Ken Miller Confuses Weak Assertions of Common Ancestry With Darwinian Evolution of Blood Clotting Cascade (Updated)
Update 8/7/13: Since this response to Ken Miller was posted, even stronger evidence of function for the beta-globin pseudogene has been reported in the scientific literature, further refuting Miller’s argument. See Dover Revisited: With Beta-Globin Pseudogene Now Found to Be Functional, an Icon of the “Junk DNA” Argument Bites the Dust.
In his book Only a Theory, one of Dr. Kenneth Miller’s main response to Michael Behe’s arguments for the irreducible complexity of the blood clotting cascade is that sequence similarities between various blood clotting factors demonstrates that they share a common ancestry. Indeed, in his response to me on the irreducible complexity of the blood clotting cascade, Miller again conflates evidence for common ancestry with evidence for Darwinian evolution. At best, Miller’s only evidence shows evidence of common ancestry–not Darwinian evolution–but on closer inspection it seems that even Miller’s arguments for common ancestry may be weak.
As a first example of such a fallacious argument, Miller confuses evidence for common ancestry with evidence for Darwinian evolution in his book Only a Theory:
if two of the proteins, such as factors 9 and 10, diverged millions of years ago, as the pathway suggests, then we should be able to take any organism we like and discover that the pattern of relationship between their various factor 9 proteins matches the one we see for their factor 10 proteins, which similarly matches the one we see for factor 7. (Ken Miller, Only a Theory, p. 64)
Dr. Miller then concludes that Darwinian evolution is supported because “analysis of the detailed sequences of these proteins matches the prediction of evolution perfectly, it passes the test.” (p. 65)
There are two main problems with Miller’s argument.
First, Evidence of Common Ancestry is NOT Evidence of a Darwinian Pathway
As Michael Behe aptly observes, “modern Darwinists point to evidence of common descent and erroneously assume it to be evidence of the power of random mutation” (Behe, The Edge of Evolution, p. 95). Behe puts it even more clearly in Darwin’s Black Box:
“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?” (Darwin’s Black Box, pp. 175-176)
Thus Miller’s observations about comparative similarities in orthologous DNA sequences in no way refutes irreducible complexity nor does it demonstrate a stepwise Darwinian evolutionary pathway.
Incidentally, when I was a graduate student at UC San Diego, I took a graduate seminar where Miller’s authority, Russell Doolittle, was brought in to tell us what was wrong with Michael Behe’s arguments for irreducible complexity in blood clotting. The main point of Doolittle’s lecture was to draw trees tracing protein relationships, all based upon mere comparison of sequence similarity. His argument that trees based upon sequence similarity somehow demonstrate Darwinian evolution and refute irreducible complexity left me unimpressed–it committed the very fallacy Behe warned about in Darwin’s Black Box. I came to a deeper realization at that point of just how strong Behe’s argument was.
Second, Conflicting Phylogenetic Trees Show Miller’s Prediction Often Fails
I would go further than Behe and contend that Miller’s evidence not only does not provide evidence for Darwinian evolution, but it also doesn’t even provide very good evidence for common descent.
On the surface, his example of coherence between the phylogenetic trees generated by the different organisms is not surprising. For example, if you compared blood clotting factor 9 in a fish, a horse, and a human, and found that the factors in the horse and human were more similar to one another than they were to the factor in the fish, no one would find that observation very startling. Molecule-based phylogenetic trees are simply nested hierarchies reflecting comparative genetic similarities. All this data shows is that organisms that are more similar on the outside tend to be more similar on the inside.
Let’s scrutinize Miller’s “prediction of evolution” more closely. Miller’s prediction seems to be that taking different orthologous genes found in various species and using them, one at a time, to construct phylogenetic trees, will produce very similar and congruent trees. While perhaps this is found to be true for these few blood clotting factors, anyone who follows this field knows that systematists regularly bang their heads against the wall because this “prediction of evolution” commonly does NOT turn out to be true. To give a few examples:
- The Cytochrome C phylogenetic tree is often touted as allegedly matching and confirming the traditional phylogeny of many animal groups, and this is said to bolster the case for common descent. But evolutionists rarely talk about the Cytochrome B tree, which has striking differences from the classical animal phylogeny. As one article in Trends in Ecology and Evolution stated: “the mitochondrial cytochrome b gene implied…an absurd phylogeny of mammals, regardless of the method of tree construction. Cats and whales fell within primates, grouping with simians (monkeys and apes) and strepsirhines (lemurs, bush-babies and lorises) to the exclusion of tarsiers. Cytochrome b is probably the most commonly sequenced gene in vertebrates, making this surprising result even more disconcerting.”
- A 2006 paper in the journal PLoS Biology entitled, “Bushes in the Tree of Life.” The authors acknowledge that “a large fraction of single genes produce phylogenies of poor quality,” observing that one study “omitted 35% of single genes from their data matrix, because those genes produced phylogenies at odds with conventional wisdom.”
- An article in the journal New Scientist stated earlier this year that “problems began in the early 1990s when it became possible to sequence actual bacterial and archaeal genes rather than just RNA. Everybody expected these DNA sequences to confirm the RNA tree, and sometimes they did but, crucially, sometimes they did not. RNA, for example, might suggest that species A was more closely related to species.” This type of problem was observed even among higher organisms, as the article lamented: “[t]he problem was that different genes told contradictory evolutionary stories,” leading one scientist to say regarding the relationships of these higher groups, “We’ve just annihilated the tree of life.”
Many (and I mean many) more similar examples could be given, but these demonstrate the point: it’s not uncommon that one gene yields one phylogenetic tree, while a different gene yields an entirely different phylogenetic tree. Miller’s “prediction of evolution” is falsified all the time.
