Evidence for Intelligent Design from
Biochemistry
Michael J.
Behe Discovery
Institute August 10,
1996
|
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.
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 few
mice 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, in one fell swoop, for
natural selection to have anything to act on.
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.
The Cilium
Now, 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. Inhumans, 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
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 composedof 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.
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.
Blood Clotting
Now let's talk about
a different biochemical system of blood clotting. Amusingly, the way
in which the blood clotting system works is reminiscent of a Rube
Goldberg machine.
The name of Rube Goldberg; the great
cartoonist who entertained America with his silly machines, lives on
in our culture, but the man himself has pretty much faded from view.
Here's a typical example of his humor. In this cartoon Goldberg
imagined a system where water from a drain-pipe fills a flask,
causing a cork with attached needle to rise and puncture a paper cup
containing beer, which sprinkles on a bird. The intoxicated bird
falls onto a spring, bounces up to a platform, and pulls a string
thinking it's a worm. The string triggers a cannon which frightens a
dog. The dog flips over, and his rapid breathing raises and lowers a
scratcher over a mosquito bite, causing no embarrassment while
talking to a lady.
When you think about it for a moment you
realize that the Rube Goldberg machine is irreducibly complex. It is
a single system which is composed of several interacting parts, and
where the removal of any one of the parts causes the system to break
down. If the dog is missing the machine doesn't work; if the needle
hasn't been put on the cork, the whole system is useless.
It
turns out that we all have Rube Goldberg in our blood. Here's a
picture of a cell trapped in a clot. The meshwork is formed from a
protein called fibrin. But what controls blood clotting? Why does
blood clot when you cut yourself, but not at other times when a clot
would cause a stroke or heart attack? Here's a diagram of what's
called the blood clotting cascade. Let's go through just some of the
reactions of clotting.
When an animal is cut a protein called
Hageman factor sticks to the surface of cells near the wound. Bound
Hageman factor is then cleaved by a protein called HMK to yield
activated Hageman factor. Immediately the activated Hageman factor
converts another protein, called prekallikrein, to its active form,
kallikrein. Kallikrein helps HMK speed up the conversion of more
Hageman factor to its active form. Activated Hageman factor and HMK
then together transform another protein, called PTA, to its active
form. Activated PTA in turn, together with the activated form of
another protein (discussed below) called convertin, switch a protein
called Christmas factor to its active form. Activated Christmas
factor, together with antihemophilic factor (which is itself
activated by thrombin in a manner similar to that of proaccelerin)
changes Stuart factor to its active form. Stuart factor,working with
accelerin, converts prothrombin to thrombin. Finally thrombin cuts
fibrinogen to give fibrin, which aggregates with other fibrin
molecules to form the meshwork clot you saw in the last
picture.
Blood clotting requires extreme precision. When a
pressurized blood circulation system is punctured, a clot must form
quickly or the animal will bleed to death. On the other hand, if
blood congeals at the wrong time or place, then the clot may block
circulation as it does in heart attacks and strokes. Furthermore, a
clot has to stop bleeding all along the length of the cut, sealing
it completely. Yet blood clotting must be confined to the cut or the
entire blood system of the animal might solidify, killing it.
Consequently, clotting requires this enormously complex system so
that the clot forms only when and only where it is required. Blood
clotting is the ultimate Rube Goldberg machine.
The
Professional Literature
Other examples of irreducible
complexity abound in the cell, including aspects of protein
transport, the bacterial flagellum, electron transport, telomeres,
photosynthesis, transcription regulation, and much more. Examples of
irreducible complexity can be found on virtually every page of a
biochemistry textbook. But if these things cannot be explained by
Darwinian evolution, how has the scientific community regarded these
phenomena of the past forty years? A good place to look for an
answer to that question is in the Journal of Molecular
Evolution. JME is a journal that was begun specifically to deal
with the topic of how evolution occurs on the molecular level. It
has high scientific standards, and is edited by prominent figures in
the field. In a recent issue of JME there were published eleven
articles; of these, all eleven were concerned simply with the
comparison of protein or DNA sequences. A sequence comparison is an
amino acid-by-amino acid comparison of two different proteins, or a
nucleotide-by-nucleotide comparison of two different pieces of DNA,
noting the positions at which they are identical or similar, and the
places where they are not. Although useful for determining possible
lines of descent, which is an interesting question in its own right,
comparing sequences cannot show how a complex biochemical system
achieved its function; the question that most concerns us here. By
way of analogy, the instruction manuals for two different models of
computer putout by the same company might have many identical words,
sentences, and even paragraphs, suggesting a common ancestry
(perhaps the same author wrote both manuals), but comparing the
sequences of letters in the instruction manuals will never tell us
if a computer can be produced step by step starting from a
typewriter.
