Biologists Use the Fluid Mosaic Model to Describe Membrane Structure

Biologists Use the Fluid Mosaic Model to Describe Membrane Structure

Describe the fluid mosaic model of plasma membrane

fluid mosaic model
explains various observations regarding the construction of functional cell membranes. Co-ordinate to this biological model, in that location is a lipid bilayer (two molecules thick layer consisting primarily of amphipathic phospholipids) in which protein molecules are embedded. The phospholipid bilayer gives fluidity and elasticity to the membrane. Small amounts of carbohydrates are likewise found in the cell membrane. The biological model, which was devised by Seymour Jonathan Singer and Garth L. Nicolson in 1972, describes the cell membrane as a 2-dimensional liquid that restricts the lateral improvidence of membrane components. Such domains are defined by the existence of regions within the membrane with special lipid and protein cocoon that promote the formation of lipid rafts or protein and glycoprotein complexes. Another fashion to define membrane domains is the association of the lipid membrane with the cytoskeleton filaments and the extracellular matrix through membrane proteins.[1]
The electric current model describes important features relevant to many cellular processes, including: cell-cell signaling, apoptosis, cell segmentation, membrane budding, and jail cell fusion. The fluid mosaic model is the most acceptable model of the plasma membrane. Its main function is to separate the contents of the cell from the outside.

Chemic makeup


Components Location Functions
Phospholipid The main textile of plasma membrane It provides selective permeability to the cell membrane.
Carbohydrates Fastened to proteins on outside membrane layers Information technology helps in cell-to-cell recognition.
Cholesterol Betwixt phospholipids and phospholipid bilayers Information technology helps the plasma membrane to retain its fluidity.
Proteins Embedded within or on the surface of phospholipid layers These form channels to allow the motility of molecules.

Experimental evidence


The fluid belongings of functional biological membranes had been determined through labeling experiments, 10-ray diffraction, and calorimetry. These studies showed that integral membrane proteins lengthened at rates affected by the viscosity of the lipid bilayer in which they were embedded, and demonstrated that the molecules within the cell membrane are dynamic rather than static.[2]

Previous models of biological membranes included the Robertson Unit Membrane Model and the Davson-Danielli Tri-Layer model.[ane]
These models had proteins nowadays equally sheets neighboring a lipid layer, rather than incorporated into the phospholipid bilayer. Other models described repeating, regular units of protein and lipid. These models were non well supported by microscopy and thermodynamic information, and did non suit evidence for dynamic membrane properties.[1]

The Frye-Edidin experiment showed that when ii cells are fused the proteins of both diffuse around the membrane and mingle rather than being locked to their area of the membrane.

An important experiment that provided evidence supporting fluid and dynamic biological was performed by Frye and Edidin. They used Sendai virus to force homo and mouse cells to fuse and class a heterokaryon. Using antibody staining, they were able to show that the mouse and human proteins remained segregated to separate halves of the heterokaryon a brusque time after cell fusion. However, the proteins eventually diffused and over fourth dimension the edge between the two halves was lost. Lowering the temperature slowed the rate of this diffusion past causing the membrane phospholipids to transition from a fluid to a gel phase.[3]
Singer and Nicolson rationalized the results of these experiments using their fluid mosaic model.[2]

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The fluid mosaic model explains changes in structure and behavior of cell membranes nether unlike temperatures, as well as the association of membrane proteins with the membranes. While Singer and Nicolson had substantial bear witness drawn from multiple subfields to support their model, recent advances in fluorescence microscopy and structural biology take validated the fluid mosaic nature of jail cell membranes.

Subsequent developments


Membrane asymmetry


Additionally, the two leaflets of biological membranes are asymmetric and divided into subdomains equanimous of specific proteins or lipids, allowing spatial segregation of biological processes associated with membranes. Cholesterol and cholesterol-interacting proteins tin concentrate into lipid rafts and constrain cell signaling processes to only these rafts.[four]
Another form of disproportion was shown by the work of Mouritsen and Bloom in 1984, where they proposed a Mattress Model of lipid-protein interactions to accost the biophysical prove that the membrane can range in thickness and hydrophobicity of proteins.[5]

Non-bilayer membranes


The beingness of not-bilayer lipid formations with important biological functions was confirmed subsequent to publication of the fluid mosaic model. These membrane structures may be useful when the cell needs to propagate a non bilayer form, which occurs during cell segmentation and the formation of a gap junction.[6]

