A Response to Dr. Dawkins’ “The Information Challenge”

In September, 2007, I posted a link to a YouTube video where Richard Dawkins was asked to explain the origin of genetic information, according to Darwinism. I also posted a link to Dawkins’ rebuttal to the video, where he purports to explain the origin of genetic information according to Darwinian evolution. The question posed to Dawkins was, “Can you give an example of a genetic mutation or evolutionary process that can be seen to increase the information in the genome?” Dawkins famously commented that the question was “the kind of question only a creationist would ask …” Dawkins writes, “In my anger I refused to discuss the question further, and told them to stop the camera.” Dawkins’ highly emotional response calls into question whether he is capable of addressing this issue objectively. This will be a response assessing Dawkins’ answer to “The Information Challenge.”

Part 1: Specified Complexity Is the Measure of Biological Complexity.

Dawkins writes, “First you first have to explain the technical meaning of ‘information’.” While that sounds reasonable, Dawkins pulls a bait-and-switch and defines information as “Shannon information” — a formulation of “information” that applies to signal transmission and does not account for the type of specified complexity found in biology.

It is common for Darwinists to define information as “Shannon information,” which is related to calculating the mere unlikelihood of a sequence of events. Under their definition, a functionless stretch of genetic junk might have the same amount “information” as a fully functional gene of the same sequence-length. ID-proponents don’t see this as a useful way of measuring biological information. ID-proponents define information as complex and specified information — DNA which is finely-tuned to do something. Stephen C. Meyer writes that ID-theorists use “(CSI) as a synonym for ‘specified complexity’ to help distinguish functional biological information from mere Shannon information — that is, specified complexity from mere complexity.” As the ISCID encyclopedia explains, “Unlike specified complexity, Shannon information is solely concerned with the improbability or complexity of a string of characters rather than its patterning or significance.”

The Inconvenient Truth for Dawkins: The difference between the Darwinist and ID definitions of information is equivalent to the difference between getting 10 consecutive losing hands in a poker game versus getting 10 consecutive royal flushes. One implicates design, while the other does not.

It is important to note ID proponents did not invent the notion of “specified complexity,” nor were they the first to observe that “specified complexity” is the best way to describe biological information. My first knowledge of the term being used comes from leading origin of life theorist Leslie Orgel, who used it in 1973 in a fashion that closely resembles the modern usage by ID proponents:

[L]iving organisms are distinguished by their specified complexity. Crystals are usually taken as the prototypes of simple, well-specified structures, because they consist of a very large number of identical molecules packed together in a uniform way. Lumps of granite or random mixtures of polymers are examples of structures which are complex but not specified. The crystals fail to qualify as living because they lack complexity; the mixtures of polymers fail to qualify because they lack specificity.

Leslie E. Orgel, The Origins of Life: Molecules and Natural Selection,” p.189 (Chapman & Hall: London, 1973).

Orgel thus captures the fact that specified complexity requires both order and a specific arrangement of parts or symbols. This matches the definition given by Dembski, where he defines specified complexity as an unlikely event that conforms to an independent pattern. This establishes that specified complexity is the appropriate measure of biological complexity.

Additionally, Richard Dawkins’ article admits that “DNA carries information in a very computer-like way, and we can measure the genome’s capacity in bits too, if we wish.” That’s an interesting analogy, reminiscent of the design overtones of Dawkins concession elsewhere that “[t]he machine code of the genes is uncannily computer-like. Apart from differences in jargon, the pages of a molecular biology journal might be interchanged with those of a computer engineering journal.” (Richard Dawkins, River Out of Eden: A Darwinian View of Life, p. 17 (New York: Basic Books, 1995).) Of course, Dawkins believes that the processes of random mutation and unguided selection ultimately built “[t]he machine code of the genes” and made it “uncannily computer-like.” But I do not think a scientist is unjustified in reasoning that in our experience, machine codes and computers only derive from intelligence.

Part 2: Does Gene Duplication Increase Information Content?

In this section, I will show why merely citing gene duplication does not help one understand how Darwinian evolution can produce new genetic information. Dawkins’ main point in his “The Information Challenge” article is that “[n]ew genes arise through various kinds of duplication.” So his answer to the creationist question that so upset him is gene duplication. Yet during the actual gene-duplication process, a pre-existing gene is merely copied, and nothing truly new is generated. As Michael Egnor said in response to PZ Myers: “[G]ene duplication is, presumably, not to be taken too seriously. If you count copies as new information, you must have a hard time with plagiarism in your classes. All that the miscreant students would have to say is ‘It’s just like gene duplication. Plagiarism is new information- you said so on your blog!'”

