Why Darwin Matters (13 page)

Dembski’s Law of Conservation of Information is purposely constructed to resemble such physical laws as the conservation of momentum or the laws of thermodynamics. But these laws were based on copious empirical data and experimental results from the real world, not inferred from logical argument alone as Dembski’s law is. Further, no other recognized theory of information—such as that proposed by the mathematician and information pioneer Claude Shannon—includes a law or principle of conservation, and no one working in the information sciences today uses or recognizes
Dembski’s law as scientifically useful, regardless of its design inference.

Even if Dembski’s LCI were validated, it is irrelevant to the theory of evolution, because it is abundantly clear that information in the natural world—through DNA, for example—is transferred and increased by natural processes. Microbiologist Lynn Margulis, for example, has demonstrated that complex eukaryote cells, such as those of which we are made, evolved from simpler prokaryote cells. The genomes of eukaryote cells increased in size—and thus in complex specified information—by incorporating simpler genomes of prokaryote cells.
⁴²
Intelligent Design theorists respond to this by saying the Intelligent Designer created complex eukaryote cells. If that is so, why does it appear that the Intelligent Designer cobbled these cells together out of parts lying around in the pre-Cambrian soup? In fact, complex eukaryote cells are a grab bag of goodies from the prokaryote world, including mitochondria, which contain their own genome. Ever heard of mitochondrial DNA (from which human lineages may be traced through females)? Our cells already have a nucleus containing a complete genome. What is another genome doing in our mitochondria? Evolution offers an answer: They are vestigial features of eukaryote cells that evolved from prokaryote cells. Intelligent Design, in contrast, offers nothing more than “then a miracle occurs.”

Richard Dawkins cogently answers the information challenge by reconstructing the evolution of hemoglobin—the oxygen-carrying protein in blood. Human hemoglobin contains four protein chains called
globins
that are similar to each other but not identical. The alpha globins each contain a chain of 141 amino acids coded by seven genes on Chromosome 11—four are pseudogenes that do not produce proteins, two produce adult hemoglobin, and one produces embryo hemoglobin. Similarly, beta globins each contain a chain of
146 amino acids coded by six genes on Chromosome 16, some of which are disabled and one used only in embryos. Letter-by-letter analysis of the genes coding for hemoglobin reveals that the two sets of genes on Chromosomes 11 and 16 are distantly related and share a common globin gene from a common ancestor five hundred million years ago. That gene duplicated, after which both copies were passed down for half a billion years, one evolving into the alpha cluster on Chromosome 11 and the other evolving into the beta cluster on Chromosome 16. Gene duplications led to the increase in complexity of the gene clusters, leading to the existence today of nonfunctional pseudogenes. Since this alpha-beta split happened five hundred million years ago we can predict that we should find the same alpha-beta split in all animals that evolved within the last half billion years. Sure enough, that is precisely what we find. As a final test, the jawless lamprey fish, the only surviving vertebrate predating the alpha-beta split, should lack this genetic divide. And sure enough, it does. Blood hemoglobin is explained by evolution, not Intelligent Design. Q.E.D.
⁴³

In general, DNA has the elements of historical contingency and evolutionary history, not design. DNA is information, and if the Law of Conservation of Information requires the input of an Intelligent Designer in order to increase specified complexity of the genome, we have to wonder why the Intelligent Designer added to our genome junk DNA, repeated copies of useless DNA, orphan genes, gene fragments, tandem repeats, and pseudogenes, none of which are involved directly in the making of a human being. In fact, of the entire human genome, it appears that only a tiny percentage is actively involved in useful protein production. Rather than being intelligently designed, the human genome looks more and more like a mosaic of mutations, fragment copies, borrowed
sequences, and discarded strings of DNA that were jerry-built over millions of years of evolution.
⁴⁴

We Cannot Observe Evolution: No laboratory experiments or field observations reveal evolution in action
.

Another regular on the Intelligent Design circuit is the hunt for “evolution in action.” Scientists have not, and probably can never, provide examples of evolution at work that would satisfy an Intelligent Design creationist. It is one thing to infer in the fossil record the creation of a new anatomical structure, or the birth of a new species; it is quite another to witness it in the laboratory. And what examples we do have of evolution in action in the lab, creationists claim is not evolution.

But not only does science have an incredibly rich fossil record, the process of evolution can be seen at work at a number of different levels. Diseases are prime examples of natural selection and evolution at work, and on time scales we can witness, all too painfully. The AIDS virus, for example, continues to evolve in response to the drugs used to combat it—the few surviving strains of the virus continue to multiply, passing on their drug-resistant genes. Creationists respond that this is an example of microevolution, not macroevolution. Fair enough.

For an example of macroevolution, then, check out the research by the University of Michigan biologist James Bardwell, reported in the February 20, 2004, edition of
Science
, in which an
E. coli
bacterium that was forced to adapt or perish improvised a novel molecular tool. “The bacteria reached for a tool that they had, and made it do something it doesn’t normally do. We caught evolution in the act of making a big step.” The big step was a new way of
making molecular bolts called
disulfide bonds
, which are stiffening struts in proteins that also help the proteins fold into their proper, functional, three-dimensional shapes. This new method restarted the bacterium’s motor and enabled it to move toward food before it starved to death.