Membrane curvature


The membrane bilayer is non ever flat. Local curvature of the membrane tin be caused past the asymmetry and non-bilayer organization of lipids equally discussed in a higher place. More than dramatic and functional curvature is achieved through BAR domains, which bind to phosphatidylinositol on the membrane surface, assisting in vesicle formation, organelle formation and cell partitioning.[7]
Curvature evolution is in abiding flux and contributes to the dynamic nature of biological membranes.[8]

Lipid motility inside the membrane


During the decade of 1970, it was acknowledged that individual lipid molecules undergo gratuitous lateral diffusion within each of the layers of the lipid membrane.[9]
Diffusion occurs at a loftier speed, with an average lipid molecule diffusing ~2 µm, approximately the length of a large bacterial cell, in about 1 second.[9]
Information technology has also been observed that individual lipid molecules rotate chop-chop around their own axis.[9]
Moreover, phospholipid molecules can, although they seldom exercise, migrate from one side of the lipid bilayer to the other (a procedure known every bit flip-flop). Still, flip-bomb might exist enhanced by flippase enzymes. The processes described above influence the disordered nature of lipid molecules and interacting proteins in the lipid membranes, with consequences to membrane fluidity, signaling, trafficking and part.

Restrictions to bilayer fluidity


In that location are restrictions to the lateral mobility of the lipid and protein components in the fluid membrane imposed past the formation of subdomains within the lipid bilayer. These subdomains arise past several processes
binding of membrane components to the extracellular matrix, nanometric membrane regions with a particular biochemical composition that promote the germination of lipid rafts and protein complexes mediated by protein-protein interactions.[1]
Furthermore, protein-cytoskeleton associations mediate the germination of “cytoskeletal fences”, corrals wherein lipid and membrane proteins tin diffuse freely, but that they can seldom go out.[1]
Restriction on lateral diffusion rates of membrane components is very of import considering information technology allows the functional specialization of detail regions within the jail cell membranes.

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Lipid rafts


Lipid rafts are membrane nanometric platforms with a detail lipid and protein composition that laterally diffuse, navigating on the liquid bilipid layer. Sphingolipids and cholesterol are of import building blocks of the lipid rafts.[10]

Poly peptide complexes


Cell membrane proteins and glycoproteins do not be as single elements of the lipid membrane, as showtime proposed by Singer and Nicolson in 1972. Rather, they occur equally diffusing complexes within the membrane.[1]
The assembly of unmarried molecules into these macromolecular complexes has of import functional consequences for the prison cell; such as ion and metabolite transport, signaling, prison cell adhesion, and migration.[1]

Cytoskeletal fences (corrals) and bounden to the extracellular matrix


Some proteins embedded in the bilipid layer interact with the extracellular matrix outside the cell, cytoskeleton filaments inside the cell, and septin ring-similar structures. These interactions take a strong influence on shape and structure, as well as on compartmentalization. Moreover, they impose concrete constraints that restrict the costless lateral improvidence of proteins and at to the lowest degree some lipids within the bilipid layer.[1]

When integral proteins of the lipid bilayer are tethered to the extracellular matrix, they are unable to lengthened freely. Proteins with a long intracellular domain may collide with a argue formed by cytoskeleton filaments.[eleven]
Both processes restrict the diffusion of proteins and lipids directly involved, as well every bit of other interacting components of the cell membranes.

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Due south.cerevisiae
Septin ring-like structures (in dark-green) can pinch prison cell membranes and divide them into subdomains.

Septins are a family of GTP-binding proteins highly conserved amid eukaryotes. Prokaryotes accept like proteins chosen paraseptins. They form compartmentalizing ring-similar structures strongly associated with the jail cell membranes. Septins are involved in the formation of structures such equally, cilia and flagella, dendritic spines, and yeast buds.[12]

Historical timeline


  • 1895
    – Ernest Overton hypothesized that cell membranes are made out of lipids.[13]
  • 1925
    – Evert Gorter and François Grendel found that cerise blood cell membranes are formed by a fatty layer two molecules thick,
    they described the bilipid nature of the cell membrane.[14]
  • 1935
    – Hugh Davson and James Danielli proposed that lipid membranes are layers composed by proteins and lipids with pore-similar structures that allow specific permeability for certain molecules. And then, they suggested a model for the cell membrane, consisting of a lipid layer surrounded by protein layers at both sides of information technology.[15]
  • 1957
    – J. David Robertson, based on electron microscopy studies, establishes the “Unit Membrane Hypothesis”. This, states that all membranes in the cell,
    i.due east.
    plasma and organelle membranes, have the same construction: a bilayer of phospholipids with monolayers of proteins at both sides of it.[16]
  • 1972
    – SJ Vocalist and GL Nicolson proposed the fluid mosaic model equally an explanation for the information and latest evidence regarding the construction and thermodynamics of cell membranes.[2]
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Notes and references


  1. ^









    Nicolson GL (2014). “The Fluid—Mosaic Model of Membrane Structure: Notwithstanding relevant to understanding the structure, function and dynamics of biological membranes after more than forty years”.
    Biochimica et Biophysica Acta (BBA) – Biomembranes.
    (half-dozen): 1451–146. doi:10.1016/j.bbamem.2013.10.019. PMID 24189436.

