V.J. Torley and our colleague Cornelius Hunter have continued their discussion about common descent, a subject on which, as John West notes, advocates of intelligent design don’t all agree. Airing such disagreements, if done in a respectful and substantive manner, is of course a healthy thing. Writing at Uncommon Descent, Dr. Torley raises an interesting point, directed at Dr. Hunter and citing theistic evolutionist Dennis Venema:
In the comments to one of your posts, you thanked a reader for linking to an article stating that the protein vitellogenin confers several beneficial effects upon bees, in addition to being used to make egg yolks. Humans possess a broken copy of the gene which makes this protein; they no longer need it. So my final question is: why do you not consider this gene to be vestigial — especially when Dr. Jeffrey Tomkins’s claim that the remaining gene [vitellogenin] fragments in human beings are functional has been soundly refuted by Dr. Dennis Venema?
Actually, if you read Venema’s response to Tomkins, Venema appears to concede Tomkins’s central point that the VIT1 gene could be functional. Here’s what Venema writes:
He [Tomkins] argues that the 150 base pair fragment of VIT1 is “not a real pseudogene” but rather regulatory DNA for an unrelated gene — DNA that functions to direct where and when another gene is transcribed. This gene falls into a class of genes known as “long non-coding RNAs” — genes that are transcribed into RNA but do not code for proteins. These genes are thought to arise quite easily over the course of evolution, and many are thought to have little or no function (for a good but technical review, see here). Specifically, the VIT1 fragment Tomkins acknowledges sits in an intron of this gene (part of the gene that is spliced out of the RNA copy after it is transcribed from DNA). Tomkins summarizes the evidence — such as it is — that suggests this sequence might have a regulatory function. If this fragment is a functional part of an unrelated gene, he argues, it makes sense to understand it as the result of special creation, rather than the evolutionary remnant of a once-functional VIT1 gene in the lineage leading to humans.
Tomkins has presented evidence that the VIT1 pseudogene sits in part of an intron that is transcribed and produces long non-coding RNAs of the type we know often have function. What does Venema say next? Does he contest this evidence for functionality? No. According to Venema the “major problem” with Tomkins’s argument isn’t the evidence for functionality in the VIT1 pseudogene. Rather, he focuses on critiquing a false dichotomy that Tomkins has supposedly advanced:
The major problem with this argument is that it subscribes to a false dichotomy: that this sequence is either a VIT1 pseudogene fragment or a functional part of another gene. From an evolutionary perspective, there is no issue with it being both. Part of evolutionary theory is the expectation that occasionally some sequences, after losing their original function, may come under natural selection to be repurposed to another function. The technical term for this process is exaptation, and many examples of it are known. Certainly a long, non-coding RNA gene could arise at this location in the human genome and this sequence could be exapted as a regulatory sequence — but there is no hint of admitting this possibility in Tomkins’ work. Once again we are reminded that he is not writing for a scientifically informed audience, but rather for a lay audience that will not know about the possibility of exaptation and expect him to provide evidence that it is not a factor in this situation. Rather, it seems enough to Tomkins to suggest that the sequence is functional — and that this alone will be enough for him to convince his readership that this fragment is “not a real pseudogene.”
Of course Venema is correct that finding function for this pseudogene is no refutation of Darwinian evolution. But his focus on this point distracts from the main issue here. And what’s that?
The main issue is that evolutionists have commonly argued that non-functionality in shared pseudogenes is what provides evidence for common ancestry. They argue that God would not put “broken” shared DNA in multiple species and thus this must be evidence for common ancestry over intelligent design (or special creation, or whatever). We’ve seen many theistic and atheistic evolutionists treat pseudogenes in precisely this manner:
Richard Dawkins writes that “genomes are littered with nonfunctional pseudogenes, faulty duplicates of functional genes that do nothing.” (Richard Dawkins, A Devil’s Chaplain: Reflections on Hope, Lies, Science, and Love (New York: Mariner Books, 2004), 99, emphasis added.)
Kenneth Miller writes that the “human genome is littered with pseudogenes, gene fragments, ‘orphaned’ genes, ‘junk’ DNA, and so many repeated copies of pointless DNA sequences that it cannot be attributed to anything that resembles intelligent design. ” (Kenneth Miller, “Life’s Grand Design,” Technology Review, 97 (February/March, 1994): 24-32, emphasis added.)
