The book: “Darwin’s Black Box:” The Biochemical Challenge to Evolution was written to challenge evolution. Author Michael Behe convinced himself that the biochemistry of the retina provides evidence of some kind of super-mind which, like a footprint in the snow is evidence of an animal, the biochemistry proves God was her. It doesn’t. All it proves is part of the body is mind-numbingly complex. How it came into existence isn’t evidence of a creator anymore than the existence of a footprint in the snow proves there’s a creator of the universe. It’s such a mind-numbingly boring exegesis that is deserves reading to prove the reaction is complex. Here’s part of Behe’s description:
Quote: “When light first strikes the retina a photon interacts with a molecule called 11-cis-retinal, which rearranges within picoseconds to trans-retinal. (A picosecond is one trillionth of a second.) The change in the shape of the retinal molecule forces a change in the shape of the protein, rhodopsin, to which the retinal is tightly bound.
“The protein’s metamorphosis alters its behavior. Now called metarhodopsin II, the protein sticks to another protein, called transducin. Before bumping into metarhodopsin II, transducin had tightly bound a small molecule called GDP. But when transducin interacts with metarhodopsin II, the GDP falls off, and a molecule called GTP binds to transducin. (GTP is closely related to, but critically different from, GDP.)
“GTP-transducin-metarhodopsin II now binds to a protein called phosphodiesterase, located in the inner membrane of the cell. When attached to metarhodopsin II and its entourage, the phosphodiesterase acquires the chemical ability to “cut” a molecule called cGMP (a chemical relative of both GDP and GTP). Initially there are a lot of cGMP molecules in the cell, but the phosphodiesterase lowers its concentration, just as a pulled plug lowers the water level in a bathtub. Another membrane protein that binds cGMP is called an ion channel. It acts as a gateway that regulates the number of sodium ions in the cell. Normally the ion channel allows sodium ions to flow into the cell, while a separate protein actively pumps them out again. The dual action of the ion channel and pump keeps the level of sodium ions in the cell within a narrow range. When the amount of cGMP is reduced because of cleavage by the phosphodiesterase, the ion channel closes, causing the cellular concentration of positively charged sodium ions to be reduced. This causes an imbalance of charge across the cell membrane that, finally, causes a current to be transmitted down the optic nerve to the brain. The result, when interpreted by the brain, is vision. If the reactions mentioned above were the only ones that operated in the cell, the supply of 11-cis-retinal, cGMP, and sodium ions would quickly be depleted. Something has to turn off the proteins that were turned on and restore the cell to its original state. Several mechanisms do this. First, in the dark the ion channel (in addition to sodium ions) also lets calcium ions into the cell. The calcium is pumped back out by a different protein so that a constant calcium concentration is maintained. When cGMP levels fall, shutting down the ion channel, calcium ion concentration decreases, too. The posphodiesterase enzyme, which destroys cGMP, slows down at lower calcium concentration. Second, a protein called guanylate cyclase begins to resynthesize cGMP when calcium levels start to fall. Third, while all of this is going on, metarhodopsin II is chemically modified by an enzyme called rhodopsin kinase. The modified rhodopsin then binds to a protein known as arrestin, which prevents the rhodopsin from activating more transducin. So the cell contains mechanisms to limit the amplified signal started by a single photon. Trans-retinal eventually falls off of rhodopsin and must be reconverted to 11-cis-retinal and again bound by rhodopsin to get back to the starting point for another visual cycle. To accomplish this, trans-retinal is first chemically modified by an enzyme to trans-retinol— a form containing two more hydrogen atoms. A second enzyme then converts the molecule to 11-cis-retinol. Finally, a third enzyme removes the previously added hydrogen atoms to form 11-cis-retinal, a cycle is complete.
But Behe neglected to tell us about the length of time that was available for an organism to develop what is a rather routine set of activities during fetal development. Instead of deciding his description was evidence of God, he should tell us about the trillions upon trillions of times the retinal tissue developed until it reached it present state. Given a sufficient amount of time the reproduction cycle could easily produce such a thing.