Duplicating Genes Doesn’t Increase Biological Information in Any Important Sense

I now have 2 questions to ask of Darwinists who claim that the mechanism of gene duplication explains how Darwinian evolutionary processes can increase the information content in the genome:

  • (1) Does gene duplication increase the information content?
  • (2) Does gene duplication increase the information content?

Asking the question twice obviously does not double the meaningful information conveyed by the question. How many times would the question have to be duplicated before the meaningful information conveyed by the list of duplicated questions is twice that of the original question? The answer is that the mere duplication of a sentence does NOT increase the complex and specified information content in any meaningful way. Imagine that a builder of houses has a blueprint to build a new house, but the blueprint does not contain enough information to build the house to the specifications that the builder desires. Could the builder obtain the needed additional information merely by photocopying the original blueprint? Of course not.

Darwinists Must Give Detailed Accounts of how a Duplicated Gene Acquires its New Function

The Darwinist would probably reply to my objection by saying, “Well, it isn’t just gene duplication that increases the genetic information — such information is increased when gene duplication is coupled with the subsequent evolution of one of the new copies of the gene.” Aye, there’s the rub.

Darwinists laud the mechanism of gene duplication because they claim it shows how one copy of a gene can perform the original function, freeing up the other copy to mutate, evolve, and acquire a new function. But the new genetic information must somehow be generated during that subsequent evolution of the gene. To explain how Darwinian processes can generate new and meaningful genetic information, Darwinists must provide a detailed account of how a duplicate copy of a gene can evolve into an entirely new gene. But ask Darwinists for details as to how the duplicate copy then starts to perform some new function, and you probably won’t get any. At least, Dawkins didn’t given us any details (as I explain below) about this in his “The Information Challenge” article, which I am rebutting here.

A recent study in Nature admitted, “Gene duplication and loss is a powerful source of functional innovation. However, the general principles that govern this process are still largely unknown.” (Ilan Wapinski, Avi Pfeffer, Nir Friedman & Aviv Regev, “Natural history and evolutionary principles of gene duplication in fungi,” Nature, Vol. 449:54-61 (September 6, 2007).) Yet the crucial question that must be answered by the gene duplication mechanism is, exactly how does the duplicate copy acquire an entirely new function? Stephen Meyer explains in Proceedings of the Biological Society of Washington that it is difficult to imagine how duplicated genes acquire new functions since they must successfully undergo “neutral evolution” and traverse a random walk in order to acquire a new function:

[N]eo-Darwinists envision new genetic information arising from those sections of the genetic text that can presumably vary freely without consequence to the organism. According to this scenario, non-coding sections of the genome, or duplicated sections of coding regions, can experience a protracted period of “neutral evolution” (Kimura 1983) during which alterations in nucleotide sequences have no discernible effect on the function of the organism. Eventually, however, a new gene sequence will arise that can code for a novel protein. At that point, natural selection can favor the new gene and its functional protein product, thus securing the preservation and heritability of both.

This scenario has the advantage of allowing the genome to vary through many generations, as mutations “search” space of possible base sequences. The scenario has an overriding problem, however: the size of the combinatorial space (i.e., the number of possible amino acid sequences) and the extreme rarity and isolation of the functional sequences within that space of possibilities. Since natural selection can do nothing to help generate new functional sequences, but rather can only preserve such sequences once they have arisen, chance alone—random variation—must do the work of information generation—that is, of finding the exceedingly rare functional sequences within the set of combinatorial possibilities. Yet the probability of randomly assembling (or “finding,” in the previous sense) a functional sequence is extremely small.

Stephen C. Meyer, “The origin of biological information and the higher taxonomic categories,” Proceedings for the Biological Society of Washington, Vol. 117(2):213-239 (2004).

The Inconvenient Truth for Dawkins: At best, the mechanism of gene duplication shows how a hiker can get to the foot of a hiking trail, but never explains how the hiker finds the peak of the mountain, while doing a random, blindfolded walk. We don’t need to know that genes can make copies of themselves; we need to know how the duplicate gene evolves, step-by-step, into an entirely new gene.

