After the Human Genome Project was completed in 2003, a startling discovery was made. Only about 2 percent of the entire human genome codes for proteins. Scientists naturally asked, what is the other 98 percent doing?
Evolutionary biology was ready with an answer. For decades, they had claimed that the vast majority of the human genome was essentially genetic garbage — “junk DNA.” This idea had deep roots in evolutionary thinking — which loves to claim humanity and other living things are poorly designed.
A 1969 paper titled “Non-Darwinian Evolution” in the journal Science proposed that “99 percent of mammalian DNA is not true genetic material.” Three years later, the great Japanese biologist Susumu Ohno coined the term “junk DNA” and predicted that “at least 90% of the mammalian genomic DNA appears to represent ‘nonsense.’”
Atheist evolutionary biologists loved the idea. Richard Dawkins wrote in his 2003 book "A Devil’s Chaplain" that “genomes are littered with nonfunctional … junk.” But even theistic evolutionists — Christians who believe God created life through evolution — found junk DNA an expedient argument to bolster their theory.
In his 2006 book "The Language of God," Francis Collins — who headed the Human Genome Project — wrote that some “45 percent of the human genome” is little better than “genetic flotsam and jetsam.”
Meanwhile, proponents of intelligent design (ID) developed a very different view of so-called "junk DNA."
In 1994, pro-ID scientist Forrest Mims wrote a letter to Science warning against assuming that “junk” DNA was “useless.” Four years later, mathematician William Dembski articulated the ID view: “Consider the term ‘junk DNA. … Design encourages scientists to look for function where evolution discourages it.”
But why does intelligent design predict function for junk DNA? It’s simple.
ID theory starts by observing what intelligent minds can do, and then searches nature to see if there’s evidence of a mind at work.
We know from our observation-based experience that intelligent agents do things for a reason. Engineers only put functional parts into cell phones. Every time an email is written, an intelligence generates informational sequences with a purposeful message. ID predicts function.
But which view is right? In 2012, a groundbreaking discovery started a paradigm shift in this debate.
A consortium of hundreds of scientists involved in the ENCODE Project published results in the top journal Nature showing that over 80 percent of the human genome is biochemically active. They showed the vast majority of the genome is converted into RNA — a process called “transcription” that is normally a telltale sign of function. One lead ENCODE researcher predicted that as more human cell types are studied, “that 80 percent will go to 100 percent.”
These discoveries had a dramatic effect on biological thinking. Even Francis Collins changed his tune. Speaking at a scientific conference in 2015, he admitted:
"In terms of junk DNA, we don’t use that term anymore because I think it was pretty much a case of hubris to imagine that we could dispense with any part of the genome as if we knew enough to say it wasn’t functional."
Collins explained that most of so-called “junk” is regulating the production of proteins, called gene expression. By 2021, one mainstream scientific paper declared that “the days of ‘junk DNA’ are over.”
These discoveries represented a spectacular fulfillment of ID’s prediction that we would discover function for junk DNA, and a colossal failure for evolution.
Unsurprisingly, evolutionary biologists weren’t going to take this sitting down. One biologist, Dan Graur at the University of Houston, worried that “If ENCODE is right, then Evolution is wrong.” He shifted the goalposts by proposing that if most of our genome is producing RNA, then that “transcription is … stochastic” — i.e., it’s just randomly produced junk RNA!
But Graur’s view has been receding as we discover more and more functions for RNA. A newly published paper in the journal Genome Biology and Evolution dealt a serious blow to “junk RNA.”
This paper, along with a 2024 paper in Nature, took sections of mammalian DNA that are transcribed into RNA and reversed them. If transcription is random and uncontrolled, then scrambling their DNA should not change the amount of RNA that’s produced. But if RNA is produced in a controlled, regulated, and functional manner, then transcription in the scrambled sequence should drop dramatically. And that’s exactly what they found. As the paper found, “most transcription is not a consequence of background noise.”
To be sure, there’s still much we don’t know about the genome. But the more we study genetics, the more function we discover. Evolution’s love affair with viewing our bodies as clumsy accidents is hindering science. In contrast, when we view DNA as intelligently designed, we can make useful predictions that bear good scientific fruit, advancing our knowledge of how cells work.