It is a particularly important experiment because Bardwell developed a strain of mutant bacteria unable to make disulfide bonds, which are critical for the ability of a bacterium’s flagellum to work—the same flagellum that Intelligent Design theorists are so fond of presenting as an example of irreducible complexity. The researchers put these nonswimming bacteria to the test by placing them on a dish of food where, once they had exhausted the food they could reach, they either had to repair the broken motor or starve. The bacteria used in the experiment were forced to use a protein called
thioredoxin
, which normally destroys disulfide bonds, to make the bonds instead. In a process similar to natural selection, one researcher made random alterations in the DNA encoding thioredoxin and then subjected thousands of bacteria to the swim-or-starve test. He wanted to see if an altered version of thioredoxin could be coerced to make disulfides for other proteins in the bacteria. Remarkably, a mutant carrying only two amino acid changes—amounting to less than 2 percent of the total number of amino acids in thioredoxin—restored the ability of the bacteria to move. The altered thioredoxin was able to carry out disulfide bond formation in numerous other bacterial proteins all by itself, without relying on any of the components of the natural disulfide bond pathway. The mutant bacteria managed to solve the problem in time, swim away from starvation, and multiply.

Of course, Intelligent Design theorists will respond that the researcher acted as an intelligent designer would have in nature, and thus this supports their case; but, in fact, the researcher was acting as
the force of natural selection, and thus this is evidence for evolution in action. Bardwell concluded that “the naturally occurring enzymes involved in disulfide bond formation are a biological pathway whose main features are the same from bacteria to man. People often speak of Computer Assisted Design (CAD), where you try things out on a computer screen before you manufacture them. We put the bacteria we were working on under a strong genetic selection, like what can happen in evolution, and the bacteria came up with a completely new answer to the problem of how to form disulfide bonds. I think we can now talk about Genetic Assisted Design (GAD).”

Perhaps we should now talk about GAD instead of GOD.

Microevolution and Macroevolution: Life shows signs of intermittent intelligent design intervention that accounts for large-scale changes
.

Ever since Darwin, creationists have argued that natural selection can account for minor changes within a species, but cannot produce new species, new body forms, or new lineages. The argument presented today is a more sophisticated version in which, according to some (but not all) theorists, several billion years ago an Intelligent Designer created the first cell with the necessary genetic information to produce all of the irreducibly complex systems we see today. Then the laws of nature and evolution took over to create diversity within each species. When totally new and more complex species, body forms, and lineages appear in the fossil record, these are signs of the Intelligent Designer stepping in, intervening with a new design element. Microevolution proceeds by natural selection, but macroevolution is in the hands of the Designer.

First, how does one distinguish the processes of microevolution (evolution within and below the species level) from those of macro-evolution (evolution above the species level)? Within evolutionary
biology there has been considerable debate about whether the microevolutionary process of natural selection operating on individuals within populations can by itself account for the diverse macroevolutionary forms of life. Today, the new science of evolutionary developmental biology, “evo-devo” for short, reveals that the wide diversity of forms evolved through an interaction of the embryological development of forms and the subsequent pruning of these forms by natural selection.

For example, it turns out that the bodily architecture of vertebrates is the product of blueprint
Hox
genes that direct the construction of repeating parts, such as ribs and vertebrae. In embryological development, various structures form or do not form depending on whether the
Hox
genes are expressed or not. Natural selection operates on expressed forms only, since these result in organisms that survive long enough to pass on their genes for the future expression of those forms. Similarly, the wide variety of eyes found throughout the animal kingdom—from the compound eyes of flies to the camera eyes of vertebrates—evolved under the control of the commonly shared
Pax-6
gene, which directs the production of photoreceptor cells and light-sensing proteins. Each type of complex eye we find today evolved from simpler photoreceptive structures in a distant common ancestor of arthropods, cephalo-pods, and vertebrates. Evo-devo biologist Sean Carroll explains that

the ancestor possessed two kinds of light-sensitive organs, each one endowed with a distinct type of photoreceptor, as well as with light-sensitive proteins called R-opsin and C-opsin, respectively. One organ was a simple two-celled prototype eye; the other, called the brain photoclock, was a part of the animal’s brain and played a role in running the animal’s daily clock. The arthropod and squid retinas incorporated the photoreceptor from the simple prototype eye, whereas the vertebrate eye incorporated both kinds of photoreceptor into its retina.
⁴⁵

Instead of eyes evolving forty or more different times in evolutionary history, it appears that this simple genetic complex led to the embryological development and evolutionary refinement of a two-part system; in some species one part is incorporated, and in others both are.

More generally, instead of an extensive genetic tool kit with genes for constructing each and every bodily structure, evo-devo shows that a small set of gene complexes such as the
Hox
genes and the
Pax-6
genes are expressed in novel ways that can generate large-scale changes in a nonincremental fashion. This explains why the human genome is not especially different from the mouse genome. It is not the number of genes that counts so much as how genes are turned on or off. Evolution involves old genes developing new tricks.

Second, a species is a group of actually or potentially interbreeding natural populations reproductively isolated from other such populations. We see evolution at work in nature today, isolating populations and creating new species, that is, new populations reproductively isolated from other such populations. As the new isolated populations drift genetically away from the parent populations, they eventually can no longer interbreed, making new species.
⁴⁶
If evolution can do this, why can’t it also create higher-order categories of organisms?

Third, some speciation may be precipitated by characteristics adapted to distinct environments that then drive populations into reproductive isolation, which leads to the creation of a new species. Similarly, sexual selection—female mate selection of males—may drive populations to diverge into different species. If females prefer certain traits in males, such as coloration, within one population, the males can change so dramatically that they are no longer appealing to females of another population, thereby making the
two populations reproductively isolated: thus a new species. Research shows that speciation occurs more often in polygamous species than in monogamous species, further evidence linking sexual selection to the origin of new species.
⁴⁷