. Cunningham CC. Actin polymerization and intracellular solvent flow in cell surface blebbing. J. Cell Biol. 1995; 129(6):1589-99. [PMID: 7790356]
  3. Blaser H, Reichman-Fried M, Castanon I, Dumstrei K, Marlow FL, Kawakami K, Solnica-Krezel L, Heisenberg C, and Raz E. Migration of zebrafish primordial germ cells: a role for myosin contraction and cytoplasmic flow. Dev. Cell 2006; 11(5):613-27. [PMID: 17084355]
  4. Keller H, Rentsch P, and Hagmann J. Differences in cortical actin structure and dynamics document that different types of blebs are formed by distinct mechanisms. Exp. Cell Res. 2002; 277(2):161-72. [PMID: 12083798]
  5. Keller H, and Eggli P. Protrusive activity, cytoplasmic compartmentalization, and restriction rings in locomoting blebbing Walker carcinosarcoma cells are related to detachment of cortical actin from the plasma membrane. Cell Motil. Cytoskeleton 1998; 41(2):181-93. [PMID: 9786092]
  6. Paluch E, Piel M, Prost J, Bornens M, and Sykes C. Cortical actomyosin breakage triggers shape oscillations in cells and cell fragments. Biophys. J. 2005; 89(1):724-33. [PMID: 15879479]
  7. Pollard TD, and Borisy GG. Cellular motility driven by assembly and disassembly of actin filaments. Cell 2003; 112(4):453-65. [PMID: 12600310]
  8. Charras GT, Coughlin M, Mitchison TJ, and Mahadevan L. Life and times of a cellular bleb. Biophys. J. 2007; 94(5):1836-53. [PMID: 17921219]