Casey Luskin
https://townhall.com/columnists/casey-luskin/2026/09/20/intelligent-design-bears-good-scientific-fruit-in-the-study-of-junk-dna-n2683215
Ho J, Douse C, Marazzi I. Transposable element DNA and RNA: Drivers of gene expression, evolution, and disease
Cell, 189, 3513-3540
Summary
Transposable elements (TEs) comprise nearly half of mammalian genomes and have shaped genome architecture, chromatin organization, and transcriptional landscapes. Thanks to recent advances in long-read sequencing and functional (epi)genomics, the focus has shifted from TE families to individual TE loci, revealing widespread, locus-specific regulatory roles. While most TEs have lost the capacity to mobilize, they still retain a DNA form and, when transcribed, an RNA form, both of which can affect genome regulation. TEs can serve as alternative promoters, exons, splicing regulators, and 3′ end modulators. They can also act as enhancers, drive three-dimensional (3D) genome organization, and give rise to long non-coding RNAs (lncRNAs) that serve as platforms for transcriptional and chromatin regulators. Mechanistically, TE repression involves DNA methylation, histone modification, phase-separated condensates, RNA modifications, RNA degradation, and nuclear compartmentalization, yet this repression can be selectively lifted during development or stress to expand regulatory potential. TEs therefore contribute to cell-type identity, developmental transitions, and responses to environmental stimuli, while their dysregulation is linked to human disorders including neurodegeneration, cancer, and autoimmune disease. TEs also hold translational promise as biomarkers and tools for gene and cell engineering. In summary, the pervasive integration of TEs as mini-genes, structural scaffolds, and regulatory elements redefines our view of the genome: rather than a gene-centric landscape dotted with repetitive “junk,” mammalian DNA is a TE-rich ecosystem in which TEs drive gene regulatory networks and evolution.
Cell, 189, 3513-3540
Summary
Transposable elements (TEs) comprise nearly half of mammalian genomes and have shaped genome architecture, chromatin organization, and transcriptional landscapes. Thanks to recent advances in long-read sequencing and functional (epi)genomics, the focus has shifted from TE families to individual TE loci, revealing widespread, locus-specific regulatory roles. While most TEs have lost the capacity to mobilize, they still retain a DNA form and, when transcribed, an RNA form, both of which can affect genome regulation. TEs can serve as alternative promoters, exons, splicing regulators, and 3′ end modulators. They can also act as enhancers, drive three-dimensional (3D) genome organization, and give rise to long non-coding RNAs (lncRNAs) that serve as platforms for transcriptional and chromatin regulators. Mechanistically, TE repression involves DNA methylation, histone modification, phase-separated condensates, RNA modifications, RNA degradation, and nuclear compartmentalization, yet this repression can be selectively lifted during development or stress to expand regulatory potential. TEs therefore contribute to cell-type identity, developmental transitions, and responses to environmental stimuli, while their dysregulation is linked to human disorders including neurodegeneration, cancer, and autoimmune disease. TEs also hold translational promise as biomarkers and tools for gene and cell engineering. In summary, the pervasive integration of TEs as mini-genes, structural scaffolds, and regulatory elements redefines our view of the genome: rather than a gene-centric landscape dotted with repetitive “junk,” mammalian DNA is a TE-rich ecosystem in which TEs drive gene regulatory networks and evolution.
Abstract
The human genome encodes the blueprint of life, but the function of the vast majority of its nearly three billion bases is unknown. The Encyclopedia of DNA Elements (ENCODE) project has systematically mapped regions of transcription, transcription factor association, chromatin structure and histone modification. These data enabled us to assign biochemical functions for 80% of the genome, in particular outside of the well-studied protein-coding regions. Many discovered candidate regulatory elements are physically associated with one another and with expressed genes, providing new insights into the mechanisms of gene regulation. The newly identified elements also show a statistical correspondence to sequence variants linked to human disease, and can thereby guide interpretation of this variation. Overall, the project provides new insights into the organization and regulation of our genes and genome, and is an expansive resource of functional annotations for biomedical research.
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