This post is the fourth in this series addressing Dr. Jeffrey Tomkins’ argument against “vitellogenin” (VIT) pseudogenes as evidence for common descent . The first post in the series is here, and new readers are strongly encouraged to browse it before reading below. In this post, we examine how Tomkins deals with the one (and only) VIT pseudogene fragment he acknowledges to exist in the human genome.
In the last post in this series, we saw how Tomkins – in his attempt to refute the striking evidence for common ancestry that human vitellogenin (VIT) pseudogenes provide – chose to ignore the entirety of the evidence except for one fragment, 150 base pairs long, of the human VIT1 pseudogene. From this starting point, he then attempts to convince his readership that this fragment is not a VIT pseudogene fragment at all, but rather part of a gene with a function unrelated to egg yolk formation.
Even as we turn to evaluating that argument, it’s important to remember that doing so is secondary to what we have already addressed: Tomkins has chosen to ignore almost all of the evidence for human VIT pseudogenes, and all of the evidence for VIT pseudogenes in other placental and marsupial mammals. Even if Tomkins’ case for the one fragment he chooses to address was airtight, it would not even begin to be a satisfactory rebuttal of the evidence for a scientifically informed audience.
Tomkins on shared synteny
As we have seen in prior posts, the shared synteny between the human and chicken genomes for the VIT1 region is an important piece of evidence for their common ancestry. Though Tomkins is aware of the importance of this line of evidence, he addresses it dismissively:
One of the supporting arguments for the vtg pseudogene fragment being authentic is that it shares gene neighborhood synteny with chicken. When this was investigated, it was found that gene synteny surrounding the chicken vtg1 gene (~360,000 bases) compared to the region surrounding the alleged vit1 fragment in human, was completely different except for the presence of the LTD1 [sic, what Brawand et. al call ELTD1] gene which was about three times the distance (~100,000 bases) from the alleged vit fragment as its homolog is in chicken (~38,000 bases). [Emphasis mine]
Tomkins is recognizing that the ELTD1 gene is the same in humans and chickens, but he claims that the rest of the surrounding area is “completely different” and that it is further away from VIT1 in humans than in chickens. Of course, admitting that the ELTD1 gene sits beside the functional VIT1 gene in chickens and the VIT1 pseudogene fragment in humans is a concession to shared synteny – but notice how Tomkins treats this evidence. His primary claim is that aside from the ELTD1 gene sequences, these regions are “completely different” in humans and chickens. (Additionally, he points out that the number of base pairs between the human and chicken sequences and ELTD1 differs – though I am unclear why he would think this supports his case, unless he is not willing to consider that insertion and/or deletion mutations in this region may have altered the distances over time.) His primary claim – that these regions are “completely different” is incorrect, as we can see from the data in the original paper, and diagrammed here:
ABOVE: Shared synteny between humans and chickens spanning the VIT1 region. Black bars between the two chromosomes indicate sequence matches. There are several matches between the functional VIT1 in chicken and the human genome, though the human VIT1 sequences are fragmentary. This figure is based on data from Brawand et al., 2008.
Not only are there several sequence matches in the region between the VIT1 fragment and the ELTD1 gene, some of those sequences are VIT1 pseudogene fragments that Tomkins is ignoring. Additionally, there are matches that extend beyond the ELTD1 gene and the VIT1 fragments, which establish that these sequences share synteny.
I am not exactly sure why Tomkins would claim that these sequences, which do indeed have matches, are completely different. It may be that they are “completely different” under the particular (and highly idiosyncratic) methods he has used to do genome comparisons in the past, for which he has been criticized, even by other young-earth creationists and supporters of Intelligent Design (see here and here, for example). In any case, Tomkins’ claim in this instance is simply wrong, and would greatly mislead a non-specialist audience.
Pseudogene or functional gene?
Having rebutted the synteny evidence to his satisfaction, the rest of the case that Tomkins attempts to make is straightforward to understand: He 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.
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.”
Cair Paravel, prefab houses, and exaptation
Perhaps returning to our prior analogies of synteny will be helpful here. Recall that when the Pevensie children (of Chronicles of Narnia fame) were coming to the realization that they were in the ruins of Cair Paravel, they had to clear away a mass of ivy from a wall before they could access the door to the treasure chamber. This wall had previously held up the roof of the great hall above the dais, but now it was a support for the ivy, and undoubtedly a host of animal life within it. The “function” of the wall, then, had changed over time. None of the children, of course, pointed to this “new function” as incompatible with their hypothesis that the wall had formerly been used for a different purpose. The observation that the wall was now a home for plants, insects and perhaps even birds was not a problem, since the children understood that these new properties could have been accumulated over time as the original function was diminished. Moreover, they correctly understood that the weight of the evidence around them strongly suggested that this transformation indeed had taken place.
Our second analogy was the neighborhood of prefabricated houses in my hometown – originally constructed as identical, and gradually becoming more distinct over time as each house has its independent history shaped by renovations and alterations. Suppose in this neighborhood one homeowner decided to relocate the bathroom into an addition, and repurpose the original bathroom into a laundry room. Careful examination of the laundry room might show how the plumbing was adapted from its original function to serve in this new capacity. Imagine, for example, that the drain for the toilet remained in its original position, but was capped and recessed under the floor. Though the room might have been converted to a new function, it still would retain some features that indicated its prior history – and examining other houses in the neighborhood would only confirm our suspicions. Merely discussing how the washing machine was hooked up properly (perhaps where the sink had once been) would do nothing to convince us that the toilet drain under the tiles was anything other than the clear sign the room had once been a bathroom.
Put more simply, evidence of function does not erase the evidence for prior history.
Even though the evidence that this sequence is functional in humans is rather thin, the main issue is that even if its function were convincingly demonstrated in the future, it would not remove the evidence that this sequence was once part of a functional VIT gene – evidence that Tomkins has either not addressed, or denied outright.
In the next post in this series, we’ll leave Tomkins behind and delve into the biology of how a lineage might shift from laying eggs to placental reproduction – a shift that has also occurred in lineages other than the one leading to placental mammals.