Long Terminal Repeats Function as Promoters for the NAIP Gene in Mammals
Both Christians and skeptics alike expect superior designs to exist throughout nature if, indeed, the all-powerful, all-knowing Creator described in the Bible made the universe and all that’s in it. For evolutionists, any example of an imperfection in nature strikes against biblical creation. For this reason many evolutionary biologists regard “junk” DNA as one of the most potent pieces of evidence for biological evolution.
According to this view, junk DNA results when undirected biochemical processes and random chemical and physical events transform a functional DNA segment into a useless, molecular artifact. This “junk” piece of DNA remains part of an organism’s genome solely because of its attachment to functional DNA. In this way, the junk DNA persists from generation to generation.
Evolutionists also highlight the fact that in many instances identical (or nearly identical) segments of junk DNA appear in a wide range of related organisms. Frequently the identical junk DNA segments reside in corresponding locations in these genomes. For evolutionists, this clearly indicates that these organisms shared a common ancestor. Accordingly, the junk DNA segment arose prior to the time that the organisms diverged from their shared evolutionary ancestor. Evolutionists ask, “Why would a Creator purposely introduce nonfunctional, junk DNA at the exact location in the genomes of different, but seemingly related, organisms”?
Recent studies on junk DNA provide a response to this question—one that evolutionists find surprising, yet hard to deny. Junk DNA possesses function. (For a detailed discussion of some of these discoveries see Who Was Adam?)
One such discovery was reported recently in the journal Plos Genetics by a team of scientists from the University of British Columbia (UBC). These researchers studied the structure of the promoter sequence for the gene that encodes the neuronal apoptosis inhibitory protein (NAIP) in humans, mice, and rats.
Promoters are part of a gene’s regulatory domain. Gene structure is complex, broadly consisting of two regions: the protein-coding region and the regulatory region. The protein coding region contains the information that the cell’s biochemical machinery needs to produce the protein encoded by that gene. The regulatory region controls the expression of the gene and, hence, the production of the protein. In effect, the regulatory region operates as a combined “on/off switch” and “volume control knob” that controls or regulates gene expression.
Promoters are one of the two key domains within the regulatory region of a gene. The promoter serves as the binding site for a massive protein complex called RNA polymerase. This enzyme initiates gene expression by producing a messenger RNA molecule, which contains a copy of the information found in the protein-coding region of the gene. The messenger RNA molecule will eventually make its way to a subcellular particle, called a ribosome. It’s here that the messenger RNA directs protein production. The strength of RNA polymerase binding at the promoter controls the amount of messenger RNA produced, and hence the amount of protein generated at the ribosome. In this sense, the promoter functions as a volume control knob of sorts.
The research team from UBC discovered that promoter sequences for the NAIP gene in humans, mice, and rats belong to a class of junk DNA called long terminal repeats (LTRs). In other words, it appears that for the NAIP gene LTRs regulate its expression. LTRs function as promoters. This work follows on the heels of other studies (“Transposable Elements in Mammals Promote Regulatory Variation and Diversification of Genes With Specialized Functions”; “Origin of a Substantial Fraction of Human Regulatory Sequences from Transposable Elements”; “Transposable Elements Are Found in a Large Number of Human Protein-Coding Genes” ) that likewise demonstrate the central role LTRs play in gene expression.
Discoveries like the one made by the UBC team undermine one of evolutionâ€™s best arguments. But the functional utility of LTR sequences is not the most fascinating aspect of this work. The team from UBC discovered that when analyzed from an evolutionary perspective, the LTR promoter sequences for the NAIP gene acquired the same function independently, multiple times in humans, mice, and rats!
Evolutionary biologists maintain that through a process called neofunctionalization, junk DNA sequences can acquire function. In the case of LTRs, they argue that these sequences—initially introduced into the genome of organisms through retroviral infections—become promoter sequences when they randomly move throughout the genome, settling in the regulatory region of genes. Once in this region, LTRs can undergo a transformation, allowing them to serve as a binding site for RNA polymerase. When this happens, the LTR sequences can now function as a promoter for that particular gene. Events like these are expected to be relatively rare, however, since random insertion of DNA sequences into genes will be deleterious more often than not.
This evolutionary scenario, at least on the surface, seems reasonable. But the fact that the sequence of events appears to have happened multiple times, independently, for the LTRs of the NAIP gene of humans and rodents raises questions about the validity of this explanation. If the genomes of organisms are the product of evolutionary processes, then identical features like promoters derived from LTR sequences should not independently recur.
Chance governs biological and biochemical evolution at its most fundamental level. This is clearly the case for the neofunctionalization of LTRs. Evolutionary pathways consist of a historical sequence of chance genetic changes operated on by natural selection, which also consists of chance components. The consequences are profound. If evolutionary events could be repeated, the outcome would be dramatically different every time. The inability of evolutionary processes to retrace the same path makes it highly unlikely that the same biological and biochemical designs should repeatedly appear throughout nature.
The concept of historical contingency embodies this idea and is the theme of the late Stephen Jay Gould’s book Wonderful Life. According to Gould,
“No finale can be specified at the start, none would ever occur a second time in the same way, because any pathway proceeds through thousands of improbable stages. Alter any early event, ever so slightly, and without apparent importance at the time, and evolution cascades into a radically different channel.”
To help clarify the concept of historical contingency, Gould used the metaphor of “replaying life’s tape.” If one were to push the rewind button, erase life’s history, and let the tape run again the results would be completely different each time. The very essence of the evolutionary process renders evolutionary outcomes nonrepeatable.
And yet, it appears as if evolution would have had to repeat itself in humans, mice, and rats to explain the promoter structures of the NAIP gene. This recognition runs counter to predictions that logically emanate from the concept of historical contingency and raises questions about the validity of the evolutionary explanation for life’s history. In the abstract of their paper, the scientists who made this discovery remark at how unexpected this result is: “The independently acquired LTRs have assumed regulatory roles for orthologous genes, a remarkable evolutionary scenario [my emphasis].”
Unwittingly, the work conducted by the team from UBC—scientists committed to biological evolution—not only erodes one of the best arguments for evolution, but at the same time raises questions about the evolutionary paradigm. Is junk DNA the best evidence for evolution? It sure doesn’t seem to be.