Pseudogene Decoy Reveals Hidden Evidence for Design
Do you remember the movie Dave?
In this romantic comedy, the president of the United States suffers a stroke while having an extramarital affair and is in a coma. The chief of staff cooks up a scheme where Dave (Kevin Kline), an uncanny look-alike, is employed to impersonate the president.
Though the movie’s plot is a bit far-fetched, the premise has one foot in reality. Throughout history, heads of state, politicians, and military leaders have used political decoys to distract attention away from them and afford them some protection.
Decoys also play a role in biochemical systems. Recently, researchers discovered that the products of pseudogenes may function as biomolecular decoys, protecting the “real” gene products from breakdown.1 As it turns out, this new insight has important implications for the biology of cancer. It also provides potent evidence for the intelligent design of biochemical systems.
Evolutionary biologists consider pseudogenes the dead, useless remains of once functional genes. According to this view, severe mutations destroyed the capacity of the cell’s machinery to read and process the information contained in these genes. Still, pseudogenes possess the tell-tale signatures that allow molecular biologists to recognize them as genes, albeit nonfunctional ones.
Molecular biologists recognize several classes of pseudogenes. Duplicated pseudogenes are the largest class. Scientists posit that these DNA segments arose when gene(s) underwent duplication in the genome, after which the duplicated copies experienced severe mutations, rendering them unrecognizable as a functional gene by the cell’s machinery. Loss of duplicated gene function has little, if any, effect on an organism’s fitness since an intact copy of the functional gene still exists.
Pseudogenes and the Case for Biological Evolution
Evolutionary biologists traditionally have viewed pseudognes as “junk” DNA and consider them among the most compelling pieces of evidence for biological evolution. Identical (or nearly identical) segments of junk DNA often occur in a wide range of related organisms and reside in corresponding locations in these genomes. For evolutionists, this occurrence clearly indicates that these organisms shared a common ancestor. They believe these junk DNA segments arose prior to the time when the organisms diverged from their shared evolutionary predecessor.
Skeptics often ask, “Why would a Creator purposely introduce nonfunctional, junk DNA at the exact same location in the genomes of different, but seemingly related, organisms?”
However, as I’ve pointed out before, researchers are beginning to recognize that pseudogenes are not purposeless junk. (Go here, and here to read a couple of articles about the biological roles of pseudogenes.)
Adding to these earlier studies is new work indicating that pseudogenes control gene expression by acting as decoys to protect gene products from destruction.
The researchers who made this discovery focused on PTEN, a gene that suppresses tumors. When this gene is functionally impaired it leads to the onset of several different types of cancer. Furthermore, the researchers learned that cancer also results if mutations occur in PTEN’s corresponding pseudogene, PTENP1. This finding means that the PTENP1 pseudogene must be functional.
Researchers discovered that expression of PTEN can be down regulated by small RNA molecules (miRNA). The tiny molecules bind to messenger RNA produced from PTEN. The miRNA then directs the breakdown of the messenger RNA, and prevents the PTEN protein from carrying out its cellular role. Left unchecked, the miRNA molecules would direct the breakdown of most of the PTEN messanger RNA, thus suppressing the activity of PTEN gene products and leading to the onset of cancer.
However, the similarity between PTENP1 and PTEN allow the PTENP1 messenger RNA to also bind miRNA molecules. This means PTENP1’s messenger RNA breaks down instead of PTEN’s. In other words, the gene product of the PTENP1 pseudogene operates as a decoy, which allows for the appropriate levels of PTEN messenger RNAs production.
Such decoy mechanisms appear to be widespread among genes. The researchers also uncovered similar relationships for a number of gene/pseudogene pairs, including the KRAS gene and KRAS1P pseudogene, which are also implicated in the onset of certain cancers.
This new insight stands as a landmark discovery. It promises to prove an important advance in understanding the biology of cancer and in developing a fundamental understanding of how the genome is structured and how it operates.
Pseudogenes and the Case for Intelligent Design
The importance of functional pseudogenes (as well as other classes of junk DNA) undermines the best argument for evolution. If functional, then junk DNA sequences in genomes do make sense from a creation standpoint. So, too, does the corresponding location of junk DNA sequences in the genomes of related organisms. The common location likely reflects functional significance and could be understood as reflecting shared design instead of shared ancestry. In the case of pseudogenes, similarity to the “real” gene could be understood to reflect its functional role, not necessarily its evolutionary origin.
It looks as if pseudogenes are functional elements in the genome that have been merely impersonating junk DNA all along.
1. Laura Poliseno et al., “A Coding-Independent Function of Gene and Pseudogene mRNAs Regulates Tumour Biology,” Nature 465 (2010): 1033–40.