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Faith and the Structure of Life
MICHAEL J. BEHE
Many scientists are unable or unwilling to accept the notion that a designer stands behind the complexity of life. But biochemist Michael Behe shows how the alternative explanation, Darwin's theory, just canít explain it all. In his own field of molecular biology Darwinís idea utterly breaks down.
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-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-the 'simple' light sensitive spot-came from. On the contrary, Darwin dismissed the question of the eye's ultimate origin:
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. To get a flavor of what a theory of evolution must explain let's take Darwin's example of the eye and examine a few of the molecular details of vision that have been discovered by modern science. 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.
This description 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. The details of life are handled by molecular machines. Darwin's theory will stand or fall on its ability to explain them.
So how can we decide if Darwin's theory can account for the complexity of molecular life? It turns out that Darwin himself set a standard. He acknowledged that:
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.
Let's consider an everyday example of irreducible complexity: the humble mousetrap. The mousetraps that my family uses consist of a number of parts. There are: 1) a flat wooden platform to act as a base; 2) a metal hammer, which does the actual job of crushing the little mouse; 3) a spring with extended ends to press against the platform and the hammer when the trap is charged; 4) a sensitive catch which releases when slight pressure is applied, and 5) a metal bar which connects to the catch and holds the hammer back when the trap is charged. Now you can't catch a mouse with just a platform, add a spring and catch a few more mice, add a holding bar and catch a few more. All the pieces of the mousetrap have to be in place before you catch any mice. Therefore the mousetrap is irreducibly complex.
An irreducibly complex system cannot be produced directly by numerous, successive, slight modifications of a precursor system, because any precursor to an irreducibly complex system that is missing a part is by definition nonfunctional. An irreducibly complex biological system, if there is such a thing, would be a powerful challenge to Darwinian evolution. Since natural selection can only choose systems that are already working, then if a biological system cannot be produced gradually it would have to arise as an integrated unit for natural selection to have anything to act on.
Let me add a word of caution. Demonstration that a system is irreducibly complex is not a proof that there is absolutely no gradual route to its production. Although an irreducibly complex system can't be produced directly, one can't definitively rule out the possibility of an indirect, circuitous route. However, as the complexity of an interacting system increases, the likelihood of such an indirect route drops precipitously. And as the number of unexplained, irreducibly complex biological systems increases, our confidence that Darwin's criterion of failure has been met skyrockets toward the maximum that science allows.
Now, mousetraps are one thing, biochemical systems are another. So we must ask, are any biochemical systems irreducibly complex? Yes, it turns out that many are. A good example is the cilium. Cilia are hairlike structures on the surfaces of many animal and lower plant cells that can move fluid over the cell's surface or "row" single cells through a fluid. In humans, for example, cells lining the respiratory tract each have about 200 cilia that beat in synchrony to sweep mucus towards the throat for elimination. What is the structure of a cilium? A cilium consists of a bundle of fibers called an axoneme. An axoneme contains a ring of 9 double "microtubules" surrounding two central single microtubules. Each outer doublet consists of a ring of 13 filaments (subfiber A) fused to an assembly of 10 filaments (subfiber B). The filaments of the microtubules are composed of two proteins called alpha and beta tubulin. The 11 microtubules forming an axoneme are held together by three types of connectors: subfibers A are joined to the central microtubules by radial spokes; adjacent outer doublets are joined by linkers of a highly elastic protein called nexin; and the central microtubules are joined by a connecting bridge. Finally, every subfiber A bears two arms, an inner arm and an outer arm, both containing a protein called dynein.
Although even this seems complex, a brief description can't do justice to the full complexity of the cilium, which has been shown by biochemical analysis to contain about 200 separate kinds of protein parts.
But how does a cilium work? Experiments have shown that ciliary motion results from the chemically-powered "walking" of the dynein arms on one microtubule up a second microtubule so that the two microtubules slide past each other. The protein cross-links between microtubules in a cilium prevent neighboring microtubules from sliding past each other by more than a short distance. These cross-links, therefore, convert the dynein-induced sliding motion to a bending motion of the entire axoneme.
Now, let us consider what this implies. What components are needed for a cilium to work? Ciliary motion certainly requires microtubules; otherwise, there would be no strands to slide. Additionally we require a motor, or else the microtubules of the cilium would lie stiff and motionless. Furthermore, we require linkers to tug on neighboring strands, converting the sliding motion into a bending motion, and preventing the structure from falling apart. All of these parts are required to perform one function: ciliary motion. Just as a mousetrap does not work unless all of its constituent parts are present, ciliary motion simply does not exist in the absence of microtubules, connectors, and motors. Therefore, we can conclude that the cilium is irreducibly complex-an enormous monkey wrench thrown into its presumed gradual, Darwinian evolution.
