Vitellogenin and Common Ancestry: Reading Tomkins

| By on Letters to the Duchess

This post is the third in this series. The first is here. In this post, we examine the fate of vitellogenin genes in marsupials, and introduce how a recent young-earth creationist paper attempts to refute the evidence.

When I was a young person growing up in northern British Columbia, one area of my hometown had a significant number of houses that were nearly identical to one another. These houses were prefabricated and erected at the same time – spanning about two blocks. As it happened, I knew two families that lived in this area, and so spent time in both of their houses. Once you knew your way around one house, you knew your way around the other. Despite small differences like color and décor, the two houses were the same: the same layout, with the same rooms.

Over time, the houses in this area became more distinct from each other – some have had additions put on, others have had rooms remodelled (and I’m certain this process has continued to this day, though I haven’t been back to my hometown for many years). Despite the changes, these houses remain recognizable as coming from the same pattern – and examining a number of houses for their common features shows what that original pattern was.

In the last post in this series, we examined the evidence for shared synteny between the human and chicken genomes for the regions with functional vitellogenin (VIT) genes in chickens. (Recall that shared synteny is merely the technical term for two or more genes in the same spatial pattern - i.e. order along a chromosome -  in two or more organisms). What we saw is that there is good evidence that the regions containing VIT pseudogene fragments in the human genome once shared common ancestral sequences with the VIT regions in chickens: the regions have the same sequences in the same overall pattern, even though changes have occurred since these sequences went their separate ways:


Figure 1. Shared synteny between humans and chickens spanning the regions with functional chicken  VIT genes. Black bars between the two chromosomes indicate sequence matches. This figure is based on data from Brawand et al., 2008.


In one sense, this is like looking at two houses in that neighbourhood in my hometown. Seeing the same features in the same pattern indicates that these sequences were inherited from a common ancestral population – just like seeing the same structures in those houses indicated they were part of the original construction.

But, you might ask – what about the other houses?

Evolutionarily speaking, the observed shared synteny for the VIT regions in humans and chickens makes a prediction about what we should find in other mammals. Since the last common ancestral population of humans and chickens lived prior to the evolution of all mammals, we would expect to (at least potentially) find these regions in any other mammal we care to sequence – with the understanding that these sequences might be missing if they have been lost in a particular lineage. To return to the house analogy, we would expect shared features unless renovations in any particular house obscured them.  

The researchers thus looked for VIT genes in a diverse number of mammals, and, not surprisingly, found them in the same arrangement as seen in chickens and humans. One example comes from a marsupial mammal – the opossum. Just like for humans, the opossum VIT genes are riddled with mutations that prevent them from being translated into proteins. Despite those mutations, however, enough VIT gene remnants and their non-gene flanking sequences remain in opossums to easily identify them – nested between the same functional genes we see in humans and chickens. In fact, in opossums, more of the VIT2 and VIT3 sequences remain than in the human genome, and more of the DNA flanking VIT1 remains the same:


Figure 2. Shared synteny between opossums and chickens spanning the regions with functional chicken VIT genes. Black bars between the two chromosomes indicate sequence matches. This figure is based on data from Brawand et al., 2008.


These findings, then, match what common ancestry predicts if indeed humans, chickens, and opossums share a common ancestral population deep in the past. Opossums, since they do not lay eggs, do not require VIT genes any more than placental mammals like humans do. Nonetheless, they too have remnants of these genes in the exact places in their genomes that common ancestry would predict. Moreover, the researchers found that several other placental and marsupial mammals also have VIT pseudogenes. As you might expect, however, egg-laying mammals (such as the platypus) retain a functional VIT gene that they use to perform bulk yolk transfer to their embryos.

In summary, what we see is a broad pattern of evidence that supports the hypothesis that placental and marsupial mammals share common ancestral populations with egg-laying mammals, and more distantly, other egg-laying vertebrates such as birds. This hypothesis was originally proposed based on shared anatomy and physiology, but has now been tested down to the molecular level – and has passed with flying colors.

Reading Tomkins

With this context in mind, we are now ready to evaluate how a recent paper, written by a young-earth creationist and published by Answers in Genesis, attempts to rebut this evidence. As we saw in the first post in this series, Tomkins claims to have “debunked” this example – and shown it not to be evidence for evolution.

How Tomkins claims to achieve this in his paper is key: he focuses only on one fragment of one of the VIT pseudogenes in the human genome. This fragment is the largest continuous fragment of the human VIT1 sequence at about 150 nucleotides long. Tomkins describes it in a blog post as follows:

The main piece of evidence for the vtg pseudogene is the presence of a 150-base human DNA sequence that shares a low level of similarity (62%) to a tiny portion of the chicken vitellogenin (vtg1) gene. However, the chicken vtg1 gene is actually quite large at 42,637 bases long, so a 150-base fragment of 62% similarity represents less than 0.4% of the original gene if the evolutionary story were true!

In the paper itself, Tomkins claims that this fragment is the extent of the VIT1 pseudogene in humans: 

The sequence identified by Brawand, Wahli, and Kaessmann (2008) as being a vtg pseudogene is only 150 bases long…

Note well: this is the only sequence that Tomkins will address in his paper (!): not the other VIT1 sequence remnants surrounding this fragment; not the shared non-gene sequences that flank VIT1 in humans and chickens; nor even a mention of the VIT2 or VIT3 regions with their pseudogene fragments, nor the flanking DNA also found there. Similarly, the finding that these regions are shared with a wide array of other mammals is not mentioned. Tomkins has neatly bypassed the bulk of the evidence with this approach by removing the one fragment he discusses from its context, and ignoring the VIT2 / VIT3 region altogether.  

The true “main evidence” for the remains of VIT genes in the human genome is as we have discussed: the overall match of sequences between placental / marsupial mammals and egg-laying organisms over large spans of DNA, including flanking regions. This is the evidence that needs to be addressed – and Tomkins does not even mention it, let alone address it. It is also highly unlikely that his audience – since Tomkins is writing not for biologists but rather for laypeople who follow young-earth creationism – will be able to see this problem in Tomkins’ approach. Moreover, since Tomkins tells them that this fragment is the extent of the VIT1 pseudogene, they would have to read the original paper by Brawand and colleagues to notice this is incorrect.

In the next post in this series, we’ll see that even Tomkins’ treatment of this small VIT1 fragment has several problems.




Venema, Dennis. "Vitellogenin and Common Ancestry: Reading Tomkins" N.p., 11 Mar. 2016. Web. 26 February 2017.


Venema, D. (2016, March 11). Vitellogenin and Common Ancestry: Reading Tomkins
Retrieved February 26, 2017, from

About the Author

Dennis Venema

Dennis Venema is professor of biology at Trinity Western University in Langley, British Columbia and Fellow of Biology for BioLogos. He holds a B.Sc. (with Honors) from the University of British Columbia (1996), and received his Ph.D. from the University of British Columbia in 2003. His research is focused on the genetics of pattern formation and signaling using the common fruit fly Drosophila melanogaster as a model organism. Dennis is a gifted thinker and writer on matters of science and faith, but also an award-winning biology teacher—he won the 2008 College Biology Teaching Award from the National Association of Biology Teachers. He and his family enjoy numerous outdoor activities that the Canadian Pacific coast region has to offer. 

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