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Michael J. Behe
Discovery Institute

A Series of Eyes
How do we see? In the 19th century the anatomy of the eye was known in great detail, and its sophisticated features astounded everyone who was familiar with them. Scientists of the time correctly observed that if a person were so unfortunate as to be missing one of the eye's many integrated features, such as the lens, or iris, or ocular muscles, the inevitable result would be a severe loss of vision or outright blindness. So it was concluded that the eye could only function if it were nearly intact.

Charles Darwin knew about the eye too. In the Origin of Species, Darwin dealt with many objections to his theory of evolution by natural selection. He discussed the problem of the eye in a section of the book appropriately entitled "Organs of extreme perfection and complication." Somehow, for evolution to be believable, Darwin had to convince the public that complex organs could be formed gradually, in a step-by-step process.

He succeeded brilliantly. Cleverly, Darwin didn't try to discover a real pathway that evolution might have used to make the eye. Instead, he pointed to modern animals with different kinds of eyes, ranging from the simple to the complex, and suggested that the evolution of the human eye might have involved similar organs as intermediates.

Here is a paraphrase of Darwin's argument. Although humans have complex camera-type eyes, many animals get by with less. Some tiny creatures have just a simple group of pigmented cells, or not much more than a light sensitive spot. That simple arrangement can hardly be said to confer vision, but it can sense light and dark, and so it meets the creature's needs. The light-sensing organ of some starfishes is somewhat more sophisticated. Their eye is located in a depressed region. This allows the animal to sense which direction the light is coming from, since the curvature of the depression blocks off light from some directions. If the curvature becomes more pronounced, the directional sense of the eye improves. But more curvature lessens the amount of light that enters the eye, decreasing its sensitivity. The sensitivity can be increased by placement of gelatinous material in the cavity to act as a lens. Some modern animals have eyes with such crude lenses. Gradual improvements in the lens could then provide an image of increasing sharpness, as the requirements of the animal's environment dictated.

Using reasoning like this, Darwin convinced many of his readers that an evolutionary pathway leads from the simplest light sensitive spot to the sophisticated camera-eye of man. But the question remains, how did vision begin? Darwin persuaded much of the world that a modern eye evolved gradually from a simpler structure, but he did not even try to explain where his starting point for the simple light sensitive spot came from. On the contrary, Darwin dismissed the question of the eye's ultimate origin:

How a nerve comes to be sensitive to light hardly concerns us more than how life itself originated. He had an excellent reason for declining the question: it was completely beyond nineteenth century science. How the eye works; that is, what happens when a photon of light first hits the retina simply could not be answered at that time. As a matter of fact, no question about the underlying mechanisms of life could be answered. How did animal muscles cause movement? How did photosynthesis work? How was energy extracted from food? How did the body fight infection? No one knew.

To Darwin vision was a black box, but today, after the hard, cumulative work of many biochemists, we are approaching answers to the question of sight. Here is a brief overview of the biochemistry of vision. 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.

My explanation is just a sketchy overview of the biochemistry of vision. Ultimately, though, this is what it means to "explain" vision. This is the level of explanation for which biological science must aim. In order to truly understand a function, one must understand in detail every relevant step in the process. The relevant steps in biological processes occur ultimately at the molecular level, so a satisfactory explanation of a biological phenomenon such as vision, or digestion, or immunity must include its molecular explanation.

Now that the black box of vision has been opened it is no longer enough for an "evolutionary explanation" of that power to consider only the anatomical structures of whole eyes, as Darwin did in the nineteenth century, and as popularizers of evolution continue to do today. Each of the anatomical steps and structures that Darwin thought were so simple actually involves staggeringly complicated biochemical processes that cannot be papered over with rhetoric. Darwin's simple steps are now revealed to be huge leaps between carefully tailored machines. Thus biochemistry offers a Lilliputian challenge to Darwin. Now the black box of the cell has been opened and a Lilliputian world of staggering complexity stands revealed. It must be explained.

Irreducible Complexity
How can we decide if Darwin's theory can account for the complexity of molecular life? It turns out that Darwin himself set the standard. He acknowledged that:

If it could be demonstrated that any complex organ existed which could not possibly have been formed by numerous, successive, slight modifications, my theory would absolutely break down. But what type of biological system could not be formed by "numerous, successive, slight modifications"?

Well, for starters, a system that is irreducibly complex. Irreducible complexity is just a fancy phrase I use to mean a single system which is composed of several interacting parts, and where the removal of any one of the parts causes the system to cease functioning.

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Yea gads. Why did you have to paste the whole thing?

The answers to the questions Behe raised are not simple, but they do exist.

Firstly, quoting Darwin in reference to molecular processes is hardly fair. Darwin was unaware of the role of DNA, so he could only imagine small changes to the physical make-up of an organism (the phenotype, as biologists call it). But nowadays we think in terms of changes to the DNA (or genotype). As anyone with an inherited genetic disorder can tell you, small changes to the DNA can have big effects on the body.

Secondly, the complex web of interactions he described is by no means something custom-designed for the eye. Ion channels are found in almost every cell, and cyclic GMP and its close relative cyclic AMP are ubiquitous signalling molecules. Most of the apparatus of vision has been borrowed from earlier tricks that life had at its disposal before vision was even invented. And sometimes these borrowings show clearly how the course of evolution has run.

Quote:

[S.T.D.]

Check these out:

http://www.talkorigins.org/faqs/behe/review.html
Keith Robison reviews Michael Behe's book Darwin's Black Box, which claims that many biological systems are "irreducibly complex" -- that in order to evolve, multiple parts would have to arise simultaneously. But is it true?

http://www.talkorigins.org/faqs/behe/publish.html
This list of papers has been collected in response to Michael Behe's claim that the scientific literature is virtually silent on the topic of molecular evolution.

http://www.talkorigins.org/faqs/behe/textbooks.html
In addition to claiming that the scientific literature devotes no time to questions of molecular evolution, Michael Behe has also said that the same is true of college biochemistry textbooks. Here, the author of some of the textbooks Behe has reviewed demonstrates this claim to be false.

http://www.talkorigins.org/faqs/behe/icsic.html
One of the molecular assemblages that Michael Behe claims is "irreducibly complex" is the complement system, an arm of the vertebrate immune system so named because it "complements" the effect of antibodies. This essay outlines the functioning of the complement system and undercuts Behe's argument by showing that simpler yet still functional versions of it exist in nature.