When “Junk DNA” Isn’t Junk: Farewell to a Darwinist Standard Response

Richard Sternberg

In the Darwinist repertoire, a standard response to evidence of design in the genome is to point to the existence of “junk DNA.” What is it doing there, if purposeful design really is detectable in the history of life’s development? Of course this assumes that the “junk” really is junk. That assumption has been cast increasingly into doubt. New research just out in the journal Nature Genetics finds evidence that genetic elements previously thought of as rubbish are anything but that. The research describes tiny strands of RNA, previously thought to be junk, that now turn out to play a role in gene expression. Another finding by Dr. Geoff Faulkner shows that “retrotransposons,” a further variety of “junk” as the dogma previously taught, play a similar role.
Nearly half of the mammalian genome (less than 45 percent) is comprised of DNA sequences thought for decades to be but evolutionary flotsam and jetsam or junk: retrotransposons. Found along every one of our chromosomes, retrotransposons mobilize within our cells via RNA copies, copies that are then converted into DNA and afterward pasted into different DNA sites. To be sure, the vast majority of these “jumping gene” duplicates, well over a million elements, appear to be little more than pseudogenes, defective images of master templates that merely drift by mutations into a phylogenetic oblivion.
Retrotransposons appear to fit the neo-Darwinian story perfectly. First, the master templates of these elements seem to serve no other purpose than to promote their own replication at the expense of the cell, and so, by the criteria of Richard Dawkins’s 1976 book The Selfish Gene, retrotransposons are selfish genes par excellence. Second, the DNA progeny of such “endogenous viruses” are without a doubt marred in various ways, as just mentioned. Relative to the original, in other words, they are junk. Third, a retrotransposon inserted into a chromosome can disrupt normal gene functions, and mutations due to these sequences have long been detected. Fourth, only a comparative few retrotransposons are conserved across different groups of mammals, with most of the DNA families being restricted to certain families, genera, or even species. Humans and mice as well as mice and rats can readily be separated solely on the basis of their retrotransposon profiles. So the bulk of these sequences do not merit being retained by natural selection.

With such facts at hand, it is no wonder that retrotransposons and other “non-coding” DNAs are part of Exhibit A on the side of the neo-Darwinian prosecution, over and against the intelligent design defense.
But there have always been big holes in this tale of selfish, junk DNA. We have known since the late 1980s that retrotransposons are distributed non-randomly along chromosomes. Even though humans and mice and rats have different families of these sequences — ultimately a reflection, according to neo-Darwinists, of randomness — the linear pattern of placement of the elements is uncannily similar. Likewise, data accumulated throughout the ’80s and ’90s which indicated that normal gene regulation can be controlled by pieces of such mobile DNA. Evidence for other diverse regulatory roles of retrotransposons has also continued to mount till the present.
But it wasn’t until recently that we learned just how extensive is the informational impact of retrotransposons on the mammalian genome. The recent study by Geoffrey Faulkner et al. (“The regulated retrotransposon transcriptome of mammalian cells,”) is only the latest. Using the RNA expression profiles of the human and mouse genomes as a backdrop, a number of key facts were uncovered. For one thing, tens to hundreds of thousands of transcription start sites — the beginning points of RNA transcripts — occur in retrotransposons. According to the data they gathered, anywhere from 6 to 30 percent of RNAs in the two species arise from repetitive (aka “junk”) DNA. For another, elements that reside in or near protein-coding genes provide alternative regions to initiate transcription, many previously unknown, and they allow for the production of various non-translated RNAs. The “start RNA production” signals conveyed by retrotransposons such as the mouse-specific VL30 retrovirus-like sequences are also markedly tissue-specific. Altogether, the results point to retrotransposons being “intrinsic components of the transcription forest regions of the genome” (Faulkner et al., 2009).
This is all rather awkward for the Darwinian side, obviously. Another standard weapon in their armory is to charge intelligent-design theorists with making a “God of the gaps” argument, where gaps in scientific knowledge are assumed to be evidence of design. The reality is that the case for Darwinian evolution is much more reasonably shown to depend on gaps — in our knowledge of what “junk DNA” does, for one thing. Hence a sobriquet for the view that evolutionists are saddled with defending: “Darwin of the gaps.”

Richard Sternberg

Senior Fellow, Center for Science and Culture
Richard Sternberg is an evolutionary biologist with interests in the relation between genes and morphological homologies, and the nature of genomic “information.” He holds two Ph.D.'s: one in Biology (Molecular Evolution) from Florida International University and another in Systems Science (Theoretical Biology) from Binghamton University. From 2001-2007, he served as a staff scientist at the National Center for Biotechnology Information, and from 2001-2007 was a Research Associate at the Smithsonian’s National Museum of Natural History. Dr. Sternberg is presently a research scientist at the Biologic Institute, supported by a research fellowship from the Center for Science and Culture at Discovery Institute. He is also a Research Collaborator at the National Museum of Natural History.



Junk DNA