Junk DNA Goes the Way of the Vestigial Organs Myth

Yet Another Study Finds that “Junk DNA” has a Critical Role in Mammals:
A Parallel Scenario to the Vestigial Organs Saga

 

by Jerry Bergman, PhD

Yet another study, the fourth I have reported on, has found that what was once labeled “junk DNA” plays a critical role in life.

History of the Junk DNA Myth

When the over 3 billion DNA nucleotide bases in humans were being sequenced and analyzed, a concern was whether or not scientists should waste time on sequencing junk DNA. As one leading Whitehead Institute geneticist, Robert Weinberg, wrote: “because 95 percent of the genome seemed to consist of so-called junk DNA—’genetic garbage,’ he called it—sequencing the entire thing would be a huge waste of time. ‘I believe it will turn out to be biologically meaningless.’”[1] The functional genes, Weinberg concluded, constituted “a small archipelago of information scattered amidst a sea of drivel.”[2]

Functional genes were expected to be “a small archipelago of information scattered amidst a sea of drivel” –Robert Weinberg

It was believed that the vast majority of the genome was junk because the “genome contains molecular mile after mile of redundant sequences, chains of nucleotide pairs that are repeated endlessly for no apparent reason.”[3] As one observer wrote:

Nearly half of our DNA has been written off as junk, the discards of evolution: sidelined or broken genes, viruses that got stuck in our genome and were dismembered or silenced, none of it relevant to the human organism or human evolution.[4]

Contrasting Predictions

Many evolutionists expected much of the genome to be junk, due to their preconceived bias that mutation is the driver of evolution. According to neo-Darwinian theory, mutations provide the genetic variation that natural selection can draw upon to better adapt organisms to their environment. The vast majority of mutations are near-neutral, meaning damaging, but not by themselves lethal or deleterious. Because of this, evolutionists expected that most mutations would affect only the 95+ percent they believed to be junk DNA. That would, theoretically, not cause problems.

By contrast, creationists believed the genome of our common ancestors, Adam and Eve, was perfect. What junk existed would have been added after the Fall and would have affected a relatively small amount of the entire genome. Thus, all of it would originally have been fully functional from its inception.

The Sequence the Entire Genome Position Prevails

Stanford Nobelist Paul Berg demurred, opposing Weinberg and cautiously stating, “I want to know every single nucleotide. Only then can we decide whether it’s junk or not.”[5] Fortunately, Berg prevailed and the entire human genome was eventually sequenced.

The latest study found that knocking out a piece of presumed junk DNA resulted in pup death in mice.[6] This surprise led to the finding that the non-coding region was a gene promoter. Promoters are short DNA sequences located upstream of a gene where the required regulatory elements can bind. The binding process is required for DNA to be transcribed to RNA. Without it, a gene will not be properly transcribed and expressed, or will not be transcribed at all. The reason knocking out this promoter resulted in the death of the mice pups is because this DNA sequence, once thought of just as “junk DNA,” has a critical role both in cell proliferation and the timing of embryo implantation in mice. Similar promoters are found in many mammals, including humans.

Selfish Viruses?

Another common claim is that much of the genome is parts of “viruses that sneaked into human DNA eons ago, multiplied, but could go no further and just stayed put.”[7] This claim is not made on evidence. It’s an assumption based only on similarities of parts of human DNA with virus DNA. The fact that two sections of DNA are similar does not prove they are historically related. Another example  presuming to identify the source of promoters is the

new study led by researchers at University of California, Berkeley, and Washington University [that] explored the function of one component of this junk DNA, transposons, …. The study shows that at least one family of transposons – [were] ancient viruses that have invaded our genome by the millions.[8]

The problem with this supposition is that the promoter serves a critical role in the life of the mammal. How the mammal could have possibly survived until this putative ancient virus arrived is never explained even by hypothetical scenarios. Even granting the scenario, once the virus arrived, how was it able to take on a critical function in the correct area in harmony with the system it is part of? That was never explained, even by just-so stories.

A More Logical Solution

It is far more logical to assume the promoter was designed to function inside the cell in the role it now plays. It was this role which researchers at University of California, Berkeley, and Washington University explored. The claim that these misnamed “selfish DNA sequences [are] able to invade their host genome,” and play a critical role in viability of the mouse, and perhaps in all mammals, is not based on evidence. That it plays a critical role was already documented when the researchers “knocked out a specific transposon [gene] in mice and half of their pups died before birth.”

This is the first example of a piece of “‘junk DNA’ being critical to survival in mammals.”[9] Specifically, the “junk DNA”

regulates the proliferation of cells in the early fertilized embryo and the timing of implantation in the mother’s uterus. The researchers looked in seven other mammalian species, including humans, and also found [claimed] virus-derived regulatory elements linked to cell proliferation and timing of embryo implantation, suggesting that ancient viral DNA has been domesticated independently to play a crucial role in early embryonic development in all mammals.[10]

Pleasing Darwinists

It is obvious that these authors’  “suggestion” is mere unfounded speculation designed to appease the Darwinists. A comparable claim is that the mammalian heart, possessed by the very early mammals, originated from a “113-119 million-year-old fish from Brazil called Rhacolepis… the first definite fossilized heart found in any prehistoric animal.”[11] This theory tries to explain where the mammalian heart came from at best, but it does not explain how mammals survived until the common ancestor of mammals got the heart from the fish. This parallel illustrates the problem of obtaining organs, as well as genes, from other animals or, in this case, viruses.

