Jeffrey Tomkins is living proof that even PhD scientists can sometimes commit serious blunders. Tomkins is a geneticist and – more importantly – a creationist and he has published several “peer reviewed” papers in YEC journals such as the Answers Research Journal.
In his 2014 article “The Human GULO Pseudogene – Evidence for Evolutionary Discontinuity and Genetic Entropy” he argued that the Human GULO pseudogene (an inactivated gene that was once responsible for Vitamin C synthesis) fails to support macroevolution. Some of his claims have already been addressed elsewhere, but I want to focus on a curious mistake made by Tomkins, which seems to have gone unnoticed by most of his critics.
Macroevolutionary enigmas
In the paper, Tomkins asserted to have identified multiple evolutionary “anomalies” and “contradictions”. One of these supposed anomalies is the fact that teleosts (a group of ray-finned fishes) lack the GULO gene. From the article:
Of particular note is the growing data set showing that cartilaginous and non-teleost bony fish species are able to synthesize vitamin C while no known teleost (ray-finned) fish has this capability, which is associated with the complete absence of the GULO gene […].
Tomkins cites several papers that he believes support his claim. However, he seemingly ignored the work of Ocalewicz et al. (2010). Using Southern blot, Ocalewicz and his colleagues found a possible remnant of the GULO gene within the genome of the common carp (a teleost fish). They write:
[…] the Southern hybridization approach with the shark GULO cDNA as a probe revealed the GULO locus in the non-teleost species studied and in the common carp. The high similarity between the shark and common carp GULO locus suggest that remnants of the gene may still exist in some of the Teleostei fishes.
[my emphasis added]
To be fair, Tomkins is right when he says that teleosts are typically incapable of synthesizing ascorbic acid. But his conclusion that this is due to the “complete lack of GULO genes in all studied teleost fish genomes” seems to be unwarranted. Now we get to the crux of the matter: Why does Tomkins even think that the absence of the GULO gene in teleosts poses a macroevolutionary anomaly? In his paper, he raises the following question:
[…] how did these genes completely disappear during macroevolution in teleost fishes and then reappear in other metazoan lineages later on?
Another young earth creationist, John Mackay, has reworded Tomkins’ challenge thusly:
[…] evolutionists have to explain how the more primitive cartilaginous or non-bony fish (sharks and rays) acquired the vitamin C gene, only to lose it when they evolved into more advanced boned fish, whose land-dwelling descendants somehow regained it then yet again lost the ability due to a degenerate mutation.
However, as we are going to see, these creationist arguments are based on nothing more than fundamental misunderstandings concerning the evolution of tetrapods.
External relationships of Teleostei
Both Tomkins and Mackay seem to be convinced that evolutionary biologists promote the idea that tetrapods evolved from teleost fishes. This however is a misconception and it probably stems from the fact that Tomkins and Mackay are using the terms “teleosts” and “bony fishes” interchangeably. But teleosts only represent a subgroup of bony fishes and so, these two terms are not at all synonymous.
Bony fishes did indeed give rise to tetrapods, but those bony fishes were members of the clade Sarcopterygii (lobe-finned fish), not Actinopterygii (ray-finned fish, which includes Teleostei). As Ching et al. (2015) note:
Terrestrial vertebrates evolved in the early Devonian period (400 MYA) from lobe‐finned fishes (Sarcopterygii), which were once a numerous and diverse group of fish. Today, the lobe‐finned fishes are represented by only six species of lungfishes and two species of coelacanths. […] There is no debate that lungfishes or the coelacanths or both are more closely related to tetrapods than ray‐finned fishes […].
[my emphasis added]
And guess what… modern lobe-finned fishes (e.g. Protopterus annectens, the African lungfish) still have functional GULO genes! Therefore, the supposed “anomaly” immediately vanishes. To say it in the words of Ching et al.:
The presence of Gulo activity in kidneys of the Australian lungfish […] and the African lungfish […] probably demonstrates the path by which the ancestral fish gulo was passed on to amphibians 400 MYA.
Tomkins and Mackay could have known this, especially since both of them cite Drouin, Godin and Pagé (2011). Figure 2 of that paper makes it abundantly clear that amphibians did not evolve from teleosts. Instead, the GULO gene was lost only once in the common ancestor of teleost fishes and – contrary to Tomkins’ claims – never reappeared.
As can be plainly seen, there is nothing “anomalous” about the genetics of Vitamin C loss in teleost fishes. It seems that Tomkins made a grave mistake here, a mistake that could easily have been avoided. The fact that this blunder made it into the article anyway casts serious doubt on the reliability of creationist “peer review”.
References
- Ching G, Chew SF, Yuen K. (2015) Ascorbate Synthesis in Fishes: A Review. IUBMB Life, 67 (2): 69-76
- Drouin, G., Godin, J. R., and Pagé, B. (2011) The genetics of vitamin C loss in vertebrates. Curr. Genomics 12, 371– 378.
- Mackay J. (2014) VITAMIN C GENE? Humans share the same broken vitamin C gene as apes. Doesn’t this prove evolution?
- Ocalewicz K, Dabrowski K, Mambrini M. (2010) Evidence for the Possible Existence of a Remnant L-gulono-gamma-lactone Oxidase (GULO) Gene in a Teleost Genome. Folia Biol. 58(1-2):51-4
- Tomkins JP. (2014) The Human GULO Pseudogene—Evidence for Evolutionary Discontinuity and Genetic Entropy. ARJ, 7: 91-101
Teaching the consensus 