None of the papers discussed detailed models for
intermediates in the development of complex biomolecular structures.
In the past ten years JME has published over a thousand papers. Of
these, about one hundred discussed the chemical synthesis of
molecules thought to be necessary for the origin of life, about 50
proposed mathematical models to improve sequence analysis, and about
800 were analyses of sequences. There were ZERO papers discussing
detailed models for intermediates in the development of complex
biomolecular structures. This is not a peculiarity of JME. No papers
are to be found that discuss detailed models for intermediates in
the development of complex biomolecular structures in the
Proceedings of the National Academy of Science,
Nature, Science, the Journal of Molecular
Biology or, to my knowledge, any science journal
whatsoever.
"Publish or perish" is a proverb that
academicians take seriously. If you do not publish your work for the
rest of the community to evaluate, then you have no business in
academia and, if you don't already have tenure, you will be
banished. But the saying can be applied to theories as well. If a
theory claims to be able to explain some phenomenon but does not
generate even an attempt at an explanation, then it should be
banished. Despite comparing sequences, molecular evolution has never
addressed the question of how complex structures came to be. In
effect, the theory of Darwinian molecular evolution has not
published, and so it should perish.
Detection of
Design
What's going on? Imagine a room in which a body
lies crushed, flat as a pancake. A dozen detectives crawl around,
examining the floor with magnifying glasses for any clue to the
identity of the perpetrator. In the middle of the room next to the
body stands a large, gray elephant. The detectives carefully avoid
bumping into the pachyderm's legs as they crawl, and never even
glance at it. Over time the detectives get frustrated with their
lack of progress but resolutely press on, looking even more closely
at the floor. You see, textbooks say detectives must "get their
man," so they never consider elephants.
There is an elephant
in the roomful of scientists who are trying to explain the
development of life. The elephant is labeled "intelligent design."
To a person who does not feel obliged to restrict his search to
unintelligent causes, the straightforward conclusion is that many
biochemical systems were designed. They were designed not by the
laws of nature, not by chance and necessity. Rather, they were
planned. The designer knew what the systems would look like when
they were completed; the designer took steps to bring the systems
about. Life on earth at its most fundamental level, in its most
critical components, is the product of intelligent
activity.
The conclusion of intelligent design flows
naturally from the data itself, not from sacred books or sectarian
beliefs. Inferring that biochemical systems were designed by an
intelligent agent is a humdrum process that requires no new
principles of logic or science. It comes simply from the hard work
that biochemistry has done over the past forty years, combined with
consideration of the way in which we reach conclusions of design
every day.
What is "design"? Design is simply the purposeful
arrangement of parts. The scientific question is how we detect
design. This can be done in various ways, but design can most easily
be inferred for mechanical objects. While walking through a junkyard
you might observe separated bolts and screws and bits of plastic and
glass, most scattered, some piled on top of each other, some wedged
together. Suppose you saw a pile that seemed particularly compact,
and when you picked up a bar sticking out of the pile, the whole
pile came along with it. When you pushed on the bar it slid smoothly
to one side of the pile and pulled an attached chain along with it.
The chain in turn yanked a gear which turned three other gears which
turned a red-and-white striped rod, spinning it like a barber pole.
You quickly conclude that the pile was not a chance accumulation of
junk, but was designed, was put together in that order by an
intelligent agent, because you see that the components of the system
interact with great specificity to do something.