Mistaking Similarity as Evidence for Common Descent, and then Mistaking Common Descent as Evidence for Darwinian Evolution

Rather than giving a step-by-step mutational account of how a duplicated gene acquires a new function, Dawkins’ article substitutes bland evidence of sequence identity between different genes as evidence for Darwinian evolution by gene duplication. Dawkins gives the example of the evolution of various globin genes that he claims arose via gene duplication. His evidence is that “[c]areful letter-by-letter analysis shows that these different kinds of globin genes are literally cousins of each other, literally members of a family.” Of course the “[c]areful letter-by-letter analysis” simply means finding amino acid sequences that are similar or identical between two different proteins. David Swift explains that such claims of relationship “are inferred solely on the basis of assuming a common ancestry and then deriving a route of polypeptide evolution, typically the most parsimonious one, to fit the known present day amino acid sequences and consistent with the observed pattern of conserved amino acids.” (David Swift, Evolution Under the Microscope, p. 165 (Leighton Academic Press, 2002), emphasis in original.) At best, such sequence identity demonstrates common ancestry (if one ignores the possibility of common design), but it does not demonstrate Darwinian evolution. Michael Behe easily rebutted the over-extrapolation from sequence-similarity to Darwinian evolution in both Darwin’s Black Box and The Edge of Evolution:

“Although useful for determining lines of descent … comparing sequences cannot show how a complex biochemical system achieved its function—the question that most concerns us in this book. By way of analogy, the instruction manuals for two different models of computer put out 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….Like the sequence analysts, I believe the evidence strongly supports common descent. But the root question remains unanswered: What has caused complex systems to form?” (Michael Behe, Darwin’s Black Box, pgs. 175-176.)

“[M]odern Darwinists point to evidence of common descent and erroneously assume it to be evidence of the power of random mutation.” (Michael Behe, The Edge of Evolution, p. 95.)

Darwinists like Dawkins continue to make the mistake cited by Behe and Swift. (In fact, if you read the aforementioned “Natural history and evolutionary principles of gene duplication in fungi” article, you’ll find it gives only anecdotal or circumstantial evidence of evolution by gene duplication, not directly observed evidence, and there certainly aren’t any detailed step-by-step models for how the genes evolved.)

The Dangerous Road Faced by Duplicated Genes

If a duplicated gene cannot successfully traverse its random walk, it may die. As Lynch and Conery found, “the vast majority of gene duplicates are silenced within a few million years.” (Lynch & Conery, “The Evolutionary Fate and Consequence of Duplicate Genes,” Science Vol. 290:1151-1155 (Nov 10, 2000).) Does Richard Dawkins give a step-by-step mutational account of how globin genes evolved from one another while remaining functional at all times, such that the duplicate copies were never “silenced,” terminating their evolution? Of course not. Dawkins has not demonstrated how Darwinian evolution can take a duplicated gene and evolve it into a new gene. The problem for Dawkins is that duplicating a gene may increase your amount of Shannon information, but it does not increase the amount of specified complexity in any non-trivial sense. To explain how one gene can turn into another, Dawkins must explain how new specified and complex information can enter the genome, and give a step-by-step mutational account of the origin of some gene via gene duplication. Dawkins has provided none of this.

To understand this point, consider the following sentence (with spaces removed):


If we merely consider the Shannon information of the 33 letters (not counting spaces) in the sentence, then it has about 155 bits of Shannon Information. Now we duplicate it, like what happens in a gene duplication event:


The amount of Shannon information has now doubled (~310 bits), but we have seen no non-trivial increase in the amount of specified complexity. Still, Dawkins thinks gene duplication is the answer, and that “[i]t is by these, and similar means, that genome sizes can increase in evolution.”

The Shannon information in the doubled-string is twice the Shannon information in the shorter string if the shorter string does nothing to predict the sequence of the doubled-string. By granting this assumption, we are able to increase the Shannon information in the genome, even though this is a trivial informational increase that does not provide a meaningful increase in the specified complexity. The key questions are (a) what process is generating the new sequence, and (b) to what extent does that process predict the new sequence? In this sense, duplicating a gene would predict that the duplicate gene would be an identical copy of the original gene. From this standpoint, gene duplication actually does NOTHING to increase the Shannon information in the genome because you can predict the sequence of the new stretch of the DNA with a Probability of 1 (where Log (1) = 0), leading to an increase in the Shannon information of 0 bits. In this sense, the Shannon information in the doubled-string is not increased at all from the original, shorter string, as it remains 155 bits. Keep in mind that it is Dawkins who raised the issue of increasing Shannon information in the genome via gene duplication. Viewed in this fashion, Dawkins’ claim that gene duplication can increase the Shannon information is even more dubious: if gene duplication predicts that you will have an identical copy of the original gene, then gene duplication not only fails to increase the specified and complex information, it also fails to increase the Shannon information in the genome.