In Only a Theory, Miller attacks ID claiming it “cannot predict such patterns, and cannot even be tested” (p. 65), but unless Miller wants evolution to be falsified by the above examples, then he must too concede the point that evolution does not make clear predictions about whether individual gene-based trees should agree. At the very least, it’s clear that trees based upon individual genes commonly do not agree. What does this do to Miller’s alleged “prediction” of evolution?
In his response to me on irreducible complexity and the blood clotting cascade, Professor Miller also argued that irreducible complexity is refuted on the grounds that whales allegedly have a non-functional pseudogene instead of a functional gene for blood clotting Factor XII. Miller wrote: “Whales possess a Factor XII pseudogene, an inactivated version of the very same gene carried by land-dwelling mammals. That pseudogene is a direct mark of their common ancestry with other mammals, and disproves any suggestion that constraints on cetacean ‘design’ required the absence of Factor XII. Rather, ordinary genetic processes knocked out the gene, and today the pseudogene remains merely as evidence of their evolutionary ancestry.”
At best a shared pseudogene might provide evidence of common ancestry, but as noted above, evidence for evolutionary ancestry does not confirm a Darwinian pathway. And again, even here it’s not clear that Miller’s evidence provides unambiguous evidence for common ancestry. If Miller thinks that by slipping in the mention of a pseudogene that he’s provided conclusive evidence of common ancestry, then he should consider that the more we study “pseudogenes,” the more we’re finding that they can have function! As Evgeniy S. Balakirev and Francisco J. Ayala wrote in Annual Review of Genetics:
“Rather, pseudogenes that have been suitably investigated often exhibit functional roles, such as gene expression, gene regulation, generation of genetic (antibody, antigenic, and other) diversity. … Pseudogenes exhibit evolutionary conservation of gene sequence, reduced nucleotide variability, excess synonymous over nonsynonymous nucleotide polymorphism, and other features that are expected in genes or DNA sequences that have functional roles.”
(Evgeniy S. Balakirev, and Francisco J. Ayala, Pseudogenes, “Are They “Junk” or Functional DNA?,” Annual Review of Genetics, Vol. 37:123–51 (2003), emphasis added.)
Some papers that have reported functions for pseudogenes include:
- D. Zheng and M. B. Gerstein, “The ambiguous boundary between genes and pseudogenes: the dead rise up, or do they?,” Trends in Genetics, Vol. 23(5):219-224 (2007).
- S. Hirotsune et al., “An expressed pseudogene regulates the messenger-RNA stability of its homologous coding gene,” Nature, Vol. 423:91-96 (May 1, 2003).
- O. H. Tam et al., “Pseudogene-derived small interfering RNAs regulate gene expression in mouse oocytes,” Nature, Vol. 453:534-538 (May 22, 2008).
- D. Pain et al., “Multiple Retropseudogenes from Pluripotent Cell-specific Gene Expression Indicates a Potential Signature for Novel Gene Identification,” The Journal of Biological Chemistry, Vol. 280(8):6265–6268 (February 25, 2005).
- J. Zhang et al., “NANOGP8 is a retrogene expressed in cancers,” FEBS Journal, Vol. 273:1723–1730 (2006).
Miller seems to be too hasty in his assumption that pseudogenes are functionless “junk” and thereby evidence for common ancestry. Unfortunately, this haste has had non-trivial ramifications.
Miller’s centerpiece example of a pseudogene that provides evidence for human-ape common ancestry in both his book Only a Theory and at the Dover trial was the human beta-globin pseudogene. But the British pro-ID organization Truth in Science has shown why this argument is weak, as the beta-globin pseudogene shows evidence of conserved sequence, implying that it could have function:
The very fact that the beta-globin pseudogene appears to be conserved in humans, chimpanzees and gorillas speaks eloquently of the fact that this DNA has some important biological function. Genetic sequences are conserved and maintained when any mutation would render them non-functional (or less functional) and when any loss of activity is damaging the organism’s prospects of survival. Such sequences are said to be under purifying (or stabilising) selection which means that deleterious mutations are removed from the gene pool restricting genetic diversity. It is probably the most common mechanism of action for natural selection and leads to the maintenance of genetic integrity. It is certainly not the driving force behind evolutionary change. According to the recent review by Sasidharan and Gerstein:
Although pseudogenes have generally been considered as evolutionary ‘dead-ends’, a large proportion of these sequences seem to be under some form of purifying selection – whereby natural selection eliminates deleterious mutations from the population – and genetic elements under selection have some use .
In the case of the beta-globin pseudogene, Wanapirak et al. have reported amazing conservation in the fine structure of the DNA with identical super-helical twists in the human, mouse, bovine, rabbit and chicken genomes  . It needs to be remembered that maintenance of the genetic integrity of these structures is biochemically costly. It takes energy to duplicate DNA. The replicating machinery in the cell has built-in proof reading and excising enzymes that constantly check for mutation and damage. Numerous repair mechanisms have been identified to correct genetic damage and to excise incorrect sequences .
(The Changing Face of Pseudogenes, Truth in Science Blog)
By assuming that the beta-globin pseudogene is functionless genetic “junk,” is it possible that Dr. Miller is unintentionally discouraging scientists from discovering its true function?
Neo-Darwinian evolutionists like Ken Miller should understand that evidence of common descent is not necessarily evidence of Darwinian pathway, and that in many cases, the evidence for common ancestry is not nearly as strong as many would like to think it is. At the very least, this much is clear: None of this evidence has any bearing upon irreducible complexity of the blood clotting cascade.