from the Michael Behe book, Darwin's Black BoxEvolutionists fancifully forges so many theories and wishful thinking as to how a organism 'evolved' from a simpler state, development to a fully formed one.. But they don't explain the details, surely because they make the seeming probability of evolution occurring even smaller (supposing that it actually had any probability to occur at all!)Darwin himself found amazing and quite improbable for a eye, to have evolved through minute developments, improvement, during millions of years.. Let alone if he knew about that:Biochemical sketch ofthe eye's operation:When light first strikes the retina a photon interacts with a moleculecalled 11-cis-retinal, which rearranges within picoseconds to trans-retinal.(A picosecond is about the time it takes light totravel the breadth of a single human hair.) The change in the shape ofthe retinal molecule forces a change in the shape of the protein, rhodopsin,to which the retinal is tightly bound. The protein's metamorphosis altersits behavior. Now called metarhodopsin II, the protein sticks to anotherprotein, called transducin. Before bumping into metarhodopsin II,transducin had tightly bound a small molecule called GDP. But whentransducin interacts with metarhodopsin II, the GDP falls off, and amolecule called GTP binds totransducin. (GTP is closely related to, but critically different from, GDP.)GTP-transducin-metarhodopsin II now binds to a protein calledphosphodiesterase, located in the inner membrane of the cell. Whenattached to metarhodopsin II and its entourage, the phosphodiesteraseacquires the chemical ability to cut a molecule called cGMP (a chemicalrelative of both GDP and GTP). Initially there are a lot of cGMP moleculesin the cell, but the phosphodiesterase lowers its concentration, just as apulled 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, whilea separate protein actively pumps them out again. The dual action of theion channel and pump keeps the level of sodium ions in the cell within anarrow range. When the amount of cGMP is reduced because of cleavageby the phosphodiesterase, the ion channel closes, causing the cellularconcentration of positively charged sodium ions to be reduced. This causesan imbalance of charge across the cell membrane that, finally, causes acurrent 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 inthe cell, the supply of 11-cis-retinal, cGMP and sodium ions would quicklybe depleted. Something has to turn off the proteins that were turned onand 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 calciumions into the cell. The calcium is pumped back out by a different protein sothat a constant calcium concentration is maintained. When cGMP levelsfall, shutting down the ion channel, calcium ion concentration decreases,too. The phosphodiesterase enzyme, which destroys cGMP slows down atlower calcium concentration. Second, a protein called guanylate cyclasebegins to resynthesize cGMP when calcium levels start to fall. Third,while all