But we aren’t trying to simply change the “genome siz[e],” and thereby change the Shannon information. We’re trying to construct something functionally new. Thus, imagine that one duplicate copy of the original sentence evolves into a new sentence of the same length:


A Darwinian theorist would find that both sentences contain the word “Dawkins,” and thus share a 21% sequence identity. They would then infer that both sentences evolved from that common ancestor via Darwinian evolution. They would conclude that a duplicated version of the sentence “METHINKSDAWKINSDOTHPROTESTTOOMUCH” has evolved into “BUTIMSUREDAWKINSBELIEVESHEISRIGHT.”

David Swift explains that finding such similarities is not enough to justify the claim that Darwinian evolution has produced the observed pattern: “[F]or family trees to be credible, most if not all of the putative ancestral sequences must be functional; but this presents a major stumbling block in the production by divergence of proteins with different functions. To get from one set of conserved amino acids to another is either an unlikely big jump, or the intermediates must have biological activity; but the latter seems unlikely because it contradicts what we know about conserved amino acids.” (p. 166). Thus, in order for Darwinists to convince me that Darwinian evolution can produce new information, at minimum I need to see a step-by-step mutational account of how they can take the sentence:


and evolve it into:


by changing the first sentence one letter at a time, and having it always retain some comprehensible English meaning along each small step of its evolution. Telling me that you can duplicate the sentence does NOT answer the question posed in the video, “Can you give an example of a genetic mutation or evolutionary process that can be seen to increase the information in the genome?” As Michael Behe requested over ten years ago in Darwin’s Black Box, what is required is a “detailed, scientific [explanation of] how mutation and natural selection could build” the sentence. (Behe, Darwin’s Black Box, p. 176.)

Don’t Blame Natural Selection: It’s Just Acting upon What Mutations Provide

It’s worth noting that Dawkins finally claims that it is natural selection that “feeds information into gene pools” by selecting for mutations that help organisms survive. Thus, Dawkins would argue that the information in the environment is transferred into the genome of the organism. Fair enough. But Dawkins isn’t telling the most important part of this story. We all know that mutations must provide the raw fuel upon which natural selection can act. As Gilbert, Opitz, and Raff write:

The Modern Synthesis is a remarkable achievement. However, starting in the 1970s, many biologists began questioning its adequacy in explaining evolution. Genetics might be adequate for explaining microevolution, but microevolutionary changes in gene frequency were not seen as able to turn a reptile into a mammal or to convert a fish into an amphibian. Microevolution looks at adaptations that concern only the survival of the fittest, not the arrival of the fittest. As Goodwin (1995) points out, “the origin of species—Darwin’s problem—remains unsolved.

Scott Gilbert, John Opitz, and Rudolf Raff (1996) “Resynthesizing Evolutionary and Developmental Biology,” Developmental Biology 173, 1996, p. 361.

Natural selection can (given the right population circumstances, etc.) preserve traits that confer a survival advantage, and it is very effective at weeding out traits that are disadvantageous. But natural selection can only act upon what mutations provide. Thus, we can’t account for the survival of particular mutations until we account for the arrival of particular mutations. We cannot account for the increase in information content of genomes until we consider how random mutations produce the raw fuel that natural selection can preserve.

My Information Challenge Reiterated:

So here is my “Information Challenge”: For the sake of the argument, I will grant that every stage of the evolutionary pathway I requested above will survive, and thus I’ll give natural selection every possible benefit of the doubt. What I need is a step-by-step mutation account of how one sentence evolved into the other wherein the sentence remains functional — i.e., it has comprehensible English meaning — at all stages of its evolution. In short, I request to see how:


can evolve into:


by changing the first sentence one letter at a time, and having it always retain some comprehensible English meaning along each small step of its evolution. This seems like a reasonable request, as it is not highly different from what Darwinists are telling me can happen in nature.

How would Dawkins reply? Would he get angry and complain that this is “the kind of question only a creationist would ask”? Or would he dodge the question like he did in his “The Information Challenge” article? Personally, I’d like to see an answer to the question.

Part 3: Dawkins “Junk”-DNA Blunder.

