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5.1C: Membrane Fluidity - Biology

5.1C: Membrane Fluidity - Biology


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The mosaic nature of the membrane, its phospholipid chemistry, and the presence of cholesterol contribute to membrane fluidity.

Learning Objectives

  • Explain the function of membrane fluidity in the structure of cells

Key Points

  • The membrane is fluid but also fairly rigid and can burst if penetrated or if a cell takes in too much water.
  • The mosaic nature of the plasma membrane allows a very fine needle to easily penetrate it without causing it to burst and allows it to self-seal when the needle is extracted.
  • If saturated fatty acids are compressed by decreasing temperatures, they press in on each other, making a dense and fairly rigid membrane.
  • If unsaturated fatty acids are compressed, the “kinks” in their tails push adjacent phospholipid molecules away, which helps maintain fluidity in the membrane.
  • The ratio of saturated and unsaturated fatty acids determines the fluidity in the membrane at cold temperatures.
  • Cholesterol functions as a buffer, preventing lower temperatures from inhibiting fluidity and preventing higher temperatures from increasing fluidity.

Key Terms

  • phospholipid: Any lipid consisting of a diglyceride combined with a phosphate group and a simple organic molecule such as choline or ethanolamine; they are important constituents of biological membranes
  • fluidity: A measure of the extent to which something is fluid. The reciprocal of its viscosity.

Membrane Fluidity

There are multiple factors that lead to membrane fluidity. First, the mosaic characteristic of the membrane helps the plasma membrane remain fluid. The integral proteins and lipids exist in the membrane as separate but loosely-attached molecules. The membrane is not like a balloon that can expand and contract; rather, it is fairly rigid and can burst if penetrated or if a cell takes in too much water. However, because of its mosaic nature, a very fine needle can easily penetrate a plasma membrane without causing it to burst; the membrane will flow and self-seal when the needle is extracted.

The second factor that leads to fluidity is the nature of the phospholipids themselves. In their saturated form, the fatty acids in phospholipid tails are saturated with bound hydrogen atoms; there are no double bonds between adjacent carbon atoms. This results in tails that are relatively straight. In contrast, unsaturated fatty acids do not contain a maximal number of hydrogen atoms, although they do contain some double bonds between adjacent carbon atoms; a double bond results in a bend of approximately 30 degrees in the string of carbons. Thus, if saturated fatty acids, with their straight tails, are compressed by decreasing temperatures, they press in on each other, making a dense and fairly rigid membrane. If unsaturated fatty acids are compressed, the “kinks” in their tails elbow adjacent phospholipid molecules away, maintaining some space between the phospholipid molecules. This “elbow room” helps to maintain fluidity in the membrane at temperatures at which membranes with saturated fatty acid tails in their phospholipids would “freeze” or solidify. The relative fluidity of the membrane is particularly important in a cold environment. A cold environment tends to compress membranes composed largely of saturated fatty acids, making them less fluid and more susceptible to rupturing. Many organisms (fish are one example) are capable of adapting to cold environments by changing the proportion of unsaturated fatty acids in their membranes in response to the lowering of the temperature.

In animals, the third factor that keeps the membrane fluid is cholesterol. It lies alongside the phospholipids in the membrane and tends to dampen the effects of temperature on the membrane. Thus, cholesterol functions as a buffer, preventing lower temperatures from inhibiting fluidity and preventing higher temperatures from increasing fluidity too much. Cholesterol extends in both directions the range of temperature in which the membrane is appropriately fluid and, consequently, functional. Cholesterol also serves other functions, such as organizing clusters of transmembrane proteins into lipid rafts.


Tetrahymena Thermophila

Alejandro D. Nusblat , . Aaron P. Turkewitz , in Methods in Cell Biology , 2012

B Sterol Metabolism

Sterols affect membrane fluidity and permeability ( Ohvo-Rekila et al., 2002 ). In addition, they are essential components of the “lipid rafts” that have been characterized principally in animal cells, which are currently understood as membrane microdomains whose formation depends upon the affinity of sterols for sphingolipids. The partitioning of proteins in lipid rafts may be important for regulation of signal transduction pathways ( Simons and Toomre, 2000 ). Sterols also serve as precursors of bile salts and steroid hormones in mammals, brassinosteroids in plants, and fungi and ecdysteroids in arthropods.

