In Adam and the Genome, which we’ve been reviewing here, Trinity Western University biologist Dennis Venema offers lengthy discussions of whole genome duplications (WGDs), even though this issue has, you guessed it, nothing to do with whether Adam and Eve existed. Venema, a theistic evolutionist associated with BioLogos, is very impressed by what he calls the evidence for the ability of WGDs to produce new genes. He writes:
[T]he base of the vertebrate lineage had two rounds of WGD, greatly increasing the number of genes available to be converted into modified functions — something that [Stephen] Meyer, to my knowledge, has not acknowledged or responded to.
(Adam and the Genome, p. 81)
But Venema is wrong here on multiple levels.
Stephen Meyer in his book Darwin’s Doubt addresses many lines of evidence and argument purported to support Darwinian evolution, and he deals with them forthrightly and effectively. It was impossible for Meyer to discuss everything in evolutionary biology, but he does spend quite a bit of time talking about gene duplication — most of Chapter 11, in fact, as well as part of Chapter 10. He even discusses duplication of genomes. Here’s how he introduces the subject:
[N]eo-Darwinists envision new genetic information arising from sections of the genetic text that can vary freely without consequence to the organism. According to this scenario, noncoding sections of the genome or duplicated sections of coding regions undergo a protracted period of “neutral evolution” in which alterations in nucleotide sequences have no discernible effect on the fitness of the organism. Functional genes and proteins gradually rise from a nonfunctional valley floor to a functional mountain peak — generating a new gene. Natural selection plays a role, but not until a new functional gene has arisen.
Evolutionary biologists typically picture this process beginning with a gene duplication event. Although several different mechanisms can generate gene duplicates in DNA,16 the most common mechanism occurs during the crossing- over step of meiosis (a kind of cell division that produces sex cells, or gametes, in sexually reproducing organisms).
(Darwin’s Doubt, p. 198)
Footnote 16 here refers to a paper that reviews various mechanisms that can duplicate genes. The footnote reads:
Matthew Hahn notes that, “There appear to be 4 major mechanisms by which DNA is duplicated: (1) unequal crossing- over, (2) duplicative (DNA) transposition, (3) retrotransposition, and (4) polyploidization” (“Distinguishing Among Evolutionary Models for the Maintenance of Gene Duplicates,” 606.)
(Darwin’s Doubt, p. 436)
Polyploidization is, of course, another word for whole genome duplication. In fact the paper he cites by Hahn equates polyploidization with “whole genome duplication”:
The fourth major mechanism of duplicate gene formation is polyploidization. Whole-genome duplications result in new gene copies of every gene in a genome and, obviously, all the flanking regulatory sequences.
(Matthew W. Hahn, “Distinguishing Among Evolutionary Models for the Maintenance of Gene Duplicates.” Journal of Heredity 100: 605-617 (2009))
So Venema is wrong: Meyer does acknowledge whole genome duplication as a mechanism of creating more DNA.
The Main Issue
But that’s really not the main issue here because duplicating DNA is the easy part. No one doubts that whole genome duplications generate new DNA. There are many mechanisms that can do this, as Meyer explains. The issue is how gene duplicates can acquire new functions.
According to proponents of gene duplication, the evolution of new genes is a basically two-step process: (1) First a gene duplicates. (2) Then it mutates to find a new function (called “recruitment”).
Step (1) may at best indicate common ancestry, but it doesn’t bear at all upon whether step (2) can occur or has occurred. Evolutionary explanations for the origin of new genes cannot simply rely upon duplication, for there must be duplication followed by recruitment to a new function.
For all we know, genes may easily duplicate. But new protein functions are difficult for random mutation to find because functional sequences are rare in sequence space. This would make it highly unlikely that WGD events can explain how new genes arise.
Meyer explains that indeed it is very difficult for gene duplicates to be recruited to new functions:
But this scenario faces an overriding problem: the extreme rarity of sequences capable of forming stable folds and performing biological functions. Since natural selection does nothing to help generate new folded, functional sequences, but rather can only preserve such sequences once they have arisen, random mutations alone must search for the exceedingly rare folded and functional sequences within the vast sea of combinatorial possibilities.
