They’ve been called selfish. They’ve been labeled as parasites. They’ve been demonized as viral interlopers clogging up our chromosomes with useless copies, taking advantage of our replication mechanisms to perpetuate themselves. These characterizations of retrotransposons, retroviruses, and transposable elements (TEs), also called “jumping genes,” fit the Darwinian picture of entities in it for themselves, getting all they can at the expense of others, in a mindless race for fitness and survival. Recent studies indicate a changing attitude toward one of design. Though it’s too early to tell, TEs may turn out to be a Cinderella story — in line for restoration to the status of essential parts of our genomes, our health, and our lives.
“Myelin Is a Gift from Retroviruses”
Michael Denton has written about the big advantage myelin gives to neurons. “This design allows for what is termed ‘saltatory conduction,” he writes, “where the nerve impulse, instead of travelling sedately and continuously down the axon, jumps from node to node, vastly increasing the speed of transmission.”
Now John Hewitt writes at Phys.org that “Myelin is a gift from retroviruses.” It’s not the only gift from these “opportunistic” elements that “make up over half our genome” —
Functional retrotransposons have been progressively implicated in all manner of things neurobiological.The maintenance of stem cell identity and mosaicism, incidence of neurological diseases and fusion of cells in the brain by sundry spike proteins are all now understood to be jobs for transposable elements. Writing in the bioRxiv preprint server, researchers have now discovered that vertebrate myelin likely originated when retrovirally derived elements inserted in the genome at key positions to trigger massive expression of their signature protein, Mbp (myelin basic protein). [Emphasis added.]
Hewitt continues to cast these TEs into evolutionary roles, but a design interpretation becomes possible when we compare his story with the fate of the junk DNA story. First there were a few examples found of function in the junk. Those numbers grew, to where now some believe all noncoding DNA is functional. In a previous article at Phys.org, Hewitt had admitted that the ENCODE results startled scientists into reconsidering the role of TEs. That project along with earlier studies showed that TEs were being translated, and appeared to be active in somatic cells, not just in germline cells.
Alongside these prodigious announcements was a parallel observation that much more of the genome is actually transcribed than had formerly been appreciated. Rather than just a few genes being expressed here or there, studies revealed that upwards of 80 percent of our entire genome is likely translated into some kind of RNA. With half a genome’s worth of retroviral additions, many of these transcriptions are undoubtedly retrotransposons one sort or another.
TEs: Enemies, Frenemies, or Friends?
More intimations of a change in attitude about transposons appeared this year. At The Scientist, Christie Wilcox wrote about “Adapting with a little help from jumping genes.”
TEs, also called transposons or jumping genes, are often cast in a negative evolutionary light. And there is a reason for that: when these sequences insert themselves into new places in the genome, they can mess up genes or alter their expression. They’re sometimes called junk DNA, or worse, genomic parasites, the idea being that they would mutate their host genomes into oblivion if they weren’t almost always silenced by epigenetic modifications such as methylation. But recent research is illuminating the intricacies of TE function and adding texture to this simplistic model.
Wilcox quotes scientists who relate their changes in thinking. The trend these days is to see transposons less as “parasites” and more as “symbionts” that can cause benefit or harm, depending on where they land in the genome. For instance, by regulating genes near to their insertion points, they can “preadapt” an organism to changes in the environment. Here’s an interesting case involving one of evolution’s favorite icons, the peppered moth:
Arguably the most immediate and dramatic impacts TEs have on genomes occur when they insert into active genes. They can jump into coding regions, altering protein sequences, or they can insert into noncoding regions and alter gene splicing or expression. This is what happened in peppered moths, when a 22-kb TE inserted into the cortex gene and led to overproduction of melanin, turning dark the normally lightly bespeckled moths and improving their survival in polluted environments.
Notice the wholesale change in the story. (This is assuming that the dark moths land on blackened tree trunks, which as Jonathan Wells has documented, is factually incorrect; we’re just using Wilcox’s opinion as an indication of a change in attitude.) Instead of positing a random single-nucleotide mutation being selected blindly in the old neo-Darwinian way of thinking, a sequence of coded information is now used in the explanation. A Darwinist would have to argue that code able to help the moth just “happened” to pre-exist and landed in the right spot of a gene to turn it dark. It’s possible to imagine that, but more difficult to support as a blind process. Wilcox shares another case of preadaptation by a transposon:
Unlike point mutations, some TEs come preloaded with genetic motifs that may affect the expression of nearby genes. Certain populations of Drosophila carry the TE insertion FBti0019386, for example, which contains transcription factor binding sites that are activated during a bacterial infection and that increase expression of the immune-related gene Bin1. Flies carrying FBti0019386 are more likely to survive inoculation with a pathogenic strain of Pseudomonas.
One other example is that TEs may become activated by stress. This could indicate that they stand ready to assist the organism in hard times by regulating gene expression.
An Evolving Picture
Like Hewitt, Wilcox fits the new findings into an evolutionary narrative, but that slant may be difficult to maintain at the rate discoveries are coming in. Readers should recall how similar attempts were made to cast junk DNA and vestigial organs in Darwinian terms. In the end, it was function that won out, and design explanations were vindicated. Design theorists may be once again ahead of the curve in explaining these mysterious pieces of mobile code — mysterious, because questions remain that will continue to challenge both approaches:
“You can find transposable elements in virtually all the organisms that have been studied [genetically], from bacteria to eukaryotes,” notes evolutionary biologist Josefa González of the Spanish Research Council (CSIC). But while TEs are nearly universal throughout living organisms, their prevalence varies widely. In some organisms, TEs dominate, accounting for up to 90 percent of the genome, while in others, transposable elements make up only a fraction of the entire genetic code. When abundant, TEs can grow the size of the genome to enormous, unwieldy proportions that continue to baffle scientists.
The picture of TEs is changing from “selfish opportunists” to “occasional partners in regulation.” Basically, TEs are being described as larger versions of random mutations occasionally found to persist by natural selection. But can any Darwinian narrative be sustained, when the point of Darwinism is to imagine adaptation by sheer dumb luck? Why would a stretch of code many kilobases long, existing simply for its own replication, just happen to be useful to another organism?
“If Something Works”
Recall Paul Nelson’s maxim, “If something works, it’s not happening by accident.” Humans have been reproducing since their appearance on earth. And yet still today, many healthy babies are born, with all their parts in working order, and many of those grow to be strong and athletic adults. If TEs making up half the human genome were so selfish and parasitic, how could that continue for many hundreds or thousands of generations with genomes filled with parasites?
For over a decade, contributing authors at Evolution News have hinted that endogenous retroviruses and other mobile elements might have functions (McLatchie 2012, Luskin 2015, Hunter 2017, Luskin 2019). Yet questions remain about their quantities, distributions, and effects in organisms. Are the targets where TEs insert themselves random or purposeful? What happens when they cause disease — could those cases be due to broken processes? Why do proportions of TEs vary so widely between organisms? Is there a pattern in the distribution somewhere? The subject of gut biota has undergone a major rethink over the years; now, scientists understand that we have a profoundly necessary and complex relationship with our bacterial partners; sometimes they cause problems, but usually the relationship works. Could there be an analogous relationship with our TEs?
The easy way out is to call it random. Now that pro-Darwin establishment scientists and reporters are increasingly admitting that TEs are not useless or selfish after all, design theorists can take a strong lead in proposing testable hypotheses that consider foresight and software engineering principles. Code that can jump around is code nonetheless.