Why do so many people think that human evolution is a valid idea?
Recently, I came across an article that explains why. The article argues that junk DNA found in the human genome is evidence for evolution and against creation.
Argument for Common Descent This piece was written for Skeptical Inquirer by Stanley Rice, a professor of biological science at Southeastern Oklahoma State University.1 The article presents a well-written and lay accessible case for common descent and our shared evolutionary ancestry with the great apes. Not surprisingly, the crux of Rice’s case rests on shared DNA sequences found in the genomes of organisms that naturally group together (such as humans and great apes). Rightly so, Rice focuses little attention on those shared sequences which code for useful protein products. Instead, he chooses to emphasize those shared sequences that lack any function, using pseudogenes as a case study.
Many life scientists view pseudogenes as genes that have become inactivated by mutational events. Presumably, these genes were functional in our evolutionary ancestors but became damaged, leading to their inactivation. Yet, despite their lack of function, these DNA sequence elements remain within the genome. Accordingly, life scientists tend to view them as vestiges of our evolutionary history. Biologists have discovered that the same (or nearly the same) pseudogene sequences are found in the human genome and the genomes of great apes. This discovery prompts Rice to ask:
“But what if you did not evolve? Then it must have been that God created not just your living genes but also slipped a bunch of dead pseudogenes into your chromosomes as well. And not just any dead genes, but dead genes that more closely resemble those found in species similar to you than in species different from you.”2
Argument for Common Design Despite this compelling evidence, I am skeptical about human evolution for several reasons I won’t address here. Still the shared pseudogenes in the genomes of humans and the great apes can’t simply be ignored. Yet it is important to note that alternative explanations exist for the presence of pseudogene sequences in the human genome (and genomes of other creatures). Along these lines, I hold to the view that shared sequences in the human and great ape genomes can readily be explained by appealing to the concept of common design.
This idea has roots in the work of prominent biologist Sir Richard Owen. Prior to Charles Darwin, Owen provided a theoretical framework to interpret anatomical and physiological similarities shared among organisms. Owen saw these mutual features as manifestations of a common blueprint—an archetype.
The RTB creation model picks up where Owen left off, viewing the shared features in the genomes of organisms as manifestations of genomic archetypes. In other words, the genetic similarities in the genomes of humans and the great apes were intentionally introduced by the Creator, despite Rice’s dismissal of this explanation.
In the case of shared pseudogenes, the RTB creation model predicts that:
1. Nonfunctional sequences, such as pseudogenes, have functional utility that explains their presence in genomes.
2. A rationale exists for the sequence similarity between genes and their pseudogene counterparts.
As I have written in three books, The Cell’s Design, Who Was Adam?, and Thinking about Evolution, and in a series of web articles (see the Resources section) both predictions have been satisfied. In other words, despite Rice’s powerful contention, it is completely rational for someone to view the human genome and the genomes of other creatures as the product of a Creator’s handiwork, with shared genomic sequences reflecting shared design, not shared evolutionary history.
Why Nonfunctional DNA Elements? Rice brings up another class of nonfunctional DNA elements shared in the genomes of humans and great apes: endogenous retroviruses (ERVs). Many life scientists view ERVs as remnants of a viral infection. As Rice puts it, “Your chromosomes carry not only fossil genes but fossil viruses.”3 And, he asks: “Why would God have put them there?”4
ERVs comprise around 8% of the human genome. For many people, the presence of ERVs in the human genome (and the genomes of other organisms) is difficult, if not impossible, to explain from a creation model perspective. In fact, I have interacted with several people who have told me that the distribution of ERVs in the genomes of humans and great apes has convinced them of the truth of human evolution.
Again, the RTB creation model predicts:(1)that ERV sequences—just like pseudogenes—are functional, serving a vital role, and (2) a rationale exists to account for their similarity to viral genomes.
A recent study published by a team from Stanford University validates these two predictions. This team has demonstrated that ERV sequences in the human genome are expressed in the early stages of embryonic development and serve a key role in ensuring a successful pregnancy.5
Before elaborating on this study, a bit of background on retroviruses and endogenous retroviruses might be helpful. (For readers familiar with ERVs and the support these genomic elements provide for human evolution, feel free to skip to ERV Activation in Early-Stage Human Embryos.)
Retroviruses Like all viruses, retroviruses consist of genetic material surrounded by a protein capsid. Retroviruses infect organisms by invading specific cell types of the host organism. After the retroviruses attach to the target cell’s surface, the targeted cell engulfs them. Once engulfed, the viral genetic material exploits the host cell’s machinery to produce viral genetic material and viral proteins. These biomolecules then assemble into new viral particles. When the newly formed viruses escape from the invaded cell, the infection cycle repeats.
Because the genetic material of retroviruses is RNA, it has to be converted into DNA before the infectious cycle can proceed. This conversion is carried out by an enzyme called reverse transcriptase, which is delivered to the target cell along with the retroviral RNA. The enzyme uses the retroviral RNA to make DNA. The newly made DNA can then use the invaded cell’s biosynthetic pathways to direct the production of new retroviral particles. The DNA copy of the retroviral genetic material can also become incorporated into the host cell’s genome. When this insertion takes place, the retroviral DNA becomes part of the host cell’s genome. This process is called endogenization.