Another example of irreducible complexity is the system that targets proteins for delivery to subcellular compartments. The eukaryotic cell contains a number of sub-cellular compartments to perform specialized tasks, like rooms in a house. These include lysosomes for digestion, Golgi vesicles for export, and others. Unfortunately, the machinery for making proteins is outside these compartments, so how do the proteins which perform tasks in subcellular compartments find their way to their destination? It turns out that proteins that will wind up in subcellular compartments contain a special amino acid sequence near the beginning called a "signal sequence". As the proteins are being synthesized, a complex molecular assemblage called the signal recognition particle or SRP, binds to the signal sequence. This causes synthesis of the protein to halt temporarily. During the pause in protein synthesis the SRP binds the trans-membrane SRP receptor, which causes protein synthesis to resume and which allows passage of the protein into the interior of the endoplasmic reticulum (ER). As the protein passes into the ER the signal sequence is cut off.
For many proteins the ER is just a waystation on their travels to their final destinations. Proteins which will end up in a lysosome are enzymatically "tagged" with a carbohydrate residue called mannose-6-phosphate while still in the ER. An area of the ER membrane then begins to concentrate several proteins; one protein, clathrin, forms a sort of geodesic dome called a coated vesicle which buds off from the ER. In the dome there is also a receptor protein which binds to both the clathrin and to the mannose-6-phosphate group of the protein which is being transported. The coated vesicle then leaves the ER, travels through the cytoplasm, and binds to the lysosome through another specific receptor protein. Finally, in a maneuver involving several more proteins, the vesicle fuses with the lysosome and the protein is at its destination.
During its travels our protein interacted with dozens of macromolecules to achieve one purpose: its arrival in the lysosome. Virtually all components of the transport system are necessary for the system to operate, and therefore the system is irreducible. The consequences of a gap in the transport chain can be seen in the hereditary defect known as I-cell disease. It results from a deficiency of the enzyme that places the mannose-6-phosphate on proteins to be targeted to the lysosomes. I-cell disease is characterized by progressive retardation, skeletal deformities, and early death.
Detection of Design
So far my criticisms of evolution are not much different from what a number of other scientists have offered. The shortcomings of Darwinian explanations have been noted by Stuart Kauffman, Lynn Margulis, Brian Goodwin, James Shapiro, and others. Where I differ from the other critics, however, is in the conclusion I draw from the complexity of cellular systems. I argue that the systems show strong evidence of design-purposeful, intentional design by an intelligent agent. I think it is safe to say that it is the conclusion of design, much more than my criticism of Darwinism, that has attracted attention. So let's look at the idea of design.
What is "design"? Design is simply the purposeful arrangement of parts. With such a broad definition its is easy to see that anything might have been designed. The coats on a rack in a restaurant may have been arranged just-so by the owner before you came in. The trash and tin cans along the edge of a highway may have been placed by an artist trying to make some obscure environmental statement. On the campus of my university there are sculptures which, if I saw them lying beside the road, I would guess were the result of chance blows to a piece of scrap metal, but they were designed.
The upshot of this conclusion-that anything could have been purposely arranged-is that we can never positively rule out design. Nonetheless, it is a good rule of thumb to assume there is no design unless one can detect it. The scientific problem then becomes, how do we confidently detect design? When is it reasonable to conclude, in the absence of firsthand knowledge or eyewitness accounts, that something has been designed?
There are several ways to detect design. However, for discrete physical systems design is most easily apprehended when a number of separate, interacting components are ordered in such a way as to accomplish a function beyond the individual components. To illustrate, consider a Far Side cartoon by Gary Larson in which an exploring team is going through a jungle, and the lead explorer has been strung up and skewered. A companion turns to another and confides, "That's why I never walk in front." Now every person who sees the cartoon immediately knows that the trap was designed. In fact, Larson's humor depends on you recognizing the design. It wouldn't be terribly funny if the first explorer had just fallen off a cliff or a rotted tree accidentally fell on him. No, his fate was intended. But how do you know that? How does the audience apprehend that this trap was designed? You can tell that the trap was designed because of the way the parts interact with great specificity to perform a function. Like the mousetrap we saw in the beginning of the talk, no one would mistake the cartoon system for an accidental arrangement of parts. Further, all of the parts of the trap are natural components: a vine, a tree, some pieces of wood. There are no artificial, manufactured pieces. Therefore, we can come to a conclusion of design for a system composed entirely of natural parts.