(Darwin’s Doubt, p. 199)
If you want to claim that a gene duplicate was able to acquire a new function by mutation and selection, then you must demonstrate that it is mathematically feasible. Gene duplication accounts of the origin of new genes frequently involve a specific sequence of mutations that are necessary to generate the gene in question. In an article, “The NCSE, Judge Jones, and Citation Bluffs About the Origin of New Functional Genetic Information,” Casey Luskin spells out three questions that must be addressed to establish an evolutionary account of the origin of a new gene through gene duplication:
- Question 1: Is there a step-wise adaptive pathway to mutate from A to B, with a selective advantage gained at each small step of the pathway?
- Question 2: If not, are multiple specific mutations ever necessary to gain or improve function?
- Question 3: If so, are such multi-mutation events likely to occur given the available probabilistic resources?
Luskin looks at about a dozen different papers purporting to explain the evolution of new genes. He finds that:
[I]n no cases were the odds of these unlikely events taking place actually calculated. Incredibly, natural selection was repeatedly invoked in instances where the investigators did not know the function of the gene being studied and thus could not possibly have identified any known functional advantages gained through the mutations being invoked. In the case where multiple mutational steps were involved, no tests were done of the functional viability of the alleged intermediate stages. These papers offer vague stories but not viable, plausibly demonstrated explanations for the origin of new genetic information. … In not a single case did the above papers cited by Long et al. actually explain how new functional information arose. In no case was there an analysis of how natural selection could have favored mutational changes that were shown to be likely along each step of an alleged evolutionary pathway; never was any detailed step-by-step mutational pathway even given. At best, these studies offered vague and ad hoc appeals to duplication, rearrangement, and natural selection — often in a sudden, extreme, and abrupt manner — to form the gene in question. In many cases, natural selection was invoked to allegedly account for changes in the gene, even though the investigators didn’t even know the function of the gene and thereby could not identify the advantage provided by the gene’s function. In no case were calculations performed to assess whether sufficient probabilistic resources existed to produce the asserted mutational events on a reasonable timescale. In some cases, the original genetic material for the genes was unknown, or the studies asserted spontaneous “de novo” origin of genes from previously non-coding DNA. While they readily admitted that “de novo” gene emergence is rare, no attempt was made to assess whether such an unguided mechanism is even remotely plausible on mathematical probabilistic grounds.
Venema makes the same error in Adam and the Genome. By citing WGD, Venema may have explained how new DNA can be produced, but in no cases did he perform any calculations of whether it is likely that a gene duplicate (called a paralog) will acquire a new function. Instead, he simply asserts:
And here’s the rub: we know that these paralogs, whether recent or ancient, have greatly diverged from each other and acquired new functions. Moreover, many of those functions are now absolutely essential for vertebrates. If Behe’s argument is correct, none of this should have been possible. (p. 77)
But what is Venema’s evidence that “we know” they acquired their function via unguided natural evolutionary mechanisms? He provides none other than the words “we know.” It’s pure assertion, without any calculations whatsoever that these paralogs could or did diverge via natural means to acquire new functions.
Not the First Time
This is not the first time that Venema has cited whole genome duplication as evidence for the power of unguided evolutionary mechanisms to produce new genes. In 2011, Casey Luskin responded to a virtually identical argument from Venema. See, “Confusing Evidence for Common Ancestry with Evidence for Random Mutation and Natural Selection,” where Luskin writes:
[Venema] cites evidence showing that vertebrates tend to have four times as many paralogous genes as urochordates, and notes that “these modern paralogs are still present in four-fold syntenty groups that span about 25% of the human genome.” Venema then claims:
“In other words, gene duplication and divergence to produce new CSI [complex and specified information] appears to be commonplace in evolution, including the evolution of our own species. Far from being rare exceptions, multiple lines of genomics evidence point to new structures, functions and information being produced through natural means. If the Intelligent Design Movement wishes to contest that natural mechanisms cannot produce new information, they need to address this widespread and compelling pattern.”