Eukaryotic organisms can satisfy their sterol requirement by de novo synthesis in vertebrates (cholesterol), plants (stigmasterol, sitosterol, and campesterol), and fungi (ergosterol), or by obtaining them from food. Sterol auxotrophs include invertebrates (nematodes and arthropods), some ciliates (Paramecium tetraurelia), apicomplexans (Plasmodium falciparum), and some flagellated parasites (Giardia intestinalis and Trichomonas vaginalis). T. thermophila is unusual in this regard, having no detectable sterols in its membranes and, accordingly, no sterol requirement. Instead, it synthesizes tetrahymanol, a compound similar to hopanoids found in bacteria, which acts as a surrogate sterol. However, when sterols are added to the growth medium, tetrahymanol synthesis is suppressed and T. thermophila incorporates the exogenous sterol, either with or without modifications( Conner et al., 1968 ). In particular, the ciliate desaturates sterols at positions C5(6), C7(8), and C22(23) and removes the C24 ethyl group in C29 sterols (phytosterols) ( Mallory and Conner, 1971 ). By the activity of these three sterol desaturases (C-5, C-7, and C-22 sterol desaturases) and C-24 sterol deethylation, the ciliate modifies exogenous sterols and accumulates the tri-unsaturated products in its membrane.

C-22 sterol desaturases have been characterized in other eukaryotes. In T. thermophila, the C-7 and C-22 sterol-desaturating activities, found mainly in a microsomal fraction, require cytochrome b5 as shown by their inhibition with azide and cyanide ( Nusblat et al., 2005 Valcarce et al., 2000 ). This cytochrome b5 dependence is not characteristic of the C22 desaturases of plants and fungi, which require cytochrome P450. The difference is underscored by the insensitivity of the ciliate C22 desaturase to azole, a compound that strongly inhibits the corresponding plant and fungal activities. Moreover, no clear orthologs can be found in the T. thermophila genome for known C-22 sterol desaturases ( Morikawa et al., 2006 ). These observations suggest that the T. thermophila enzyme represents a new class of C-22 sterol desaturases.

The C-5 sterol desaturase present in most eukaryotic cells belongs to the fatty acid hydroxylase (FAH) superfamily of integral membrane proteins that bind an iron cofactor via a 3-histidine motif. The C-5 sterol desaturase in T. thermophila, DES5A, was identified by characterizing the phenotype resulting from deletion of a putative FAH gene ( Nusblat et al., 2009 ). The deletion mutant, which was fully viable, showed strongly diminished C-5 sterol desaturase activity, while C-7(8) and C-22(23) desaturase activities were unaffected.

The gene involved in C-24 sterol deethylation, DES24, was similarly confirmed by the disruption of putative FAH genes ( Tomazic et al., 2011 ), resulting in a strain unable to eliminate the C-24 ethyl group from different phytosterols, and probably defective at the first step in dealkylation. Interestingly, the mutant strain was highly sensitive to phytosterols in the culture media, showing defects in growth and morphology and altered tetrahymanol biosynthesis. This observation suggests that C29 sterols can impair the normal growth of Tetrahymena. While C-24 sterol deethylation activity has been characterized in other organisms including nematodes, arthropods, and green algae, the Tetrahymena enzyme represents the first molecular characterization. However, DES24 clusters phylogenetically with bacterial FAH sequences of unknown function, with no obvious orthologs in other eukaryotes, and may therefore have been acquired by lateral transfer. A variety of other observations, including substrate specificity and inhibitor studies, are also consistent with the hypothesis that the mechanism of T. thermophila C-24 deethylation differs from that in other eukaryotes.

T. thermophila, which is exposed in its environment to phytoplankton, higher plants and algae, may have developed the ability to metabolize otherwise-harmful phytosterols upon acquisition of DES24 from bacteria. Interestingly, however, Paramecium tetraurelia does not have C-24 dealkylation activity ( Conner et al., 1971 ) and requires phytosterols ( Whitaker and Nelson, 1987 ). Overall, sterol metabolism in T. thermophila seems to be the evolutionary product of a fascinating combination of gene losses (e.g., typical eukaryotic genes involved in sterol biosynthesis) combined with acquisition of bacterial genes to allow for synthesis of unusual compounds, with potentially novel mechanisms of sterol modification. This evolutionary history may be illuminated by interrogating the genomes of other Tetrahymena species as these are sequenced. In addition, further studies of the sterol pathways in T. thermophila may yield more information about lipid diversity and function.


Components of the Plasma Membrane

The plasma membrane is made up primarily of a bilayer of phospholipids with embedded proteins, carbohydrates, glycolipids, and glycoproteins, and, in animal cells, cholesterol.