It is not
only artificial mechanical systems for which design can easily be
concluded. Systems made entirely from natural components can also
evince design. For example, suppose you are walking with a friend in
the woods. All of a sudden your friend is pulled high in the air and
left dangling by his foot from a vine attached to a tree branch.
After cutting him down you reconstruct the trap. You see that the
vine was wrapped around the tree branch, and the end pulled tightly
down to the ground. It was securely anchored to the ground by a
forked branch. The branch was attached to another vine, hidden by
leaves so that, when the trigger-vine was disturbed, it would pull
down the forked stick, releasing the spring-vine. The end of the
vine formed a loop with a slipknot to grab an appendage and snap it
up into the air. Even though the trap was made completely of natural
materials you would quickly conclude that it was the product of
intelligent design.
A Complicated World
A word
of caution; intelligent design theory has to be seen in context: it
does not try to explain everything. We live in a complex world where
lots of different things can happen. When deciding how various rocks
came to be shaped the way they are a geologist might consider a
whole range of factors: rain, wind, the movement of glaciers, the
activity of moss and lichens, volcanic action, nuclear explosions,
asteroid impact, or the hand of a sculptor. The shape of one rock
might have been determined primarily by one mechanism, the shape of
another rock by another mechanism. The possibility of a meteor's
impact does not mean that volcanos can be ignored; the existence of
sculptors does not mean that many rocks are not shaped by weather.
Similarly, evolutionary biologists have recognized that a number of
factors might have affected the development of life: common descent,
natural selection, migration, population size, founder effects
(effects that may be due to the limited number of organisms that
begin a new species), genetic drift (spread of neutral, nonselective
mutations), gene flow (the incorporation of genes into a population
from a separate population), linkage (occurrence of two genes on the
same chromosome), meiotic drive (the preferential selection during
sex cell production of one of the two copies of a gene inherited
from an organism's parents), transposition (the transfer of a gene
between widely separated species by non-sexual means), and much
more. The fact that some biochemical systems were designed by an
intelligent agent does not mean that any of the other factors are
not operative, common, or important.
Curiouser and
Curiouser
So as this talk concludes we are left with what
many people feel to be a strange conclusion: that life was designed
by an intelligent agent. In a way, though, all of the progress of
science over the last several hundred years has been a steady march
toward the strange. People up until the middle ages lived in a
natural world. The stable earth was at the center of things; the
sun, moon, and stars circled endlessly to give light by day and
night; the same plants and animals had been known since antiquity.
Surprises were few.
Then it was proposed, absurdly, that the
earth itself moved, spinning while it circled the sun. No one could
feel the earth spinning; no one could see it. But spin it did. From
our modern vantage it's hard to realize what an assault on the
senses was perpetrated by Copernicus and Galileo; they said in
effect that people could no longer rely on even the evidence of
their eyes.
Things got steadily worse over the years. With
the discovery of fossils it became apparent that the familiar
animals of field and forest had not always been on earth; the world
had once been inhabited by huge, alien creatures who were now gone.
Sometime later Darwin shook the world by arguing that the familiar
biota was derived from the bizarre, vanished life over lengths of
time incomprehensible to human minds. Einstein told us that space is
curved and time is relative. Modern physics says that solid objects
are mostly space, that sub atomic particles have no definite
position, that the universe had a beginning.
Now it's the
turn of the fundamental science of life, modern biochemistry, to
disturb. The simplicity that was once expected to be the foundation
of life has proven to be a phantom. Instead, systems of horrendous,
irreducible complexity inhabit the cell. The resulting realization
that life was designed by an intelligence is a shock to us in the
twentieth century who have gotten used to thinking of life as the
result of simple natural laws. But other centuries have had their
shocks and there is no reason to suppose that we should escape them.
Humanity has endured as the center of the heavens moved from the
earth to beyond the sun, as the history of life expanded to
encompass long-dead reptiles, as the eternal universe proved mortal.
We will endure the opening of Darwin's black box.
Michael J.
Behe is Associate Professor of Chemistry at Lehigh University in
Pennsylvania and a Fellow of the Discovery Institute’s Center for
Renewal of Science & Culture.
|
|