Bleb (cell biology)

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In cell biology, a bleb is a protrusion, or bulge, of the plasma membrane of a cell, caused by localized decoupling of the cytoskeleton from the plasma membrane.[1] Blebbing or zeiosis is the formation of blebs.

The process of apoptosis, with blebbing shown in the middle illustration


Bleb growth is driven by intracellular pressure generated in the cytoplasm by the contractile cell cortex.

Bleb formation can be initiated in two ways: 1) through local rupture of the cortex or 2) through local detachment of the cortex from the plasma membrane.[2] This generates a weak spot through which the cytoplasm can flow, leading to the expansion of a bulge of membrane. The cytoplasmic flow is driven by hydrostatic pressure inside the cell.[3][4]

Physiological functions[edit]

During apoptosis (programmed cell death), the cell's cytoskeleton breaks up and causes the membrane to bulge outward.[5] These bulges may separate from the cell, taking a portion of cytoplasm with them, to become known as apoptotic bodies. Phagocytic cells eventually consume these fragments and the components are recycled.

Blebbing also has important functions in other cellular processes, including cell locomotion, cell division, and physical or chemical stresses. The types of blebs vary greatly, including variations in bleb growth rates, size, contents, and actin content. It also plays an important role in all five varieties of necrosis, a generally detrimental process. However, cell organelles do not spread into necrotic blebs.


In 2004, a chemical known as blebbistatin was shown to inhibit the formation of blebs. This agent was discovered in a screen for small molecule inhibitors of nonmuscle myosin IIA and was shown to lower the affinity of myosin with actin,[6][7][8] thus altering the contractile forces that impinge on the cytoskeleton-membrane interface.


  1. ^ Fackler OT, Grosse R (Jun 2008). "Cell motility through plasma membrane blebbing". J Cell Biol. 181 (6): 879–84. doi:10.1083/jcb.200802081. PMC 2426937. PMID 18541702. 
  2. ^ Charras, G; Paluch, E (Sep 2008). "Blebs lead the way: how to migrate without lamellipodia.". Nature reviews. Molecular cell biology 9 (9): 730–6. doi:10.1038/nrm2453. PMID 18628785. 
  3. ^ Charras, GT; Yarrow, JC; Horton, MA; Mahadevan, L; Mitchison, TJ (May 19, 2005). "Non-equilibration of hydrostatic pressure in blebbing cells.". Nature 435 (7040): 365–9. doi:10.1038/nature03550. PMID 15902261. 
  4. ^ Tinevez, JY; Schulze, U; Salbreux, G; Roensch, J; Joanny, JF; Paluch, E (Nov 3, 2009). "Role of cortical tension in bleb growth.". Proceedings of the National Academy of Sciences of the United States of America 106 (44): 18581–6. doi:10.1073/pnas.0903353106. PMID 19846787. 
  5. ^ Vermeulen K, Van Bockstaele DR, Berneman ZN (Oct 2005). "Apoptosis: mechanisms and relevance in cancer". Ann Hematol. 84 (10): 627–39. doi:10.1007/s00277-005-1065-x. PMID 16041532. 
  6. ^ Straight AF,Cheung A, Limouze J, Chen I, Westwood NJ, Sellers JR, and Mitchison TJ (March 2003). "Dissecting temporal and Spatial control of cytokinesis with a myosin II inhibitor". Science 299 (5613): 1743–47. Bibcode:2003Sci...299.1743S. doi:10.1126/science.1081412. PMID 12637748. 
  7. ^ Kovács M, Tóth J, Hetényi C, Málnási-Csizmadia A, Sellers JR (Aug 2004). "Mechanism of blebbistatin inhibition of myosin II". J Biol Chem. 279 (34): 35557–63. doi:10.1074/jbc.M405319200. PMID 15205456. 
  8. ^ Limouze J, Straight AF, Mitchison T, Sellers JR (2004). "Specificity of blebbistatin, an inhibitor of myosin II". J Muscle Res Cell Motil. 25 (4–5): 337–41. doi:10.1007/s10974-004-6060-7. PMID 15548862. 


External links[edit]

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