The way some evolutionary biologists and some uncritical reporters in the media talk, probabilistic miracles are routine events. Natural selection is omnipotent so it can handle any observation in biology. Since evolution is already a fact, no other explanation or argument is needed. It exists; therefore it evolved.

Genes from Scratch

Take the case of de novo genes. Darwin skeptics argue that the origin of a new gene or protein by chance is so fantastically improbable, it will never happen anywhere in the history of the universe, even under the most favorable circumstances.* No problem, say these evolutionists; since evolution is a fact, it happened. This is a variation on a formulation offered here last year, “To solve a problem, declare it solved.” Watch the faith of evolutionists at Trinity College Dublin when they consider the origin of orphan genes. They report, “Genes from scratch — far more common and important than we thought.”

Over time, genes change via random mutations. Some of these changes result in serious defects and are rarely passed on to the next generations, others have little impact, and others confer significant advantages, which become favoured due to natural selection and end up being passed on to future generations.

This is the main source of genetic novelty and how organisms differ from each other. However, genetic novelty can also be generated by totally new genes evolving from scratch. [Emphasis added.]

They exist; therefore they evolved. Totally new genes evolved from scratch. 

Evolution Supplied the Miracles

These evolutionists are aware that the existence of orphan genes looks like a tough problem for Darwinism. But looks are deceiving.

Orphan genes pose a tough evolutionary problem though. They don’t look like other genes, so where do they come from? One idea is that they can originate seemingly from nothing: over long, evolutionary timescales, a completely novel gene can emerge de novo out of a region in the genome that is made up of junk DNA. Alternatively, with enough time, two ‘cousin’ genes can diverge so much that we can no longer identify the relationship between them. Thus, a gene may at a glance appear to be an orphan without having really emerged de novo.

Surely they are not going to pursue option 1, that orphan genes appeared out of junk DNA? And yet we see them discount option 2, that orphan genes are descendants of genes that diverged long ago. Only about a third of them seem to have come about from pre-existing genes, they reckon. What can they do?

Their method of determining how orphan genes originated is simple. Here it is: they counted them. Since they exist, it must have been a cinch for evolution to create them. Professor of genetics Aoife McLysaght explains:

“To our surprise, at most, around one third of orphan genes result from divergence. So, in turn, this suggests that most unique genes in the species we looked at are the result of other processes, including de novo emergence, which is therefore much more frequent than scientists initially thought.” 

From the junkpile of non-coding DNA, strands with “potential” to be functional exist, waiting for their moment in the light. Once they show some function, natural selection is fully capable of amplifying them into genes from scratch. Assistant professor of computational systems biology Anne-Ruxanda Carvunis has no problem with declaring the problem solved. Evolution is a fact, remember? It’s the Darwin skeptics’ fault if they can’t see the logic.

“Order seems like something that’s hard to achieve, but our results go completely opposite to that. We found that simple order is rampant everywhere in the genome. The propensity to make simple shapes that are stable is already there, waiting to be exposed. De novo gene birth is thus becoming less and less mysterious as we better understand molecular innovation.”

Perhaps a refresher on the difference between order and complexity would help. 

Masters of Fitness

Their paper in Nature Communications shows that the team of 16, including Carvunis and McLysaght, did perform some busy work to argue for the innovative power of evolution. For instance, they found an orphan gene in yeast that was not present in its assumed evolutionary ancestor. Simple answer: its existence served as “confirming the de novo origination of” the gene. Why, all that non-coding junk must be pregnant with “proto-genes” just waiting for their moment to emerge! Once they show a little talent (are “preadapted”), natural selection is sure to make them masters of fitness.

Recent evidence demonstrates that novel protein-coding genes can arise de novo from non-genic loci. This evolutionary innovation is thought to be facilitated by the pervasive translation of non-genic transcripts, which exposes a reservoir of variable polypeptides to natural selection.

These emerging proto-genes, rather than being stumbling beginners, must be even more likely to race to the fitness goal.

Mutations that cause changes to the sequence or expression of established genes are typically constrained by preexisting selected effects—the specific physiological processes mediated by the gene products that are maintained by natural selection. In contrast, emerging proto-genes are expected to mostly lack such constraints because they do not have selected effects. This would leave them more readily accessible to evolutionary changes that have the potential to increase fitness (adaptive changes). We reasoned that this initial potential for adaptive changes would give way as proto-genes mature and the adaptive changes engender novel selected effects, in turn increasing constraints and reducing the possibility of future change. This reasoning is akin to Sartre’s “existence precedes essence” dictum, and predicts that mutations affecting the sequence or regulation of proto-genes should impact fitness differently than mutations affecting the sequence or regulation of established genes. Specifically, proto-genes are predicted to evolve under weaker constraints, and thereby to display a higher potential for adaptive change, than established genes (Fig. 1a).

Who Needs Probability? 

Well. If Jean-Paul Sartre, the famous biochemist, says it, it must be so. There may be no Designer, but there is adaptive potential in junk DNA. And so these proto-genes, like rowdy youngsters full of unconstrained energy, are more likely to increase their fitness rapidly without being bogged down by the hang-ups of their elderly fuddy-duddies. Their essence as functional, innovative genes is established by their existence. Who needs thermodynamics to overcome the configurational entropy hurdle described by Charles Thaxton, Walter Bradley and Roger Olsen in the new expanded edition of The Mystery of Life’s Origin? Genes exist de novo. Therefore, they evolved.**

Listen to Paul Nelson on ID the Future describe the extent of orphan genes, with examples from various genomes. He considers both options evolutionists use for their origins: divergence from common ancestry and de novo appearance.

*On ID the Future, Center for Science & Culture biologist Ann Gauger answers the question, “Is it easy to get a new protein?” with Doug Axe’s calculations about probability of a new protein fold by chance. She also addresses the example of nylonase, which is often put forward as an icon of evolutionary potential for innovation. For an illustration of the improbability of a functional protein, see “The Amoeba’s Journey” from Illustra Media’s film Origin.

**A companion paper in eLife by Vakirlis, Carvunis, and McLysaght (open access), “Synteny-based analyses indicate that sequence divergence is not the main source of orphan genes,” argues that sequence divergence is an insufficient explanation for orphan genes:

The persistent presence of orphans and TRGs [taxonomically restricted genes] in almost every genome studied to date despite the growing number of available sequence databases demands an explanation. Studies in the past 20 years have mainly pointed to two mechanisms: de novo gene emergence and sequence divergence of a pre-existing gene, either an ancestrally present or one acquired by horizontal transfer.

Horizontal transfer “is not known to be frequent in metazoa,” they say. By conservatively underestimating the number of orphans, and overestimating the number originating by sequence divergence, they find the divergence explanation inconsistent with the data. 

As a result, we can be confident that those genes without detectable similarity really are orphans and TRGs, but in turn we also know that some will have spurious similarity hits giving the illusion that they have homologues when they do not in reality.

The eLife paper focuses on refuting the divergence explanation, but does not conclude that de novo appearance is likely. They leave the answer to the “mystery of orphan genes” to future studies:

Overall, our findings are consistent with the view that multiple evolutionary processes are responsible for the existence of orphan genes and suggest that, contrary to what has been assumed, divergence is not the predominant one. Investigating the structure, molecular role, and phenotypes of homologues in the ‘twilight zone’ will be crucial to understand how changes in sequence and structure produce evolutionary novelty.

Image credit: Arek Socha via Pixabay.