Second verse, same as the first,
A whole lot louder, and a whole lot worse
Venema recently issued a second challenge, also published on the BioLogos Foundation website, to our model. Specifically, Venema focuses on pseudogenes which are often cited as evidence in favor of human evolution.
Evolutionary biologists consider pseudogenes dead, useless remains of once-functional genes. Presumably, severe mutations destroyed the cellular machinery’s capacity to “read” and process the information contained in these genes. Still, pseudogenes possess telltale signatures that allow molecular biologists to identify them as one-time genes.
There are three types of pseudogene: unitary, duplicated, and processed. Evolutionary biologists believe that unitary pseudogenes arise when functional genes experience a mutation and, as a consequence, lose function. Duplicated pseudogenes supposedly result when genes are duplicated, generating two or more copies. After the duplication event takes place, one of the copies experiences a mutation, rendering it nonfunctional. Processed pseudogenes, evolutionary biologists say, originate through a complex pathway that involves reverse transcription of messenger RNA (after it has undergone splicing and other biochemical processing), followed by integration of the resulting DNA into the genome.
The figure below is an artist’s depiction of how evolutionary biologists believe the three types of pseudogenes originate.
In his critique, Venema points out that when biologists compare the genomes of organisms they often find that the same pseudogenes appear in corresponding locations juxtaposed to the same genes. Evolutionary biologists make use of shared pseudogenes to construct evolutionary trees and, thus, take them as evidence for common descent. After all, why would an all-powerful, all-knowing, all-good Creator create the same nonfunctional, junk DNA sequences in seemingly related organisms? According to evolutionary biologists, the pattern observed for the distribution of pseudogenes makes sense if life-forms evolved from a common ancestor.
When evolutionary biologists present this argument, they make a number of assumptions, all of which appear to have questionable validity based on recent research results. For the pseudogene evidence to have potency: (1) pseudogenes must lack function; (2) their origin must be due to rare, random events; and (3) their juxtaposition to other genes must be arbitrary.
As it turns out, molecular geneticists have learned that a number of pseudogenes have function, including duplicated and processed pseudogenes. (I would refer interested readers to Who Was Adam? and The Cell’s Design for a discussion of a number of discoveries that ascribe function to pseudogenes. We also offer articles on our website that describe the discovery of functional utility for pseudogenes: here, here, and here.)
In his critique, Venema does acknowledge that research shows some pseudogenes are functional, but he dismisses this point by claiming that such pseudogenes are rare. This assertion, however, is not supported by the latest work. In fact, two of the articles on our website discuss papers (published in peer-reviewed journals) that emphasize how widespread pseudogene function actually is.
Researchers have discovered that the genesis of certain classes of junk DNA is not rare and random, but occurs frequently and in a repeatable manner. (Go here and here to read recent articles.) Scientists have also learned that the order of genes along a chromosome plays a functional role as well.
In other words, the latest discoveries raise questions about the validity of the assumptions necessary to conclude that shared pseudogene sequences evince biological evolution. As part of his criticism of RTB’s human origins model, Venema claims that we selectively ignore advances that go against our model and fail to interact appropriately with the scientific literature. Yet, most evolutionary biologists, including Venema, fail to acknowledge the discoveries mentioned here and their implications for the evolutionary paradigm. The latest insights into junk DNA, including pseudogenes, undercut the best evidence for human evolution.
But as Venema points out in his critique, researchers have yet to discover function for unitary pseudogenes. He posits that this creates devastating problems for RTB’s human origins model. But is that the case? Can the RTB model make sense of shared seemingly nonfunctional junk DNA sequences? I will address this question next week.