An Evangelical Geneticist’s Critique of Reasons to Believe’s Testable Creation Model, Pt. 2
In part one of this series, Dr. Venema examined how Reasons to Believe (RTB) represents comparative human-chimpanzee genomics in its “Testable Creation Model.” In this section, he continues his evaluation of the RTB model by examining how it handles pseudogene evidence for human evolution. The full paper with complete footnotes can be found here.
The RTB Model and Pseudogenes
Pseudogenes (literally, “false genes”) are the remnants of once-functional genes that persist in genomes after they lose function. Pseudogenes are often shared among species in a nested pattern that strongly supports common ancestry. Additionally, the human genome harbors pseudogene remnants of genes devoted to non-mammalian ways of life. For those unfamiliar with this line of evidence for evolution, Darrel Falk and I have recently written about pseudogenes in the human genome for a lay audience. Since shared pseudogenes are such clear indicators of common ancestry, RTB has also expended significant effort on discussing pseudogene data in their major works. As such, pseudogene evidence is a second opportunity to test the scientific reliability of the RTB model.
Understanding the difference between two specific classes of pseudogenes is important for evaluating the RTB literature: specifically, processed versus unitary pseudogenes. Processed pseudogenes are the remains of RNA copies of genes that have inserted themselves into chromosomes, whereas unitary pseudogenes are the remains of genes that have been inactivated due to mutation. In the case of processed pseudogenes, the original gene remains intact and functional.
One of the most compelling features of pseudogene evidence for common ancestry is that pseudogenes (of all kinds) form nested hierarchies. Consider an example phylogeny (evolutionary history, or family tree) for four modern species (A, B, C and D) given in the figure below.
Phylogenies can be assembled using genome sequence similarity (grouping more closely related organisms together) as well as through other measures, such as anatomy. A phylogeny assembled through these criteria (which agree and reinforce one another) can be used to predict what the distribution of various pseudogenes will be in the four modern species. For example, pseudogenes from the very distant past (and thus present in the common ancestor of the whole group) will appear in all modern species, with the same mutations. Pseudogenes shared by species A and C (e.g. the pseudogene form of “gene X” in the diagram) are best explained as having been present in their common ancestor. Since the common ancestor of A and C is also the common ancestor of species B, observing a shared pesudogene between A and C makes a precise prediction: if the species do share common ancestry and we have the phylogeny correct, species B should have the same pseudogene with the same mutation. The pseudogenes should be present in a nested hierarchy. Note too that mutations may happen in a lineage after its last known speciation event (e.g. “Gene Z” in species C). In this case, this pseudogene should be unique to that species: we should not find it in the other species in the phylogeny.
One example of a nested, hierarchical pattern of unitary pseudogenes in primates is that of olfactory receptor pseudogenes. An analysis of these pseudogenes in humans, chimpanzees, gorillas and orangutans produces a nested hierarchy that independently groups these species into a phylogeny identical to the one assembled from sequence homology data: humans share the most pseudogenes in common with chimpanzees, less pseudogenes in common with gorillas, and so on (see below):
Most importantly, the nested hierarchical pattern is not violated: for example, all the pseudogenes present in both gorillas and humans (and thus in the common ancestor of these species) are present in chimpanzees (since the common ancestor of humans and gorillas is also the common ancestor of chimpanzees). Not one of these pseudogenes is out of place. A second, equally powerful line of pseudogene evidence for common ancestry is the presence of pseudogenes that show adaptation to manners of life that do not make sense for the organism in question. Whereas humans do need (at least some) olfactory receptors, the human genome contains pseudogene remnants of genes that mammals do not need. One example that I have discussed previously is the vitellogenin pseudogene found in the human genome. Vitellogenin is a protein component of egg yolk, and as such is a functional gene in amniotic (egg-laying) organisms. Humans are of course placental mammals, yet we have the vitellogenin gene present in our genomes as a unitary pseudogene. The two functional genes flanking the human vitellogenin pseudogene are the same two genes flanking the functional vitellogenin gene in chickens. These data make perfect sense if humans are descended from egg-laying ancestors and share common ancestry with chickens. It is very difficult to rationalize this data from an antievolutionary perspective. Since the common ancestor of humans and chickens was a reptile, this indicates that the vitellogenin pseudogene should be present in all non-egg-laying mammals. Studies so far have found this unitary pseudogene in wide variety of additional species ranging from dogs to wallabies. As expected, egg-laying mammals such as the platypus retain a functional version of this gene.
