A short history of blebbing

  title={A short history of blebbing},
  author={Guillaume T. Charras},
  journal={Journal of Microscopy},
  • G. Charras
  • Published 1 September 2008
  • Biology
  • Journal of Microscopy
Blebs are protrusions of the cell membrane. They are the result of actomyosin contractions of the cortex, which cause either transient detachment of the cell membrane from the actin cortex or a rupture in the actin cortex. Then, cytosol streams out of the cell body and inflates the newly formed bleb. During expansion, which lasts ∼30 s, the bleb is devoid of actin and the surface area increases through further tearing of membrane from the cortex and convective flows of lipids in the plane of… 

A RhoA and Rnd3 cycle regulates actin reassembly during membrane blebbing

This study revealed that epidermal growth factor receptor kinase substrate 8 (Eps8) and ezrin are important regulators of rapid actin reassembly for the initiation and retraction of protruded blebs.

Membrane shrinkage and cortex remodelling are predicted to work in harmony to retract blebs

It is demonstrated that cortex retraction alone cannot account for bleb retraction and suggested that the mechanism works in tandem with membrane shrinking, and an emergent hysteresis loop is observed in the intracellular pressure, which suggests a potential mechanism through which a secondary bleb can be initiated as a primary bleb contracts.

Membrane bleb: A seesaw game of two small GTPases

It is proposed that a Rnd3 and RhoA cycle underlies the core machinery of continuous membrane blebbing, which is widely used for migration across species.

Assembly and composition of the cellular actin cortex

It is discovered by localisation and silencing studies, that formin Diaph1 and the Arp2/3 complex are needed for the cortex nucleation, as both localised to the cortex and depletion of either led to cortical defects.

Interaction and fusion dynamics between cellular blebs.

Multiscale Computation of Cytoskeletal Mechanics During Blebbing

A general multiscale interaction procedure is applied to the problem of cellular blebbing and is efficient enough to show cellular level effects produced by changes at the microscopic level, such as biochemical reaction rates.

abLIM1 constructs non-erythroid cortical actin networks to prevent mechanical tension-induced blebbing

Actin-binding protein abLIM1 governs the formation of dense interconnected cortical actin meshwork in non-erythroid cells to prevent mechanical tension-induced blebbing during cellular activities such as spreading and migration.



Reassembly of contractile actin cortex in cell blebs

The Rho pathway was important for cortex assembly in blebs, and Ezrin played no role in actin nucleation, but was essential for tethering the membrane to the cortex.

Life and times of a cellular bleb.

It is shown that bleb nucleation depends on pressure, membrane-cortex adhesion energy, and membrane tension, and is tested experimentally to find that retracting blebs are fivefold more rigid than expanding blebs, an increase entirely explained by the properties of the newly formed cortical actin mesh.

Actin polymerization and intracellular solvent flow in cell surface blebbing

It is postulated that blebs occur when the fluid-driven expansion of the cell membrane is sufficiently rapid to initially outpace the local rate of actin polymerization, and the rate of intracellular solvent flow driving this expansion decreases as cortical gelation is achieved, thereby leading to decreased size and occurrence of blebs.

Protrusive activity, cytoplasmic compartmentalization, and restriction rings in locomoting blebbing Walker carcinosarcoma cells are related to detachment of cortical actin from the plasma membrane.

The findings suggest that the dynamic events at the front of blebbing metazoan cells are similar to those previously found in Amoeba proteus but different from those found in lamellipodia.

Cortical actomyosin breakage triggers shape oscillations in cells and cell fragments.

It is found that adherent cells, when detached from their substrate, developed a membrane bulge devoid of detectable actin and myosin, and a constriction ring at the base of the bulge oscillated from one side of the cell to the other.

Dissection of amoeboid movement into two mechanically distinct modes

It is shown that Dictyostelium cells moving in a physiological milieu continuously produce `blebs' at their leading edges, and that focal blebbing contributes greatly to their locomotion, and concludes that amoeboid motility comprises two mechanically different processes characterized by the production of two distinct cell-surface protrusions, blebs and filopodia-lamellipodia.

A micromechanic study of cell polarity and plasma membrane cell body coupling in Dictyostelium.

Membrane tether formation from blebbing cells.

Implications of a poroelastic cytoplasm for the dynamics of animal cell shape.

Apoptotic Membrane Blebbing Is Regulated by Myosin Light Chain Phosphorylation

The model system described here should facilitate future studies of MLCK, Rho, and other signal transduction pathways activated during the execution phase of apoptosis and also implicate Rho signaling in these active morphological changes.