Francis Collins and Karl Giberson write in The Language of Science and Faith that pseudogenes are “broken,” and it is “not remotely plausible” that “God inserted a piece of broken DNA into our genomes.” In their view, pseudogenes shared across different species establish “conclusively that the data fits a model of evolution from a common ancestor.” (Karl Giberson and Francis Collins, The Language of Science and Faith: Straight Answers to Genuine Questions (InterVarsity Press, 2011), 49, emphasis added.)
Darrel Falk writes that one “might be tempted suggest that the reason why God put a deletion into the ape lineage is because it would make the gene more ideally suited to carrying out its purposes in apes. That might well have been a valid argument if this was a functioning gene. However, it is not. The gene has no function. ” (Darrel Falk, Coming to Peace with Science (IVP Academic, 2004), 188, emphasis added.)
Denis Alexander writes: “[O]ur own genomes are loaded with ‘pseudogenes,’ stretches of DNA that are so similar to functional genes that there is no doubt where they came from, yet so full of mutations that they are functionally incapable of making protein, as can be shown experimentally in the laboratory” (Creation or Evolution, p. 112). He goes on to say that “pseudogenes … have lost their function” (p. 204), calling them ” derelict genetic fossils” (p. 205) or a “dysfunctional gene” (p. 206). He even calls them “nonfunctional genes” (p. 119).
Even Venema makes a big deal about the idea that pseudogenes are non-functional: “Pseudogenes (literally, ‘false genes’) are gene sequences that have been inactivated by mutation that persist in the genome as nonfunctional sequences. … once inactivated, a pseudogene accumulates mutations only slowly because the proofreading mechanisms that govern DNA replication do not distinguish between functional and nonfunctional DNA sequences.” (Emphasis added.)
In fact, in that same article, Venema goes on to say this specifically about the vitellogenin pseudogene. Immediately after calling pseudogenes “nonfunctional,” he gives the example of the vitellogenin pseudogene:
The human genome thus contains the mutated remains of a gene devoted to egg yolk formation in egg-laying vertebrates at the precise location predicted by shared synteny derived from common ancestry.
So Venema calls pseudogenes “nonfunctional,” gives the “vitellogenin pseudogene” as his primary example, and then goes on to use the supposed nonfunctionality of the vitellogenin pseudogene as evidence against intelligent design and for common ancestry.
He says much the same on BioLogos’s website where he uses similar language to say that “pseudogenes are remnants of once-functional genes” and repeatedly calls them “non-functional.” (See here and here.) And again he uses the vitellogenin pseudogene as an example, citing “the mutated remains of the vitellogenin gene.”
Now Venema argues that the vitellogenin “pseudogene” in humans simply lost its original function and is now being used for a different function. Perhaps, he might argue, even if we are using the vitellogenin “pseudogene” for some function, the fact that we aren’t using it to make egg yolk shows that we inherited it from a common ancestor we shared with chickens. This too would be a misguided argument.
First, proteins often have multiple domains that allow a protein to interact with different molecules in different contexts within a cell. At best, the human vitellogenin “pseudogene” only represents a small fraction of the chicken version of the gene. One could initially surmise that the fragment (or fragments) of the vitellogenin “pseudogene” that humans have (and use for some function) may not be the part (or parts) crucial only for making egg yolk in chickens. We may be using it for a non-egg-yolk related function that’s also found in chickens.
But in this case, according to Tomkins (2015), the human “vitellogenin pseudogene” seems to be producing a long non-coding RNA (lncRNA), not a protein. LncRNAs are known to have all kinds of functional roles in humans, and are especially known to be involved in gene regulation. In this more likely case, perhaps the chicken vitellogenin gene produces not only egg yolk-related proteins, but also RNAs that have other roles or functional interactions in chickens. We may be using our “vitellogenin pseudogene” for a similar RNA-based function or interaction that chickens do. For example, perhaps in addition to producing a protein, the chicken vitellogenin gene also produces RNAs with some regulatory role, and humans use our version of the “vitellogenin gene” for some similar RNA-based regulatory role. Indeed, Venema’s discussion of the human “vitellogenin gene” seems to admit that something like this could be a possibility.
