Shared mistakes as evidence of common ancestry

One piece of evidence for common ancestry that I don’t see brought up as much is the genetic ‘mistakes’ shared within various clades. Creationists sometimes try, and fail, to address specific shared mistakes (such as the GULO pseudogene), but I don’t think many creationists are aware of the extent of this evidence and how well it supports common ancestry. Let’s go over just a few examples.

Bird evolution

Although the fossil record is replete with examples of toothed avialans (e.g., Archaeopteryx, Confuciusornis, Ichthyornis), no extant birds have true teeth. According to creationists, toothy birds are part of different ‘kinds’ than modern birds (which also fall into several different ‘kinds’), so they share no common ancestry (Garner, Wood, and Ross 2013; Brophy 2021). Under this hypothesis, there should be no evidence that organisms in the lineage of modern birds had teeth. In contrast, the common ancestry hypothesis predicts that evidence of teeth should be found in the genomes of modern birds.

The latter prediction is vindicated by genetics. As demonstrated by Harris et al. (2006), modern chickens (Gallus gallus domesticus) possess the entire genetic repertoire with which to build teeth. Chicken embryos that carry the talpid2 mutation begin to develop teeth, and not just any teeth, crocodilian teeth, also vindicating the conclusion from phylogenetics that birds are most closely related to crocodilians.

The evidence doesn’t just stop here. Not just chickens, but all modern birds, possess the genes needed to build teeth, and they all share the same eleven inactivating mutations in these genes (Meredith et al. 2014). Within modern birds (Neornithes), the different clades also share mutations in these now pseudogenized tooth genes, forming a nested hierarchy as predicted by common ancestry.


Table 1 of Meredith et al. (2014). There are eleven inactivating mutations in the tooth formation genes of all birds (Neornithes), and many others shared by all members of Palaeognathae, Neognathae, Galloanserae, and Neoaves respectively.

This evidence is conclusive against separate ancestry. Creationists who wish to dispute this and claim that different ‘kinds’ of birds were specially created by God are forced to jump to one of two conclusions:

  1. God created each ‘kind’ of bird with crocodilian teeth, and the genes involved in tooth development were subsequently lost in every single lineage, following the exact same eleven inactivating mutations.

  2. God created each ‘kind’ of bird with these pseudogenes in order to deceive us into thinking that all birds share common ancestry and used to have teeth.

Needless to say, the first option is completely implausible, and the second option is incompatible with the Bible (see Heb. 6:18 – “it is impossible for God to lie”) and would lead to radical epistemic skepticism (we can’t trust our senses if they were created by a malevolent or duplicitous deity). Creationists could also claim that these pseudogenes somehow have a necessary function, but… good luck with proving that.

Whale evolution

This one is especially interesting to me, because there are just so many pseudogenes involved in the evolution of whales. For example, whales don’t have hind limbs, but they do possess the entire genetic repertoire needed to build hind limbs (Onbe et al. 2007; Liang et al. 2022). As demonstrated by Liang et al. (2022), cetaceans all share four inactivating deletion mutations in the HLEA regulator needed to build hind limbs.


Figure 1 of Liang et al. (2022). Four inactivating deletions in the HLEA enhancer cause lack of expression of Tlx4, directly resulting in the lack of hindlimbs in cetaceans.

Likewise, the thick rubbery skin of whales is the result of gene loss. Many hair keratin genes and sebum-producing genes have been pseudogenized or entirely deleted in whales (Nery et al. 2014; Lopes-Marquez et al. 2019). Cetaceans have also lost the GSDMA, DSG4, DSC1, and TGM5, the loss of which in mice is associated with thicker epidermis, lack of hair, and increased shedding rate, all of which are characteristics of cetacean skin (Sharma et al. 2018). Other genes associated with epidermal differentiation have been lost in the cetacean lineage (Strasser et al. 2004; Holthaus et al. 2021). Whales’ eyes are adapted to water thanks to the loss of OPN1SW and OPN1LW – although there are different inactivating mutations in this gene in odontocetes and mysticetes (McGowen et al. 2014).