The main fabric of the membrane is composed of two layers of phospholipid molecules. Phospholipid molecules have a “head” that is hydrophilic (water-loving) and polar (Figure 2). Hydrophilic polar molecules “like” water or dissolve in water. Salt and sugar are examples of hydrophilic molecules. The hydrophilic polar heads of these molecules are in contact with the watery environment outside the cell as well as the cytoplasm (composed mostly of water) inside the cell. In contrast, the interior of the membrane, composed of the tails of phospholipids, is hydrophobic (water-fearing) or non-polar (Figure 2). Hydrophilic non-polar molecules do not “like” water or dissolve in water. Oil is an example of a hydrophobic molecule.

Figure 2 Structure of a phospholipid. Notice the hydrophilic (water-loving) heads, which face the outside of the membrane and the hydrophobic (water-fearing) tails, which make up the inside of the membrane. Credit: “Phospholipid” Ain wirk wikimedia.

Proteins make up the second major chemical component of plasma membranes (Figure 1). Proteins are embedded in the plasma membrane and may go all the way through the membrane, or only be present on one side or the other. Proteins that go all the way through the membrane can serve as channels or pumps to move materials into or out of the cell. Other proteins are found on one side of the membrane or the other, but do not pass all the way through. Both types of proteins may serve as enzymes, as structural attachments for the fibers of the cytoskeleton, or as part of the cell’s recognition sites.

Carbohydrates are the third major component of plasma membranes (Figure 1). They are always found on the exterior surface of cells and are bound either to proteins (forming glycoproteins) or to lipids (forming glycolipids). These carbohydrate chains may consist of 2–60 monosaccharide units and may be either straight or branched. Along with peripheral proteins, carbohydrates form specialized sites on the cell surface that allow cells to recognize each other.

The amount of cholesterol in animal plasma membranes regulates the fluidity of the membrane and changes based on the temperature of the cell’s environment. In other words cholesterol acts as antifreeze in the cell membrane and is more abundant in animals that live in cold climates.


More Double Bonds or Unsaturated Fat:

The more phospholipids with double bonds, the more fluid the cell membrane is. This is because the double bond provides a kink within a monolayer. This prevents all of the phospholipids from packing together really closely and restricting fluidity of the membrane.

–Cold Environments: More double bonds= Better in Cold Environments

Animals living in freezing temperatures tend to have more unsaturated fat and double-bonded phospholipids in their bodies. When the environment is so cold, the cell membrane can freeze and stop moving, and that is bad. The individual phospholipids, in other words, would pack together so closely and would be more susceptible to “freezing.” Thus, animals adapted to these frigid environments have more double-bonded phospholipids in their cell membranes, due to the double bonds making kinks and spacing out the individual phospholipids from freezing together so closely.


Membrane fluidity is regulated by the C. elegans transmembrane protein FLD-1 and its human homologs TLCD1/2

Dietary fatty acids are the main building blocks for cell membranes in animals, and mechanisms must therefore exist that compensate for dietary variations. We isolated C. elegans mutants that improved tolerance to dietary saturated fat in a sensitized genetic background, including eight alleles of the novel gene fld-1 that encodes a homolog of the human TLCD1 and TLCD2 transmembrane proteins. FLD-1 is localized on plasma membranes and acts by limiting the levels of highly membrane-fluidizing long-chain polyunsaturated fatty acid-containing phospholipids. Human TLCD1/2 also regulate membrane fluidity by limiting the levels of polyunsaturated fatty acid-containing membrane phospholipids. FLD-1 and TLCD1/2 do not regulate the synthesis of long-chain polyunsaturated fatty acids but rather limit their incorporation into phospholipids. We conclude that inhibition of FLD-1 or TLCD1/2 prevents lipotoxicity by allowing increased levels of membrane phospholipids that contain fluidizing long-chain polyunsaturated fatty acids.

Editorial note: This article has been through an editorial process in which the authors decide how to respond to the issues raised during peer review. The Reviewing Editor's assessment is that all the issues have been addressed (see decision letter).

Keywords: C. elegans cell biology fluorescence recovery after photobleaching forward genetics human lipotoxicity membrane fluidity membrane homeostasis phospholipid.

Conflict of interest statement

MR, RB, ES, RD, KB, MS, JB, MP No competing interests declared, HP affiliated with AstraZeneca. The author has no other competing interests to declare.


Video Animation Showing Membrane Fluidity

This video by Stanford University demonstrates the fluidity of the plasma membrane with a neuronal cell.

[Attributions and Licenses]

This modified article is licensed under a CC BY-NC-SA 4.0 license.

Note that the video(s) in this lesson are provided under a Standard YouTube License.



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