But since Venema has cited no evidence for natural selection and random mutation, there is nothing for intelligent design to contest.
What Venema has discussed is shared functional genetic patterns across various classes of vertebrates. None of this evidence says anything about, as he claims his series would show, “a natural mechanism that does add functional, specified information to DNA sequences … natural selection acting on genetic variation produced through random mutation.” At best, these shared functional similarities that Venema has cited provide evidence of common ancestry, which is not incompatible with intelligent design. Michael Behe, for one, reminds us that evidence for common ancestry is not evidence of a Darwinian pathway:
“[M]odern Darwinists point to evidence of common descent and erroneously assume it to be evidence of the power of random mutation.
(Michael J. Behe, The Edge of Evolution: The Search for the Limits of Darwinism, p. 95 (Free Press, 2007).)”
In Darwin’s Black Box, Behe elaborates on the point:
“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 J. Behe, Darwin’s Black Box: The Biochemical Challenge to Evolution, pp. 175-176 (Free Press, 1996).)”
Luskin wrote that back in 2011, but the same applies here in response to Adam and the Genome. In fact, Venema’s arguments have hardly changed since that prior discussion. He even cites the same 2005 paper by Dehal and Boore in PLOS Biology to establish two rounds of gene duplication.
As before, Venema has not provided any evidence for the creative power of natural selection, much less has he addressed whether Adam and Eve existed. Arguably, he has not even provided compelling evidence for WGD.
Of Sea Squirts and Circumstantial Evidence
As an aside, in Adam and the Genome, the main evidence for WGD that Venema presents is that non-chordates such as sea squirts have a very different genomic organization, where paralogs are not found on different chromosomes, but are adjacent to one another. This is circumstantial evidence, though, especially given that Dehal and Boore 2005 were forced to invoke large amounts of “gene loss and rediploidization” to fit the data to a model of two rounds of genome duplication. In other words, much genetic data doesn’t neatly fit the pattern of two WGD events, so you have to invoke ad hoc explanations of gene gain or loss to explain why so many genes don’t fit.
But whether the data does or does not support WGD is immaterial to the question of whether Venema has found concrete evidence that all of these genes diverged by natural selection and random mutation. In fact, the paper he cites make clear that the writers don’t know whether these supposed whole genome duplication provided advantages that natural selection could select:
It remains unclear to what extent such large-scale genomic events have driven macroevolutionary change versus the regular accumulation of small mutations, as is the central tenet of the classical model of evolution.
(Paramvir Dehal, Jeffrey L. Boore, “Two Rounds of Whole Genome Duplication in the Ancestral Vertebrate,” PLOS Biology, Vol. 3(10):1700-1708 (October 2005))
They further observe that “the vast majority of duplicated genes were subsequently deleted, indicating that relatively few genes may have been responsible for the increased complexity seen in vertebrates.” So, again, it seems that they are not sure to what extent natural selection was driving the evolution of these supposed new duplicate copies of genes. As Luskin explained, this is inadequate:
The following is the incredibly low level of detail they provide for the alleged Darwinian evolution of vertebrate genetic structure: “We imagine that rapid and extensive evolutionary change could possibly be an emergent property of having all genes duplicated at the same time, allowing this expanded gene repertoire to evolve together.” Such vague assertions of evolutionary processes in no way demonstrate the efficacy of random mutation and natural selection. Instead, without providing any evidence that natural selection and random mutation could produce observed vertebrate diversification, they simply assert that it happened. It’s easy to tell stories when the underlying mechanisms are assumed rather than demonstrated.
Perhaps their imaginations are simply more powerful than those of ID proponents, who find it difficult to “imagine” such “rapid and extensive evolutionary change” across thousands of genes when precise, detailed Darwinian pathways are never given.
In the end, ID is not incompatible with common descent, but Venema has confused evidence for common ancestry with evidence for natural selection and random mutation. Evidence for WGD doesn’t show a Darwinian pathway. There is no evidence here against intelligent design or Michael Behe.