This is all bad enough for creationists, but there’s more. Huelsmann et al. (2019) have documented many inactivating mutations shared by all cetaceans. In terrestrial mammals, the blood coagulation system can result in thrombosis during deep diving; in cetaceans, the F12 and KLKB1 genes have been inactivated, helping them to avoid this problem. The POLM gene has also been lost, making the repair of DNA damage (caused by deep diving) more efficient. The loss of lung-expressed genes MAP3K19 and SEC14L3 aids in the collapse/reinflation of the cetacean lung during deep dives.


Adapted from Figs. 1, 2, and 3 of Huelsmann et al. (2019). (A, B) Inactivating mutations in the F12 and KLKB1 genes, shared by all cetaceans, help to prevent thrombosis during deep diving. (C, D) Inactivating mutations in the POLM gene, shared by all cetaceans, result in a more effective DNA repair mechanism adapted for deep diving. (E, F) Inactivating mutations in the MAP3K19 and SLC6A18 genes, shared by all cetaceans, result in the unique cetacean lung adapted for deep diving.

Saliva secretion, although useful in terrestrial mammals, is completely ineffective underwater; as a result, the gene SLC4A9 – the loss of which is associated with decreased saliva secretion in mice – has been inactivated in cetaceans. All of the genes involved in melatonin synthesis have also been pseudogenized in cetaceans, causing decreased time asleep and loss of the circadian rhythm, a necessary precondition for unihemispheric sleep.


Adapted from Figs. 4 and 5 of Huelsmann et al. (2019). (A, B) Inactivating mutations in the SLC4A9 gene, shared by all cetaceans, result in decreased saliva secretion. (C, D) Inactivating mutations in the AANAT, ASMT, MTNR1A, and MTNR1B genes, shared by all cetaceans, result in lack of melatonin synthesis, a necessary precondition for unihemispheric sleep.

Again, to explain this, creationists must choose one of two options: either God is malevolent and placed these genes fully functional – which would be very harmful to underwater creatures – in the genomes of cetaceans, and they were subsequently lost to the exact same inactivating mutations in all cetaceans, or he is deceptive and placed these as pseudogenes in cetacean genomes. Again, neither option is consistent with the God of the Bible, and if God is malevolent or deceptive, that means we can’t trust our senses at all.

Mammal evolution

According to universal common ancestry, mammals evolved from a more basal tetrapod ancestor, and we should expect to find evidence of this in the genome. According to special creation and separate ancestry, different mammal ‘kinds’ were created uniquely, and their genomes should reflect this. Which hypothesis is confirmed by the data? Unsurprisingly, the common ancestry hypothesis is vindicated, as all mammals share remnants of the vitellogenin gene, used to produce the egg yolk in egg-laying animals (Brawand et al. 2008).


Adapted from Figures 3 and 4 of Evograd (2019). (A) The vit1 pseudogene in humans (and other mammals) is in the exact same location in the genome as the vit1 gene in chickens. (B) There are five peaks of conserved synteny in the mammal vit1 pseudogene, spanning 7.3% of the vit1 gene of chickens (~3100 bp).

Not only is this pseudogene found in all mammals, but the same five peaks of conserved sequence (about 3100 base pairs in length) are shared by all mammals, as shown by the mVISTA analysis in the figure above. Thus, creationists must explain why remnants of this gene can be found in all mammals if mammals didn’t have egg-laying ancestors, and also why the same sequences are preserved in this (nonfunctional) pseudogene by all mammals.

YEC geneticist Jeffrey Tomkins (2015) attempted to prove the claim that this pseudogene actually has a function in mammals, but his analysis was very flawed, as shown by our very own Evograd (2019). Furthermore, even with his flawed analysis, only 150 base pairs of the ~3100bp conserved sequences can be explained. Thus, creationists are left with the same two unsatisfactory options as in the above two examples – either all mammals (including humans) were created by God with the ability to lay eggs, and we all lost that ability independently in the exact same way, or God created this pseudogene to deceive us.

Ape evolution

Here’s another example of a ‘shared mistake’ in the genomes of all apes. I just became aware of this thanks to @GutsickGibbon’s new YouTube video. All apes (Hominoidea), including humans, lack tails. According to common ancestry, apes share common ancestry with the Old World monkeys (Cercopithidae) which have tails, so there should be evidence of the loss of tails in all ape genomes. According to separate ancestry, apes form separate ‘kinds’ from tailed monkeys, so there should be no evidence that apes ever had tails.

