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This article was originally published as a chapter in the book “Design and Catastrophe: 51 Scientists Explore Evidence in Nature"
As a chemistry professor, when I study nature I see evidence of God as Creator. I have been teaching biochemistry for many years and often teach about the structure and function of cellular membranes. The cellular membrane in living cells is composed of lipids and proteins as well as some carbohydrates. The plasma membrane of animals and bacteria is a lipid bilayer that serves as a barrier between the inside of each living cell and its environment. One of the leaflets of the lipid bilayer is exposed to the outside of the cell, and the other leaflet is exposed to the inside of the cell, or the cytoplasmic side. The two leaflets are very different in composition—they are asymmetrical.
Typical lipids in the cell membrane are phospholipids such as glycolipids, sphingomyelin, phosphatidylserine, phosphatidylcholine, and phosphatidylinositol. In living cells, these types of lipids are not randomly distributed between the two bilayers. Glycolipids contain carbohydrates and are always found on the outer leaflet of the plasma membrane. They are never found on the layer that faces the cytoplasm. Sphingomyelin is also almost always found in this outer leaflet. Phosphatidylserine, however, is found primarily in the opposite side of the bilayer—the inner leaflet. How does this asymmetry arise? In the lab, when researchers work to assemble a lipid bilayer, the phospholipids and glycolipids self-assemble in a random symmetrical manner, producing a bilayer membrane with no asymmetry.[1]
Many proteins are found in biological membranes. Some are positioned across the membrane and are exposed on both sides (both the cytoplasmic side and the exterior of the cell). These are called transmembrane proteins. Some are pumps and channels, and others are receptor proteins. These proteins need to be oriented in the membrane the correct way. For example, if the ligand-binding site of the receptor protein is facing the extracellular environment and is able to bind to a hormone molecule, it will change the 3D structure of the transmembrane protein, allowing the signal to be noticed and transmitted to the inside of the living cell.
Pumps and channels must be correctly oriented in the bilayer so the ions, or molecules, being moved across the cell membrane are transported the correct way. For example, the sodium-potassium ATPase is an important pump in many cells. It always pumps sodium ions out of the cell while it pumps potassium ions into the cell. This pump requires the use of ATP (cellular energy) to pump these ions across the membrane, setting up an ion gradient. The ion gradient can then be used by other transmembrane proteins called secondary transporters to pump other important molecules or ions across the membrane. One example is the sodium-glucose linked transporter, which uses the sodium gradient to pump glucose into the cell; sodium is allowed into the cell through this transporter as glucose is pumped in. These protein pumps and transporters never “flip” in orientation— that is, protein channels and pumps do not experience “transverse diffusion.” Scientists have never found these proteins inserted into the membrane the wrong way. These specifically oriented proteins are another example of the asymmetry of cellular membranes.
However, phospholipids are able to occasionally flip from one leaflet of the bilayer to the other, undergoing spontaneous transverse diffusion. This flipping diminishes the asymmetry; after a phospholipid flips into the wrong leaflet, it is usually placed back into its original leaflet by special proteins in the cell membrane called flippases. For example, phosphatidylserine is found mostly on the inner leaflet of the plasma membrane. When it flips to the leaflet facing the exterior of the cell, the flippase notices the phosphatidylserine molecule in the wrong place and flips it back to the inner leaflet. This is important for the cell because when phagocytes (macrophages) notice phosphatidylserine molecules exposed to the outside of a cell, they recognize this and assume the cell has experienced apoptosis (cell death). Phagocytes are signaled to destroy and remove a cell that has phosphatidylserine in the outer bilayer.[2] In this case, the asymmetry of the phosphatidylserine excluded from the outer leaflet saves the cell from being destroyed by other cells.
Another attribute of the asymmetrical distribution of the phospholipids in a cellular membrane is the intrinsic membrane potential, or non-zero transmembrane potential, of the plasma membrane in living cells. This membrane potential is caused by the positively charged “head groups” of phosphatidylcholine and sphingomyelin on the extracellular side of the plasma membrane and the net negatively charged head group of phosphatidylserine that is almost entirely on the inner leaflet. This transmembrane potential is linked to varied physiological phenomena.[3]
I have wondered how this asymmetry was originally set up in a cell. A cell would not be able to function for long if the phospholipids (such as phosphatidylserine) and protein channels or pumps were inserted randomly into the cell membrane. If the asymmetry wasn’t initially present in a living cell membrane, the ion gradients needed for other cellular processes would never be established, and the cell would quickly die. While thinking about this problem, I was stopped in my tracks when I read this line in my biochemistry textbook: “This absolute asymmetry is preserved because membrane proteins do not rotate from one side of the membrane to the other and because membranes are always synthesized by the growth of preexisting membranes.”[4]
This implies that there must always be a preexisting membrane from which further cellular membranes may grow. This information fits a model in which a Creator could design and create the original cell membranes with absolute asymmetry of the lipids and proteins in them.
NOTES
[1] D Marquardt, B Geier, G Pabst. Asymmetric lipid membranes: towards more realistic model systems. Membranes 2015; 5(2):180–196. doi:10.3390/membranes5020180.
[2] M Darland-Ransom, X Wang, C-L Sun, J Mapes, K Gengyo-Ando, S Mitani, D Xue. Role of C. elegans TAT-1 protein in maintaining plasma mem-brane phosphatidylserine asymmetry. Science 2008; 320(5875):528–531. doi: 10.1126/science.1155847.
[3] B Fadeel, D Xue. The ins and outs of phospholipid asymmetry in the plasma membrane: roles in health and disease. Critical Reviews in Biochemistry and Molecular Biology 2009; 44(5):264–277. doi:10.1080/1040230903193307.
[4] JM Berg, JL Tymoczko, L Stryer. Biochemistry. 7th ed. New York: W.H. Freeman; 2012, p. 364.
Carrie A. C. Wolfe is a professor of chemistry at Union College (Lincoln, NE). She holds a PhD in Chemistry from the University of Nebraska-Lincoln. In her teaching career, she has developed curricular material on the subject of faith and science for courses on origins.