In either case, our “vitellogenin pseudogene” and the chicken version would turn into a mere example of homologous DNA performing a homologous functions — something we see all the time in biology and which can be explained by common design just as easily as by common descent. It doesn’t appear that the specific function of our “vitellogenin gene” has been explored yet, and this would be an interesting question to investigate. The hypotheses offered here could very well turn out to be true.
But doesn’t have to be the case, however, to defeat the vitellogenin argument for common ancestry. That’s because, as a second point, even if humans are using our “vitellogenin gene” for entirely different purposes than chickens do, this still doesn’t provide evidence for common ancestry. Why? Because we often see in technological designs that similar parts can be used for very different purposes. A plastic ring in one design might be used for blowing bubbles, but in another it helps seal the connections between two pipes. Or a plastic container in an outboard boat motor holds fuel, but in another technological design it holds dishwashing liquid. Using similar parts for different purposes is easily accommodated by common design.
Moreover, when we in biology see this sort of phenomenon — similar parts performing different functions — it is usually taken as evidence against common ancestry, not for it, as the textbook Explore Evolution notes:
In another surprising twist, biologists have also discovered many cases in which the same genes help to produce different adult structures. Consider, for instance, the eyes of the squid, the fruit fly, and mouse. The fruit fly has a compound eye, with dozens of separate lenses. The squid and mouse both have single-lens camera eyes, but they develop along very different pathways, and are wired differently from each other. Yet, the same gene is involved in the development of all three of these eyes.
According to neo-Darwinian theory, the development of non-homologous structures should be regulated by non-homologous genes. So, many biologists were taken aback to discover that non-homologous eyes (from an insect, a mollusk, and a vertebrate) could be regulated during their development by homologous genes, like Pax-6. Stephen Jay Gould called this discovery, “…unexpected under usual views of evolution….”
To summarize, biologists have made two discoveries that challenge the argument from anatomical homology. The first is that the development of homologous structures can be governed by different genes and can follow different developmental pathways. The second discovery, conversely, is that sometimes the same gene plays a role in producing different adult structures. Both of these discoveries seem to contradict neo-Darwinian expectations.
(Explore Evolution, Second Edition, pp. 44-45)
Thus, examples where homologous genes perform non-homologous functions are said to provide a conundrum for common ancestry; it would be a mistake to cite similar DNA being used for different purposes as evidence for common ancestry.
But this speculation about the function of the human “vitegollenin” gene is an aside, because if we look at the arguments that are actually being made and what we already know to be true, the argument from vitegollenin for common ancestry is defeated. Here is what’s really going on:
Evolutionists have often claimed that DNA elements like the VIT1 pseudogene are “non-functional.”
Evolutionists claim that these pseudogenes provide special evidence for evolution because God would not create different species with shared non-functional DNA in the same location. Therefore, they argue, pseudogenes must be evidence for shared ancestry.
Tomkins presented evidence that the VIT1 “pseudogene” is indeed functional in humans.
Evolutionists responded not by disputing Tomkins’s evidence for functionality in the human VIT1 “pseudogene.” Rather, they shifted the argument, saying in effect, “Well, common ancestry/evolution isn’t refuted simply by finding a function or a pseudogene.”
One might reply to point (4) as follows: We never said that functional pseudogenes refute evolution. But functional pseudogenes do in fact refute a central part of a major argument that evolutionists have made against ID and for common ancestry. Venema does not seem to contest the evidence that Tomkins cites showing that the vitellogenin “pseudogene” is functional. Although Venema does not explicitly concede the point, by its very nature his argument is one that accepts its functionality.
No, the evidence raised by Tomkins suggesting vitellogenin “pseudogene” functionality in humans poses a major problem for those who make the case that the vitellogenin pseudogene provides compelling evidence for common ancestry. Tomkins’s argument has hardly been “soundly refuted” by Venema.
Photo: Chicken egg yolk, by jefras a.k.a Joăo Estęvăo A. de Freitas [Public domain], via Wikimedia Commons.