Once again, the prediction of common ancestry is confirmed by the data. Within the TBXT gene of all ape genomes, which helps establish the vertebral column during development, a transposable element (AluY) has established itself in the sixth intron. As a result, the sixth exon is (mistakenly) excised by the spliceosome (see the figure below). Until recently, we didn’t know for sure whether this resulted in tail loss, but a study by Xia et al. (2024) demonstrated that inducing the same mutation in mice also resulted in tail loss.


Figure 1 of Xia et al. (2024). The (b) insertion of an AluY element into the TBXT gene of apes leads to the (c) excision of Exon 6 of the same gene, which is now known to result in tail loss.

To creationists: if apes don’t share common ancestry, then why do we all have the same inactivating mutation in the TBXT gene? ‘Common design’ can’t be the answer, because it would be more efficient to simply remove the sixth exon altogether, rather than inserting a transposable element that leads to an unintended splicing of the sixth exon. In fact, this mutation is known to be the cause of several rare disorders (including spina bifida), meaning that God would have to be malevolent to specially create us this way. Either God created all apes (including humans) with tails, and each ape kind subsequently lost them to the same mutation, or God is deceiving us by creating us with this transposable element in our genomes. Neither answer is satisfactory.

Human evolution

There are many pseudogenes shared by humans and other primates – after all, our genome contains about ~20,000 pseudogenes (Torrents et al. 2003), and we share 95-96% of our genome with chimpanzees. Here, though, I want to focus on one pseudogene, the GULO pseudogene, because this one has actually been disputed by some creationists. The GULO gene encodes an enzyme that produces vitamin C, but this gene is nonfunctional in many primates (Haplorrhini) including humans, along with a handful of other mammals. This is why humans can get scurvy if we don’t have enough vitamin C in our diet.

All members of Haplorrhini (including humans) share several inactivating mutations in the GULO pseudogene (see the figure below).


Figure 4 from Lachapelle and Drouin (2011). (A) Exons 2 and 3 have been lost in the human, chimp, and macaque lineages; galago represents the ancestral state with a working GULO gene. (B) The deleted region highlighted, showing the many shared mutations between human, chimp, and macaque, compared to the working GULO gene in the galago.

This should be very troubling for creationists, who claim that primates – especially humans – fall into different ‘kinds’ that share no common ancestry. For this reason, YEC geneticist Tomkins (2014) claims that this gene was originally created functional in each primate ‘kind’ and the five lost exons (1, 2, 5, 7, and 10) were lost independently in each lineage!

Setting aside the bad BLAST analysis that he does elsewhere in the paper, this claim is astounding to me. Why were the same exons lost in each lineage? And what about the identical substitutions, insertions, and deletions within the pseudogene found in human, chimp, and macaque (see the figure above)? Basically, Tomkins takes the first option of the two available options for creationists (independent losses or deceptive deity), which is so implausible as to basically be impossible.

Conclusion

The many shared ‘mistakes’ within the bird, whale, mammal, and primate lineages demonstrate virtually beyond a doubt that common ancestry holds true in these lineages. I’d love to see if any of our resident creationists (@colewd? @thoughtful?) would take a stab at explaining it, because I don’t think there is an explanation that fits their model.

Edit: Here are even more examples of shared pseudogenes from @evograd’s website.

It’s really such a shame that creationists are forced to ignore/explain away these facts, because they’re so interesting! In the case of whale evolution, it’s really cool to see that many of the unique features of cetaceans are the result of gene losses. As a theist, it amazes me how creative this process (evolution) that God used to create the diversity of life on earth is. Yet creationists are too focused on proving the minutia of the Bible from a literalistic standpoint to stop and think about the grandeur of it all.

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I can confidently assume that you meant to say something else.

Otherwise, fun post.

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Also interesting how much evolution of whales’ novel aquatic phenotypes are actually explained by geneloss. Proving you can have many gains of novel physiological adaptations through loss of molecular function.