  2. ^




    Vocalizer SJ, Nicolson GL (February 1972). “The fluid mosaic model of the construction of cell membranes”.
    (4023): 720–31. doi:ten.1126/science.175.4023.720. PMID 4333397. S2CID 83851531.

  3. ^

    Frye LD, Edidin Thou (1970). “The rapid intermixing of jail cell surface antigens after formation of mouse-human heterokaryons”.
    J Cell Sci.
    (ii): 319–35. doi:x.1242/jcs.7.2.319. PMID 4098863.

  4. ^

    Silvius JR (2005). “Partitioning of membrane molecules between raft and non-raft domains: Insights from model-membrane studies”.
    Biochimica et Biophysica Acta (BBA) – Molecular Jail cell Research.
    (3): 193–202. doi:ten.1016/j.bbamcr.2005.09.003. PMID 16271405.

  5. ^

    Mouritsen OG, Bloom M (1984). “Mattress model of lipid-protein interactions in membranes”.
    Biophys J.
    (ii): 141–153. doi:10.1016/S0006-3495(84)84007-two. PMC1435039. PMID 6478029.

  6. ^

    van den Brink-van der Laan E; et al. (2004). “Nonbilayer lipids affect peripheral and integral membrane proteins via changes in the lateral pressure profile”.
    Biochim Biophys Acta.
    (1–2): 275–88. doi:10.1016/j.bbamem.2004.06.010. PMID 15519321.

  7. ^

    Frost A; et al. (2009). “The BAR domain superfamily: membrane-molding macromolecules”.
    Prison cell.
    (ii): 191–6. doi:10.1016/j.cell.2009.04.010. PMC4832598. PMID 19379681.

  8. ^

    Rodríguez-García R; et al. (2009). “Bimodal spectrum for the curvature fluctuations of bilayer vesicles: pure bending plus hybrid curvature-dilation modes”.
    Phys Rev Lett.
    (12): 128101. doi:10.1103/PhysRevLett.102.128101. PMID 19392326.

  9. ^




    Alberts B, Johnson A, Lewis J, et al. (2008).
    Molecular Biology of the Cell
    (5th ed.). New York: Garland Science. pp. 621–622. ISBN978-0-8153-4105-v.

  10. ^

    Lingwood D, Simons K (2010). “Lipid rafts as a membrane-organizing principle”.
    (5961): 46–l. doi:ten.1126/science.1174621. PMID 20044567. S2CID 35095032.

  11. ^

    Grand. Vereb; et al. (2003). “Dynamic, however structured: The jail cell membrane three decades after the Singer–Nicolson model”.
    (fourteen): 8053–8058. doi:10.1073/pnas.1332550100. PMC166180. PMID 12832616.

  12. ^

    Juha Saarikangas; Yves Barral (2011). “The emerging functions of septins in metazoans”.
    EMBO Reports.
    (11): 1118–1126. doi:10.1038/embor.2011.193. PMC3207108. PMID 21997296.

  13. ^

    Overton, E (1895). “Uberdie osmotischen Eigenshafter der Lebenden Pflanzen und tierzelle”.
    VJSCHR Naturf Ges Zurich.
    twoscore: 159–201.

  14. ^

    Eastward. Gorter; F. Grendel (1925). “On Biomolecular Layers of Lipoids on the Chromocytes of the Blood”.
    Journal of Experimental Medicine.
    (iv): 439–443. doi:10.1084/jem.41.iv.439. PMC2130960. PMID 19868999.

  15. ^

    James Danielli; Hugh Davson (1935). “A contribution to the theory of permeability of thin films”.
    Journal of Cellular and Comparative Physiology.
    (4): 495–508. doi:10.1002/jcp.1030050409.

  16. ^

    John E. Heuser (1995). “In Memory of J. David Robertson”
    Newsletter of the American Society of Jail cell Biology.

Biologists Use the Fluid Mosaic Model to Describe Membrane Structure