Dawkins’ article has other problems. He writes that “most of the capacity of the genome of any animal is not used to store useful information.” This is another good example demonstrating how Neo-Darwinism led may scientists to wrongly believe that non-coding DNA was largely junk. Dawkins’ statement is directly refuted by the findings of recent studies, which the Washington Post reported that scientists have now found that “the vast majority of the 3 billion ‘letters’ of the human genetic code are busily toiling at an array of previously invisible tasks.” That strikes a fatal blow to Dawkins’ argument:

 Dawkins then (1998)Scientists now (2007)
Position regarding “Junk”-DNA:“most of the capacity of the genome of any animal is not used to store useful information”“the vast majority of the 3 billion ‘letters’ of the human genetic code are busily toiling at an array of previously invisible tasks”

Dawkins claims that there is “lots of repetitive nonsense” in the genome. But is it really “nonsense”? Recent studies are finding increasing function for allegedly non-functional repetitive DNA. Richard Sternberg surveyed the literature and found extensive evidence for function in repetitive DNA (also called repetitive elements, or “REs”). A listing of functions for REs reprinted from Sternberg’s paper is shown below:

  • satellite repeats forming higher-order nuclear structures;
  • satellite repeats forming centromeres;
  • satellite repeats and other REs involved in chromatin condensation;
  • telomeric tandem repeats and LINE elements;
  • subtelomeric nuclear positioning/chromatin boundary elements;
  • non-TE interspersed chromatin boundary elements;
  • short, interspersed nuclear elements or SINEs as nucleation centers for methylation;
  • SINEs as chromatin boundary/insulator elements;
  • SINEs involved in cell proliferation;
  • SINEs involved in cellular stress responses;
  • SINEs involved in translation (may be connected to stress response);
  • SINEs involved in binding cohesin to chromosomes; and
  • LINEs involved in DNA repair.(Richard Sternberg, “On the Roles of Repetitive DNA Elements in the Context of a Unified Genomic-Epigenetic System,” Annals of the New York Academy of Sciences, Vol. 981:154-188 (2002).)

Dawkins not only got repetitive junk-DNA wrong, he provides a shimmering example of the fact that neo-Darwinism has led many scientists to wrongly presume that junk-DNA has no function. Some Darwinists have tried to counter that claim by arguing that Neo-Darwinism also led other biologists to presume function for junk-DNA, since its mere presence in the genome implies that natural selection has preserved it for some purpose. Even if that were a good argument, the fact remains that the false junk-DNA mindset was born and bred out of the Neo-Darwinian paradigm. That paradigm misled many scientists on this point, and in fact continues to mislead them.

But it isn’t even clear that Darwinists have a good scientific justification to believe that junk-DNA, if it exists, would be naturally selected out of the genome. According to the 2006 edition of Voet and Voet’s Biochemistry, there is insufficient selection pressure on functionless repetitive “junk”-DNA to remove it from the genome:

No function has been unequivocally assigned to moderately repetitive DNA, which has therefore been termed selfish or junk DNA. This DNA apparently is a molecular parasite that, over many generations, has disseminated itself throughout the genome through transposition. The theory of natural selection predicts that the increased metabolic burden imposed by the replication of an otherwise harmless selfish DNA would eventually lead to its elimination. Yet for slowly growing eukaryotes, the relative disadvantage of replicating an additional 100 bp of selfish DNA in an 1-billion-bp genome would be so slight that its rate of elimination would be balanced by its rate of propagation. Because unexpressed sequences are subject to little selective pressure, they accumulate mutations at a greater rate than do expressed sequences.

Donald Voet and Judith G. Voet, Biochemistry, p. 1020 (Jon Wiley & Sons, 2006), emphasis added.

In other words, Darwinists like Dawkins had every reason to presume that non-coding repetitive DNA was, in Dawkins’ words, functionless “nonsense” that was, in Voet and Voet’s words, a “molecular parasite,” even though it persisted in the genome. But Voet and Voet are wrong to presume that such repetitive DNA is mere parasitic junk, given that examples of functions for it abound. Sternberg’s article concluded that “the selfish DNA narrative and allied frameworks must join the other ‘icons’ of neo-Darwinian evolutionary theory that, despite their variance with empirical evidence, nevertheless persist in the literature.” Sternberg, along with geneticist James A. Shapiro, concludes elsewhere that “one day, we will think of what used to be called ‘junk DNA’ as a critical component of truly ‘expert’ cellular control regimes.” (Richard Sternberg and James A. Shapiro, “How Repeated Retroelements format genome function,” Cytogenetic and Genome Research, Vol. 110:108-116 (2005).)

It looks like Dawkins has some work to do if he is to update all of his arguments against ID and answer “The Information Challenge.”

Casey Luskin

Associate Director and Senior Fellow, Center for Science and Culture
Casey Luskin is a geologist and an attorney with graduate degrees in science and law, giving him expertise in both the scientific and legal dimensions of the debate over evolution. He earned his PhD in Geology from the University of Johannesburg, and BS and MS degrees in Earth Sciences from the University of California, San Diego, where he studied evolution extensively at both the graduate and undergraduate levels. His law degree is from the University of San Diego, where he focused his studies on First Amendment law, education law, and environmental law.