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Yep — edited that out as soon as I re-read it.

Thanks!

I wouldn’t be surprised if creationists go the route of Kurt Wise and start claiming that all whales evolved from a pair of pakicetids on Noah’s ark in the last 4500 years. Given the many gene losses, they’ll even try to chalk it all up to genetic entropy. But that won’t happen until the old guard of creationists (Ken Ham etc.) dies out, now that they’ve denounced Kurt Wise as a “young earth evolutionist.”

The Torah does not make clear whether Pakicetids were clean or unclean animals. But it is my considered opinion that they would have been classified as clean—and thereby seven pairs of each Pakicetid “kind” would have boarded the ark. (Genesis 7:2) That probably explains the alternate version of a very old and familiar nursery rhyme and song:

Pick a pack of Pakicetids,
all valid Pakicetidae.
Seven pairs are boarding
while the rest are doomed to die.

When the flood was over,
those aboard began to spring,
stampeding through that one ark door,
and eventually fossil-ing.

— from Ken Ham’s “The Little Golden Book of Noah’s Quatrains”

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Unlikely, since they clove the hoof but didn’t chew the cud.

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Indeed. It was a setup for a joke. (But good catch.)

Some of my favorite stories told by “The Far Side” cartoonist Gary Larson are those describing the mail he would get objecting to various “errors” in his cartoonish depictions of animals. One letter said something like, “You should know that the ‘dinosaur meeting’ cartoon doesn’t make sense because pterosaurs were NOT dinosaurs.” Gary Larson’s reply to him went something like this: “Yeah. And dogs don’t talk and bears don’t drive cars through the woods.”

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Hi Andrew
Thanks for the thoughtful sharing of the papers you presented. The evidence based on shared “non functional sequences” is certainly evidence for common descent among the animals you included. This is the evidence that Mike Behe quotes for his acceptance of common descent.

What I personally don’t find compelling given the evidence of chromosome and gene differences is the assumption that these segments lack function or were not purposely disabled sequences. I also don’t think predicting the mind of God is an easy task. There are many more reasons beyond what we can imagine why God built animals in the way he did.

I still believe that multiple origins or multiple trees should be a model that is considered.

You must show that all these pseudogenes have function. You can’t just claim “function!” and run away from the implications. Are any of these sequences expressed at a higher rate than the background rate? If you knock them out does it result in any phenotypic change? Why doesn’t the ratio of synonymous:nonsynonymous changes indicate that the sequences are unconstrained? If they are unconstrained, then how does ‘common design’ or ‘common function’ explain the shared inactivating mutations?

These are all questions you need to be asking yourself if you really want to show that these pseudogenes are functional. And you need to prepare for the possibility that they are nonfunctional (as they indeed are). Tomkins tried to show that just one of these pseudogenes (vitellogenin) was functional and he utterly failed.

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Ape evolution

Here’s another example of a ‘shared mistake’ in the genomes of all apes. I just became aware of this thanks to @GutsickGibbon’s new YouTube video. All apes (Hominoidea), including humans, lack tails. According to common ancestry, apes share common ancestry with the Old World monkeys (Cercopithidae) which have tails, so there should be evidence of the loss of tails in all ape genomes. According to separate ancestry, apes form separate ‘kinds’ from tailed monkeys, so there should be no evidence that apes ever had tails.

Once again, the prediction of common ancestry is confirmed by the data. Within the TBXT gene of all ape genomes, which helps establish the vertebral column during development, a transposable element (AluY) has established itself in the sixth intron. As a result, the sixth exon is (mistakenly) excised by the spliceosome (see the figure below). Until recently, we didn’t know for sure whether this resulted in tail loss, but a study by Xia et al. (2024) demonstrated that inducing the same mutation in mice also resulted in tail loss.


Figure 1 of Xia et al. (2024). The (b) insertion of an AluY element into the TBXT gene of apes leads to the (c) excision of Exon 6 of the same gene, which is now known to result in tail loss.

