Reasons to Believe

Three (More) Reasons Why Junk DNA Is No Longer Evidence for Evolution

At one time, many researchers viewed shared junk DNA sequences as the most compelling evidence for common descent and, hence, biological evolution. This made shared junk DNA sequences one of the most significant scientific challenges to the biblical creation model.

Yet, over the last decade, numerous studies have demonstrated that practically every class of junk DNA displays function. The most comprehensive work toward this end comes from the ENCODE (ENCyclopedia Of DNA Elements) Project. Phase II results, published in September 2011, demonstrated that, at minimum, 80 percent of the human genome consists of functional elements. As Phase III results become available, it is likely that even more of the genome will be deemed functional.

Shortly after the Phase II results were published several papers appeared in the scientific literature highlighting ENCODE’s “flaws.” Many evolutionary biologists hope these critiques will undermine the project’s conclusion. Yet, in spite of these protests, it appears that the ENCODE Project conclusions will stand: a vast proportion of the human genome (and other organisms’ genomes) appears to be functional. Still, because of ENCODE deniers’ complaints it is important that ongoing research reaffirms the ENCODE results.

And it has, as this sampling of new discoveries makes plain.

Finding #1: Junk DNA Plays a Role in Embryonic Development
Two separate studies concluded that junk DNA sequences play a key role in embryonic development. 

In one study, scientists from the Karolinska Institutet (Sweden) mapped the genes that are active in human embryos the first few days after fertilization takes place.1 They learned that, of the 23,000 genes in the human genome, only 32 are transcribed two days after the zygote forms (when the embryo is in the four-cell stage) and only 129 genes are active at day three (when the embryo is in the eight-cell stage). The scientists argued that these 129 genes are responsible for kick-starting the process of embryonic development. They discovered that the promoter sequences controlling the activity (or expression) of these genes are enriched in Alu sequences, which shows that Alu sequences are critical for regulating the initial stages of embryonic development.

Traditionally, Alu sequences were considered junk. They are highly repetitive sequences of DNA (about 300 genetic letters, or base pairs, in length) belonging to a class of DNA known as SINEs (short interspersed nuclear elements). Alu sequences are unique to primates. There are over 1 million Alu elements in the human genome, making up about 11 percent of the genetic material. Evolutionary biologists have pointed out that humans and chimps share large numbers of Alu sequences, with identical (or nearly identical) sequences occurring in corresponding locations in both genomes. Evolutionists believed shared Alu elements arose prior to the divergence of humans and chimps from a shared evolutionary ancestor.

However, the fact that the Karolinska Institutet study and others have identified function for the Alu sequences means that the sequences’ presence in human and great ape genomes could be interpreted as evidence for common design, not common descent.

In the other study, Stanford University researchers determined that endogenous retroviral (ERV) DNA sequences play a key role in the early stages of embryonic development.2 The researchers determined that disruption of the transcription of ERV sequences prevents cells in the early embryo from developing into the inner cell mass and inhibits the ability of these cells to develop pluripotency (the ability to transform into the specialized cells of the human body).

Evolutionary biologists view ERV DNA sequences in the human genome as leftovers of retroviral infections, whereby the retroviral DNA becomes incorporated into the human genome. ERV sequences make up about 5 percent of the human genome and many of these sequences are also found in the chimp genome. Evolutionary biologists argue that these shared sequences reflect shared evolutionary ancestry. Presumably the retroviral infection occurred in the human-chimpanzee common ancestor. But, again, if ERVs are functional, it opens the possibility that the shared sequences are the work of a designer.

Finding #2: Duplicated Genes Are Functionally Significant
A number of human genes are duplicated and biologists view these as vestiges of evolution. There are several ways to duplicate genes. It was assumed this duplication process is random and that the duplicated sequences lack any functional significance. Oftentimes, the same duplicated genes are found in both human and chimp genomes; thus, evolutionary biologists argue duplication events took place in the human-chimp ancestor.

A recent report indicates that there may be a rationale for the existence of duplicated genes in the human genome (and the genomes of other organisms).3 These scientists were trying to understand why elephants rarely develop cancer. It turns out elephant genomes have 20 copies of the tumor suppressor gene, TP53. (Humans have one copy.) The investigators discovered that these duplicated TP53 copies actively prevent tumor growth by inducing the cancer cells to undergo aggressive apoptosis (programmed cell death).

This study makes it possible to view duplicated genes as the handiwork of a Creator and not the unintended consequence of undirected biochemical events. It also makes it reasonable to view shared duplicated genes as common design features, not the vestiges of an evolutionary history.

Finding #3: Genome Size Correlates with Reproductive Fitness
Historically, the C-value paradox was one reason why life scientists thought most DNA was junk. Biologists noted that there appeared to be no rhyme or reason to the varied genome sizes among organisms—thus, they concluded junk DNA was nonfunctional remnants of an evolutionary history. Yet some studies have demonstrated that genome size may be related to the role DNA plays in regulating the size of the cell’s nucleus.

Added to these studies is recent work by biologists from Uppsala University in Sweden. These researchers demonstrate that beetles with larger genome sizes have improved reproductive fitness.4 The relationship between genome size and beetle fecundity is unclear, but it is clear that larger genomes are beneficial.

It is exciting that ongoing research efforts, in line with the results of the ENCODE Project, continue to identify function for junk DNA. Though it may seem like wasted effort to continue dwelling on this facet of the creation-evolution controversy, it is necessary as long as ENCODE skeptics continue to rail against the conclusions of this project. As new studies reaffirm the ENCODE results, its critics will eventually realize the futility of arguing against it.

Subjects: Junk DNA

Dr. Fazale Rana

In 1999, I left my position in R&D at a Fortune 500 company to join Reasons to Believe because I felt the most important thing I could do as a scientist is to communicate to skeptics and believers alike the powerful scientific evidence—evidence that is being uncovered day after day—for God’s existence and the reliability of Scripture. Read more about Dr. Fazale Rana


  1. Virpi Töhönen et al., “Novel PRD-Like Homeodomain Transcription Factors and Retrotransposon Elements in Early Human Development,” Nature Communications 6 (September 2015), doi: 10.1038/ncomms9207.
  2. Jens Durruthy-Durruthy et al., “The Primate-Specific Noncoding RNA HPAT5 Regulates Pluripotency during Human Preimplantation Development and Nuclear Reprogramming,” Nature Genetics, published electronically November 23, 2015, doi:10.1038/ng.3449.
  3. Michael Sulak et al., “TP53 Copy Number Expansion Correlates with the Evolution of Increased Body Size and an Enhanced DNA Damage Response in Elephants,” BioRxiv, preprint, published electronically October 6, 2015, doi:
  4. Göran Arnqvist et al., “Genome Size Correlates with Reproductive Fitness in Seed Beetles,” Proceedings of the Royal Society B 282 (September 2015), doi: 10.1098/rspb.2015.1421.