For much the same reason, I suggest that many biochemical systems were designed by an intelligent agent. Our ability to be confident of the design of the cilium or intracellular transport rests on the same principles as our ability to be confident of the design of the jungle trap: the ordering of separate components to achieve an identifiable function that depends sharply on the components. Who did the designing, when, where, and how, remain open questions that may or may not be accessible to science. But the fact of design itself can be deduced from the structure of the systems which biochemists have elucidated in the past decades.
Reception of the Book
My book has been out for about eight months now, enough time for reaction to it to come in from various corners. I think it's safe to say that the reaction has been mixed. A number of reviews have been quite favorable, and a number unfavorable. Let's take a minute to see what has been said in reviews of the book by other biologists. First of all, in all the reviews of my book that I am aware of, no one claims that the biochemical systems I describe have already been explained by science. James Shreeve, reviewing the book for the New York Times says "Mr. Behe may be right that given our current state of knowledge, good old Darwinian evolution cannot explain the origin of blood clotting or cellular transport." In National Review microbiologist James Shapiro of the University of Chicago writes "There are no detailed Darwinian accounts for the evolution of any fundamental biochemical or cellular system, only a variety of wishful speculations." In Nature University of Chicago evolutionary biologist Jerry Coyne, although very unfriendly to the concept of intelligent design, states "There is no doubt that the pathways described by Behe are dauntingly complex, and their evolution will be hard to unravel.... We may forever be unable to envisage the first proto-pathways." In New Scientist Andrew Pomiankowski writes, "Pick up any biochemistry textbook, and you will find perhaps two or three references to evolution. Turn to one of these and you will be lucky to find anything better than 'evolution selects the fittest molecules for their biological function.'" So apparently everyone at least agrees that complex biochemical systems have yet to be explained.
However, none of the reviewers are willing to come to the conclusion of intelligent design. Here are their reasons:
James Shreeve, New York Times Book Review
James Shapiro, National Review
Jerry Coyne, Nature
Andrew Pomiankowski, New Scientist
It is clear from the quotations, I think, that the reviewers are not rejecting design because there is scientific evidence against it, or because it violates some principle of logic. Rather, I believe they find design unacceptable because they are uncomfortable with the theological ramifications of the theory. This viewpoint was expressed very clearly recently by the biologist Richard Lewontin. In a review of Carl Sagan's last book in the New York Review Lewontin wrote:
Pope John Paul II noted that a theory of evolution has two parts, the mechanism and the philosophy attached to that mechanism. Putting it like that, however, makes it sound as if any philosophy can be mixed and matched with any mechanism. But the situation is not really that clean cut. While Catholics and theists in general can accommodate the mechanism of Darwin to their worldview, materialists require something like Darwinism because, ultimately, materialism says that life and intelligence had to arise unaided from brute matter. A theory of intelligent design, however, holds implicitly that there is a designer capable of planning and executing the phenomenal intricacies of life on earth. Although there are, at least in theory, some exotic candidates for the role of designer that might be compatible with materialist philosophy (such as space aliens or time travelers), few people will be convinced by these, and will conclude that the designer is beyond nature. Many scientists are unable or unwilling to accept such a designer, because that goes against their prior commitment to materialism, or at least to a functional materialism in the course of their work.
Nonetheless I remain optimistic that the scientific community will eventually come around to accepting intelligent design, even if the acceptance is discreet and muted. The reason for optimism is the advance of science itself, which almost every day discovers new intricacies in nature, fresh reasons for recognizing the design inherent to life and the universe.
In the meantime, there is nothing to stop nonscientists from recognizing and appreciating that design. We are fearfully and wonderfully made, and every cell of our bodies testifies to the intelligence that pervades creation.
Adapted from Behe, M.J. 2001. "Faith and the Structure of Life." In Science and Faith, Gerard V. Bradley and Don DeMarco, eds. St. Augustine's Press, South Bend, Indiana, Chapter 2.
Published with the kind permission of Michael J. Behe and the Fellowship of Catholic Scholars.
Michael J. Behe, professor of biological sciences at Lehigh University, is author of Darwin's Black Box: The Biochemical Challenge to Evolution. Touchstone, ©1996, ISBN 0-684-82754-9. Michael Behe is on the Advisory Board of the Catholic Educator's Resource Center.
Copyright 2001 The Fellowship of Catholic Scholars