To creationists: if apes don’t share common ancestry, then why do we all have the same inactivating mutation in the TBXT gene? ‘Common design’ can’t be the answer, because it would be more efficient to simply remove the sixth exon altogether, rather than inserting a transposable element that leads to an unintended splicing of the sixth exon. In fact, Xia et al. provide evidence that this mutation may be the cause of the rare condition spina bifida, meaning it is detrimental (God would have to be malevolent to specially create us this way). Either God created all apes (including humans) with tails, and each ape kind subsequently lost them to the same mutation, or God is deceiving us by creating us with this transposable element in our genomes. Neither answer is satisfactory.

Edit: Added this to the main post.

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You have to know by now that Bill won’t do the work and won’t engage with your argument. He’s made up his mind, come up with an excuse to interpret the data as supporting separate creation, and that’s enough for him.

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Hi Andrew
I have not claimed function or type of function. You have claimed non function. I don’t find this evidence is compelling one way or another at this point. If we could show all or most are not functional then that would be interesting. If we could demonstrate that this was due to random change that became fixed in the population that would also be interesting. This would indicate that intent was not involved in all the changes.

What we are observing is different genes and chromosome types in most these animals for which we currently have no detailed natural explanation.

If Tomkins failed to demonstrate function that is not surprising as this discussion is in the first inning. To the best of my knowledge no one has been able to show reproductive connection between different species with different gene and chromosome patterns without assuming UCD,

That is not very satisfying, because we know how these segments are supposed to function. These are not random sequences with unknown purpose. Rather, they are recognizable sequences which have functions, but these have been lost due to selection, whether relaxed or active.

The sensible conclusion is that there is history there, where in a prior time and context these genes served a role which is no longer in play. They had a demonstrable purpose, but one which applies to to a very real past, and such sequences are extremely valuable for reconstructing that path. That is quite different from assuming lack of function.

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Did anyone else notice the simultaneous acceptance of evidence for common descent of all mammals and consideration of multiple origins for a subset of them?

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Listen to @RonSewell. We know these pseudogenes are non-functional because we know their original function, and we can see that they don’t do that anymore. Plus, we can determine their lack of function based on the lack of expression and ratio of synonymous to nonsynonymous mutations. That’s how pseudogenes are identified in the first place. The ball’s in your court to prove that a sequence can exhibit all the signs of a pseudogene and still be functional.

Tomkins didn’t just fail, he lied about there being any signal of expression or any sign of function at all. The discussion is not in the “first inning,” these sequences’ lack of function has already been demonstrated, you need to show that this is somehow wrong.

That’s kind of what the above post is doing. Not to mention the many other posts on this forum with conclusive evidence of common ancestry, that you have conveniently forgotten. I don’t know what “differing gene and chromosome patterns” has to do with anything; you keep showing a Venn diagram, but it does not mean what you think it means, and even if it did, that would be evidence against the mechanism of unguided evolution, not against common ancestry itself.

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I took @colewd to mean “multiple origins or multiple trees” was in general a model to be considered. In contrast to the general YEC position that there are lots of “kinds”, which would require very little common decent, my understanding is that @colewd is comfortable with common descent but is skeptical of it being truly universal (or at least that the jury is still out).

He is generally unwilling to commit to any clear position, but he refuses to believe that any two species that have 1) any difference in gene content, 2) any difference in chromosome structure, including but not limited to different counts, or 3) pairwise genetic distance greater than some small number, perhaps around 0.5% are related by descent. This would mean that a “kind” is in most cases a single species. But of course he hasn’t considered the implications so may not understand his position.

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Hi Jordan
Your assessment is correct. Common descent is a viable hypothesis IMO however universal common descent is not as there is too much evidence against it.

When universal common descent is taken as unassailable dogma all discussion of different starting points stops. This begins with the eukaryotic cell and prokaryotic cell which are very different yet assumed to share ancestry.

One of the current evidence for common descent is the sequence similarities that assume that random change disabling a functioning gene is the cause of the observed sequence.

I agree that if you can establish these differences are from random change then this is evidence for common descent between the species.

This evidence however needs to be weighed against the differences in gene and chromosome arrangements between animals and evidence of how reproductive and other natural mechanisms could account for these differences.

The idea of God guided common descent being a solution for explaining the differences in animals genetics is only valid if this is considered by scientists using the theory.

You might as well just write ‘I don’t know …’

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