Magical Repurposing

The evolutionary scenario gets even weirder. The former virus is now considered a “viral promoter.” Evolutionists claim, in this case (without evidence) that a viral gene “has been repurposed as a promoter for a mouse gene that produces a protein involved in cell proliferation in the developing embryo and in the timing of implantation of the embryo.”[12] This scenario represents a  major change in thinking about evolution. For over a century, mutations were proposed by Neo-Darwinists as the driving force of evolution. Now the Stanford and UC Berkeley scientists propose a new scenario.

[The] real significance of this story [the virus-to-promoter scenario] is it tells us how evolution works in the most unexpected manner possible. Transposons were long considered useless genetic material, but they make up such a big portion of the mammalian genome. A lot of interesting studies illustrate that transposons are a driving force of human genome evolution.[13]

This scenario falls apart upon inspection, because “different species have largely different transposons that are expressed in pre-implantation embryos, but the global expression profiles of these transposons are nearly identical among all the mammalian species” – creating a chasm between mammals and the animals they are believed to have evolved from![14]

This scenario is not purely an intellectual pursuit to understanding how evolution works. The authors suggest some real-world implications.  “The finding could have implications for human infertility…. nearly half of all miscarriages in humans are undiagnosed or don’t have a clear genetic component. Could transposons like this be involved?”[15]

Summary

“Junk DNA,” not actually being worthless but critically important, is just another one of many examples where the creation worldview has been vindicated and the evolutionary worldview has impeded research. It is exactly akin to the evolutionists’ vestigial-organ myth, where they wrongly claimed that a host of human body parts and anatomical structures were useless ancestral leftovers. The creation mindset, by contrast, correctly predicted that all of the putative “vestigial” organs would have a necessary purpose and functional use. Nevertheless, evolutionists used, and still employ, the vestigial-organ myth as an alleged proof of evolution.[16]

Both the junk DNA myth and the vestigial organs myth rely on the same religious argument. Why would God (in their thinking) build into our bodies a lot of useless organs and structures that have no function, or worse, cause problems (such as the human appendix causing appendicitis)? That particular case unraveled when the appendix was discovered to have several important intestinal digestive and immune functions. Historically, over 100 organs were assumed to be vestigial, i.e., junk, but after a century of further research, all of them have been documented to be functional. In many cases, they are very important for health. Likewise, the claim that a regulatory gene, now documented to be “critical to survival in mammals,” was due to a viral invasion of a pre-mammal cell is also irrational. The most obvious explanation is that it was designed to serve a “crucial role” in mammals from the very beginning.[17]

References

[1] Kyon, Feff, and Peter Gorner. Altered Fates: Gene Therapy and the Retooling of Human Life. W. W. Norton & Co, New York, NY, 1995, p. 533.

[2] Kyon and Gorner, 1995, p. 534.

[3] Kyon and Gorner, 1995, pp. 533-534.

[4] University of California – Berkeley. So-called junk DNA plays critical role in mammalian development. Science Daily, 18 October 2021. See also Robert Sanders post at Berkeley News.

[5] Kyon and Gorner, 1995, p. 533.

[6] Modzelewski, Andrew J., et al. A mouse-specific retrotransposon drives a conserved Cdk2ap1 isoform essential for      development. Cell, 12 October 2021; DOI: 10.1016/j.cell.2021.09.021

[7] Kyon and Gorner, 1995, p. 534.

[8] University of California – Berkeley, 2021.

[9] University of California – Berkeley, 2021.

[10] University of California – Berkeley, 2021.

[11] Long, John. The first fossilized heart ever found in a prehistoric animal. The Conversation 19 April 2016.

[12] University of California – Berkeley, 2021.

[13] University of California – Berkeley, 2021

[14] University of California – Berkeley, 2021

[15] University of California – Berkeley, 2021.

[16] Among the many examples on YouTube include: https://www.youtube.com/watch?v=OAfw3akpRe8; https://www.youtube.com/watch?v=9QDoMaPOqi4; https://www.youtube.com/watch?v=5eVjsCfjo_U&t=118s; https://www.youtube.com/watch?v=PxoDMlT08w4; https://www.youtube.com/watch?v=NAxCQwuUPHM&t=144s. and many more such examples.

[17] University of California – Berkeley, 2021.

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Dr. Jerry Bergman has taught biology, genetics, chemistry, biochemistry, anthropology, geology, and microbiology for over 40 years at several colleges and universities including Bowling Green State University, Medical College of Ohio where he was a research associate in experimental pathology, and The University of Toledo. He is a graduate of the Medical College of Ohio, Wayne State University in Detroit, the University of Toledo, and Bowling Green State University. He has over 1,300 publications in 12 languages and 40 books and monographs. His books and textbooks that include chapters that he authored are in over 1,500 college libraries in 27 countries. So far over 80,000 copies of the 40 books and monographs that he has authored or co-authored are in print. For more articles by Dr Bergman, see his Author Profile.