Unitary pseudogenes present in nested hierarchies that independently group organisms into phylogenies assembled with other data are incredibly powerful evidence for common ancestry. Additionally, the fact that the genomes of multiple placental mammals (including humans) contain a unitary pseudogene clearly adapted for egg laying (in the precise genomic location predicted by common ancestry), is very challenging to explain from an antievolutionary perspective. Accordingly, any attempt to scientifically refute common ancestry must address these types of evidence in a convincing manner.
The most extensive discussion of pseudogene evidence for common ancestry in the RTB literature is found in WWA, where an entire chapter is devoted to the topic (pp. 226 – 243). While WWA does not specifically address the fact that pseudogenes are observed in nested hierarchies, it does at least mention that unitary pseudogenes with identical mutations are shared between primates, including humans and chimpanzees (pp. 228-230, 243). The more recent RTB books, however, make no mention of these data when discussing pseudogenes. The core of RTB’s attempt to refute pseudogene evidence in all three books is their claim that pseudogenes are functional sequences: “Non-coding DNA regions (including pseudogenes, LINEs, SINEs and endogenous retroviruses) aren’t really junk after all. These elements possess function.” (p. 235)
The evidence offered for this assertion are examples of pseudogenes and other “junk DNA” that have been shown to have function, specifically processed pseudogenes, SINEs and LINEs that have been implicated in gene regulation (pp. 235-243). This argument, however, is scientifically weak: rare examples of processed pseudogenes and repetitive DNA elements such as LINEs and SINEs that have retained or gained a function does not confer similar functionality on the many thousands of such sequences for which there is good evidence that they are not functional. Beyond this weakness is a more serious flaw: evidence for unitary pseudogene function is lacking. In WWA, RTB candidly admits that evidence for unitary pseudogene function is not to be found:
“What about the genetic material without a known function, such as the GLO unitary pseudogenes that humans and chimpanzees share? Currently the RTB model offers no explanation for this feature. The model does predict, however, that as with other classes of noncoding DNA, function will one day be discovered for these uniting pseudogenes.” (p. 243)
The later RTB books, however, do not distinguish between unitary pseudogenes and other pseudogene / repetitive DNA classes. The same examples of rare functional processed pseudogenes, LINEs, SINEs and endogenous retroviruses are given, but unitary pseudogenes are not mentioned at all in either CAS or MTT. Instead, the selected functional examples of non-unitary pseudogenes are used to imply that pseudogenes in general have been demonstrated to have function. This is misleading. Unitary pseudogenes remain highly problematic for RTB, and becoming vague on this point does not overcome the difficulty they pose for the RTB model.
In summary, discussions of pseudogene evidence in the RTB model are selective, misleading and simply ignore the strongest lines of evidence that pseudogenes provide for common ancestry. The RTB approach to pseudogenes also suggests that the differences between WWA and the two more recent books may be a pattern: RTB is able and willing to provide extensive detail when the data are inconclusive, but becomes vague and imprecise when data that challenge the model become available.
As we have seen, the RTB model of human origins with respect to common ancestry is seriously flawed. It misrepresents well-established science, fails to address the strongest relevant evidence against its position, and selectively presents data in an attempt to support a pre-determined position that humans and other apes do not share ancestry. As such this model is not a model that a believer can hold with scientific integrity. It may well be that RTB offers their model in good faith: if so, however, it demonstrates that they are not qualified to address these lines of evidence in a scientific manner.
While this series presents a careful analysis designed to substantiate my conclusions for a non-specialist audience, it should be noted that the scientific flaws in the RTB model are blatantly obvious to working scientists within the biological sciences. Moreover, scientists are likely to interpret these flaws as obfuscation or deliberate deception. As such, the packaging of such arguments with an overt Gospel message seriously compromises a Christian witness within this group and raises unnecessary barriers to faith. Within the community of believers, the extent to which one’s faith is supported by such arguments is also the extent to which one is rendered vulnerable to crisis should those arguments fail: “today’s reason to believe” sets one up for tomorrow’s “reason to disbelieve” should the evidence be examined.
Dennis Venema is Fellow of Biology for The BioLogos Foundation and associate professor of biology at Trinity Western University in Langley, British Columbia. His research is focused on the genetics of pattern formation and signalling.