How “Junk” DNA Got Its Function: Evolutionary Tales Fail to Convince
Recently I wrote about various functions that have been identified for “junk” DNA. Of course, many functions have been discovered for the supposed “junk,” but these form a special case where diseases played a role. How are they being identified? It’s because when those functions go wrong, diseases result. Most evolutionists aren’t bothered by such findings of individual functions for junk DNA. They just claim that occasionally junk gets co-opted to do something useful, or even vital to our health. They offer evolutionary accounts of how the junk got its function — but those accounts often appear highly unlikely. Here are a couple of examples.
Did junk DNA cause humans to lose their tails.
Earlier this year there was a flurry of stories about how “junk DNA” may explain why humans don’t have tails. As the story goes, a transposable element called an Alu sequence got randomly inserted into a regulatory intron of a gene called TBXT, which is involved in the early development of the neural tube (which later becomes the spinal column). An evolutionary story ensues, outlined at Study Finds:
The researchers identified a specific genetic alteration — an inserted piece of DNA — present in humans and apes but absent in monkeys. This insertion, located in a gene known as TBXT, is believed to play a critical role in the development, or rather the absence, of tails in humans.
Technical paper in Nature elaborates on the story.
We demonstrate that this Alu element — inserted into an intron of the TBXT gene — pairs with a neighbouring ancestral Alu element encoded in the reverse genomic orientation and leads to a hominoid-specific alternative splicing event. … the exon-skipped transcript is sufficient to induce a tail-loss phenotype.
This particular Alu element is precisely located to allow the gene variant to arise — as the study’s lead author tweeted:
So it takes TWO to make an impact! The unique alignment of a pair of Alu elements is crucial; without it, neither element would have significance.
One scientist called this event a “strange evolutionary quirk.” Strange indeed. The story is an evolutionary framing of the study’s findings, and it’s cool research, but what is the raw data here? The raw data is simply a genetic difference that has been identified between hominoids and monkeys, and the difference is likely part of what builds the tail-less hominoid body plan. The evolutionary story thus makes a common mistake: it confuses the identification of how some aspect of human development works with an evolutionary explanation of how that aspect of the body plan originated.
Moreover, if this were a true evolutionary story, it’s doubtful that the change alone really would be “sufficient” to cause an advantageous change leading to tail-loss. The technical paper suggests other mutations were probably needed:
[E]ven if the AluY insertion substantially influenced tail-loss evolution in hominoids, additional genetic changes may have acted to stabilize the no-tail phenotype. Such possible hominoid-specific variants in tail-development-related genes may have preexisted in the ancestral genome or occurred after the AluY insertion. Such a possible set of genetic events suggest that a change to the AluY element in modern hominoids would be unlikely to result in the reappearance of the tail.
The technical paper reports that when this gene variant is induced in mice, “mice expressing the exon-skipped Tbxt isoform develop neural tube defects.” Humans can experience this genetic defect as well, and this means that undoubtedly multiple coordinated genetic changes would have been necessary to evolve the tail-less phenotype without experiencing other disease-related problems, such as neural tube defects. The paper continues:
We suggest, however, that the selective advantage must have been strong because the loss of the tail may have included an evolutionary trade-off of neural tube defects, as demonstrated by the presence of neural-tube-closure defects in mice expressing the TbxtΔexon6 transcript.
The language there is interesting: because of the highly deleterious neural-tube closure defects associated with this gene variant in mice, the only way this could change could have been selected was if it provided a “strong” selective advantage offsetting the greatly increased likelihood of disease — an “evolutionary trade-off.” It’s hard to imagine a scenario where such a greatly increased risk of disease would somehow be tolerable simply in exchange for losing your tail. Multiple other coordinated mutations would seemingly be needed to avoid serious birth defects. But when multiple mutations are needed to avoid such deleterious defects, that is highly unlikely under blind evolution and speaks to the need for foresight, planning, and intelligence.
Interestingly, a co-author of the study noted in Scientific American that this evidence shows that Alu sequences “aren’t just cluttering the genome” and are “important”
AluY was an unexpected piece of the puzzle because millions of such elements are present in our cells — and for a long time they were referred to as “junk DNA” because researchers believed they were littering the human genome at random and seemingly with no purpose. “It shows that these elements aren’t just cluttering the genome,” Yanai says. “They’re doing something important.”
Taken as a whole, this tale provides more evidence that when you mess with the “junk,” you mess with its function, and problems arise. And evolutionary stories of how the junk got its function just aren’t adding up. If this story were true, then multiple mutations would be necessary in order to avoid very severe developmental defects, something that points to planning and design, not blind evolution.
Does Junk Give Us Big Brains?
Here’s another example of a questionable evolutionary story about how junk DNA got its function: An article at Live Science says “Humans’ big-brain genes may have come from ‘junk DNA.’” They report, “the genes that enabled human brains to grow large lobes and complex information networks may have originally emerged from junk DNA.” Once again, identifying how things work is not an explanation for how they evolved. The original paper in Nature Ecology & Evolution states:
Human de novo genes can originate from neutral long non-coding RNA (lncRNA) loci and are evolutionarily significant in general, yet how and why this all-or-nothing transition to functionality happens remains unclear.
Don’t miss the words “all-or-nothing transition” — this suggests that transforming the “junk” into functional genes would have required many coordinated changes. Sure, these genes are important for human brain development, but is such a set of coordinated changes to transform “junk” into crucial genes likely to occur by blind evolution? It seems not.
Whatever the answer, this much is clear: junk DNA performs many important functions, and when evolutionists try to interpret the origins of those functions from within their paradigm, the results often fail to stand up to scrutiny.
