Skip to comments.Intelligent design: Who has designs on your students' minds?
Posted on 01/11/2006 2:50:12 PM PST by cougar_mccxxi
The intelligent-design movement is a small but growing force on US university campuses. For some it bridges the gap between science and faith, for others it goes beyond the pale. Geoff Brumfiel meets the movement's vanguard.
For a cold Tuesday night in March, the turnout is surprisingly good. Twenty or so fresh-faced college students are gathered together in a room in the student union at George Mason University in Fairfax, Virginia, the state's largest public university. They are there for the first meeting of Salvador Cordova's Intelligent Design and Evolution Awareness (IDEA) club.
(Excerpt) Read more at nature.com ...
Uh, oh. Here we go ...
After the Dover decision, he'd better apply to study cosmetology instead.
Maybe he'll do a nice dissertation saying the big bang is all bunk??? Only need one reference, so the whole thing would probably fit all on one page, don't you think?
Twenty students? Is that it? Some kind of "growing force" that is.
As opposed to the evolution-only folks, who believe that the history of biology is just a series of lucky, lucky events. Take the following description of how human vision works:
When light first strikes the retina, a photon interacts with a molecule called 11-cis-retinal, which rearranges within picoseconds to trans-retinal. The change in the shape of retinal forces a change in the shape of the protein, rhodopsin, to which the retinal is tightly bound. The protein's metamorphosis alters its behavior, making it stick to another protein called transducin. Before bumping into activated rhodopsin, transducin had tightly bound a small molecule called GDP. But when transducin interacts with activated rhodopsin, the GDP falls off and a molecule called GTP binds to transducin. (GTP is closely related to, but critically different from, GDP.)
GTP-transducin-activated rhodopsin now binds to a protein called phosphodiesterase, located in the inner membrane of the cell. When attached to activated rhodopsin and its entourage, the phosphodiesterase acquires the ability to chemically 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, like 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 which, finally, causes a current to be transmitted down the optic nerve to the brain. The result, when interpreted by the brain, is vision.
Can evolution really tell me HOW all those chemicals got to the right place at the time? Did a jiggly bug 500 million years ago just happen to create phosphodiesterase one day and pass it from generation to generation until whatever species it eventually evolved to had a use for it? Nope, evolution-fanatics CAN'T tell us that but rather give their opinions, which makes it just as much "science" as Intelligent Design. Not only that, but the opinions offered tend to be on the "and that's how the tiger got his stripes" level with a few technical words to scare the non-scientists. For human vision, the "that's how the tiger got his stripes" story probably goes something like this:
Once upon a time, a very lucky and special bacteria had a spot on it that was sensitive to light. We'll call it a chromosphere. Never mind where the spot came from or why it was sensitive to light or even why it was a vitamin-A derivative, because the bacteria had never taken any vitamin-A tablets. But that special spot gave the lucky, lucky bacteria to avoid being eaten by the Blind Blue Meanie bacteria, and thus lived longer and had more babies. This was, of course, during the time of the Cambrian explosion, which was a very lucky time. As the animal evolved, more and more chemicals came along and made vision even better. For a while, the photoreceptors were wired into the creature's big toe, but that didn't work and the photoreceptors, in a stroke of luck, wired themselves into the brain.
Throw in a few more fancy words, have it peer-reviewed by people who would be ostracised if they got suspicious about how many times luck intervened, and you now have a credible theory of the evolution of vision.
For what it's worth, I believe that evolution is a fact and that animals and plants have evolved into new species to function better within their environment. However, my education is in chemistry and chemistry involves just a little more than saying, "That hand looks like that flipper so the hand must have evolved from the flipper." Winning the lottery once is due to chance. Winning the 50 weeks in a row points implies that something other than chance is behind the winnings, no matter how much the lottery judges protest.
Natural selection, anyone?
With your description of the design of the the eye this statement seems really strange. Can you elaborate?
Your presentation portrays the vision system as some unique system unrelated to any other biological system. Light driven ion pumps occur in bacteria. Halobacter halobium contains a similar system with a proton pump, as far as the molecules go. Ion channels and transmembrane pumps are not unique here either. The 7 helix bundle transmenbrane glycoprotein with 20-28 hydrophobic amino acids is a common receptor motif. It occurs in rhodopsin, a2adrenoreceptors and muscarinic acetylcholine receptors of nerve synapses. Phosphodiesterase is also common, as is the cGDP. cGMP is a common regulator of ion channel conductance, glycogenolysis, and cellular apoptosis. It also relaxes smooth muscle tissues. In blood vessels, relaxation of vascular smooth muscles lead to vasodilation and increased blood flow.
There's no luck, or design involved in the creation of these systems. They develop as allowed by changes that occur to the cellular system, principally to the DNA coded blueprint. Ignoring, or otherwise failing to note the commonalities and similarities will certainly lead to obfuscation and a failure to understand how evolution works. Your vision mechanism occured in one cell with componenets common and similar to those found elsewhere.
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