In 1972, Singer and Nicolson proposed a new model of the plasma membrane to better explain both microscopic observations and the plasma membrane function. This new model was called the fluid mosaic model. The model has evolved somewhat over time, but still best accounts for the structure and functions of the plasma membrane as we know it today.  The fluid mosaic model describes the structure of the plasma membrane as a mosaic of components that are able to flow and change position, while maintaining the basic integrity of the membrane. Both phospholipid molecules and embedded proteins are able to diffuse rapidly and laterally in the membrane. The fluidity of the plasma membrane is necessary for the activities of certain enzymes and transport molecules.   Plasma membranes vary in thickness.  As a comparison, human red blood cells, visible via light microscopy, are approximately 1,000 times thicker than a plasma membrane. (Figure 1)

Figure 1. The fluid mosaic model of the plasma membrane structure describes the plasma membrane as a fluid combination of phospholipids, cholesterol, proteins, and carbohydrates.

The main chemical component of the membrane is the bilayer.  The phospholipid bilayer has both hydrophilic(water-loving) and hydrophobic(water-fearing) components. The hydrophilic side, composed of polar heads, are in contact with the aqueous fluid, both inside and outside the cell.  In contrast, the hydrophobic side, composed of two nonpolar fatty acid tails, face each other forming the interior of the membrane. Cholesterol is scattered within the bilayer. This serves to strengthen and provide stability to the membrane(Figure 1).

Two types of proteins make up the second major chemical component of the plasma membrane.  Peripheral proteins are found on the exterior or interior surfaces and serve to stabilize and shape the membrane. They are found only on one side of the membrane. Filaments of the cytoskeleton provide further stability to these proteins. Integral proteins are embedded in the plasma membrane and may span all or part of the membrane.  Although they are embedded within the plasma membrane, they have the ability to move laterally. Integral proteins may serve as channels to move materials into/out of the cell.

Carbohydrates are the third major component of plasma membranes. They are always found on the exterior surface of cells and are bound  to proteins (glycoproteins) or to lipids(glycolipids). These carbohydrate chains vary in length and shape.  Along with peripheral proteins, carbohydrates form specialized sites on the cell surface that allow cells to recognize each other.

EVOLUTION IN ACTION

How Viruses Infect Specific Organs

Specific glycoprotein molecules exposed on the surface of the cell membranes of host cells are exploited by many viruses to infect specific organs. For example, HIV is able to penetrate the plasma membranes of specific kinds of white blood cells called T-helper cells and monocytes, as well as some cells of the central nervous system. The hepatitis virus attacks only liver cells.

These viruses are able to invade these cells, because the cells have binding sites on their surfaces that the viruses have exploited with equally specific glycoproteins in their coats. (Figure 2). The cell is tricked by the mimicry of the virus coat molecules, and the virus is able to enter the cell. Other recognition sites on the virus’s surface interact with the human immune system, prompting the body to produce antibodies. Antibodies are made in response to the antigens (or proteins associated with invasive pathogens). These same sites serve as places for antibodies to attach, and either destroy or inhibit the activity of the virus. Unfortunately, these sites on HIV are encoded by genes that change quickly, making the production of an effective vaccine against the virus very difficult. The virus population within an infected individual quickly evolves through mutation into different populations, or variants, distinguished by differences in these recognition sites. This rapid change of viral surface markers decreases the effectiveness of the person’s immune system in attacking the virus, because the antibodies will not recognize the new variations of the surface patterns.

Figure 2. HIV docks at and binds to the CD4 receptor, a glycoprotein on the surface of T cells, before entering, or infecting, the cell. (credit: modification of work by US National Institutes of Health/National Institute of Allergy and Infectious Diseases)