Endogenous Retroviruses (ERVs) Once retroviral DNA becomes incorporated into an organism’s genome it is called an endogenous retrovirus (in contradistinction to exogenous retroviruses which exist independent of genomes). After inserting into the host’s genome, the endogenous retrovirus can still produce retroviral particles, if its DNA is transcribed by the host cell’s biochemical machinery. If the ERV infects a germ line cell (a sperm cell or an egg cell), it can be inherited, transmitted from generation to generation as a permanent feature of the genome. If the ERV DNA suffers severe mutations, it becomes disabled and remains in the genome as nonfunctional, junk DNA.
Endogenous Retroviruses and the Case for Human Evolution Many human ERVs are also found in the genomes of chimpanzees, bonobos, gorillas, and orangutans. Not only do these ERVs share many of the same sequence patterns, but they also appear in corresponding locations in the genomes.
Evolutionary biologists explain this data by assuming that the shared ancestor of humans and chimpanzees, for example, became infected by these specific retroviruses. Later these endogenized retroviruses experienced mutations that disabled them in the ancestor’s genome. These ERV sequences were retained in the genomes of humans and chimpanzees as their separate evolutionary lineages diverged from the common ancestor. According to the model, the endogenous retroviruses shared by humans and chimpanzees represent the molecular artifacts of infections that occurred millions of years ago and left their imprint on contemporary genomes via this (presumed) shared ancestor.
To echo Rice: why would the Creator introduce the same nonfunctional sequence elements in the same locations within the genomes of organisms that naturally group together (based on other biological features)? And why would he create these shared sequence elements to bear such strong similarity to retroviruses?
The Stanford University scientists‘ research helps address these questions.
ERV Activation in Early-Stage Human Embryos The researchers focused their attention on a class of endogenous retroviruses found in the human genome called HERVK. These endogenous retroviral elements have intact sequences, which code for retroviral proteins. Normally, HERVK sequences are silenced by methylation of the LTR regions of the HERVK sequences. The researchers learned that through demethylation of the LTR regions and the activity of a transcription factor (OCT-4), the HERVK sequences become transcriptionally active at the 8-cell stage of embryonic development. This activation persists until the inner cell mass of the embryo differentiates into the epiblast and the hypoblast.
In support of this discovery, the research team detected the presence of viral-like particles and the production of gag and rec retroviral proteins in the early-stage embryo cells.
The production of the rec protein is of particular significance. Researchers have discovered that the overexpression of the gene that encodes the rec protein in pluripotent stem cells increases IFITM1 levels on the cell surface. This protein is induced by interferon and inhibits the early stages of viral invasion of the cell by preventing the virus from interacting appropriately with the cell membrane. As a consequence, the process of endosome formation becomes disrupted, preventing the entry of virions into the cell.
The researchers discovered that by forcing the expression of HERVK sequences in pluripotent stem cells, they were able to inhibit the infection of the cells by the H1N1 influenza virus.
Here’s the important point: These observations indicate that the HERVK sequences offer the early-stage embryo protection against viral infections when it is particularly vulnerable. Though not addressed by the Stanford researchers, it seems reasonable to me that the generation of viral-like particles and the production of gag proteins may also function in an antiviral capacity through competitive inhibition.6 This mechanism offers an explanation for the similarity between endogenous retroviral DNA sequences and those of retroviruses.
The production of the rec protein also serves another important function. This protein interacts with messenger RNA molecules at the nuclear pore, mediating their transport out of the nucleus into the cytoplasm, where these biomolecules become translated into proteins at the ribosome. The rec protein also mediates the ribosome occupancy of messenger RNA. Both processes, in effect, regulate the expression of a wide range of genes. This regulation of gene expression undoubtedly influences cell differentiation in early embryonic development. In this scheme, the similarity between the retroviral rec protein and the rec protein found in the human genome makes sense. This similarity allows the rec protein encoded by HERVK sequences to function in the same vein as the retroviral rec protein would during a retroviral infection.
A Common Blueprint Bottom line: HERVK sequences contribute to the innate immunity of the early-stage embryo and play a role in gene regulation.
So, in response to Rice’s question: God could have intentionally designed and incorporated ERV sequences in the human genome because they serve a function that is predicated on similarities with retroviral DNA sequences. This study serves as a reminder that advances in biochemistry support a creation model that sees shared genomic sequences as a Creator’s common blueprint.
Endnotes 1. Stanley Rice, “Creationist Funhouse, Episode Six: God the Biotechnologist,” Skeptical Inquirer 45 (May/June 2021): 45–47, https://skepticalinquirer.org/2021/04/creationist-funhouse-episode-six-god-the-biotechnologist/. 2. Rice, “God the Biotechnologist,” 46. 3. Rice, “God the Biotechnologist,” 47. 4. Rice, “God the Biotechnologist,” 47. 5. Edward J. Grow et al., “Intrinsic Retroviral Reactivation in Human Preimplantation Embryos and Pluripotent Cells,” Nature 522 (June 11, 2015): 221–25; doi:10.1038/nature14308. 6. Clare Lynch and Michael Tristem, “A Co-Opted Gypsy-Type LTR-Retrotransposon Is Conserved in the Genomes of Humans, Sheep, Mice, and Rats,” Current Biology 13, no. 17 (September 2, 2003): 1518–23. doi:10.1016/S0960-9822(03)00618-3.
