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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. |
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