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Hey, friends —

I was looking over the comments I get here on YouTube, and there were a few from a persistently obnoxious creationist going by the name @ThatGuyBuster. He pops up now and then to shout non sequiturs and silly objections to evolution, and while I know nothing is going to get through to him, I figured I might poke back and explain something basic to everyone.

So he responded to one of my videos with this:

Stop lying PZ. There is no mechanism evolution has that builds news systems and you know it. There is not even an hypothesis that attempts to explain the creation of useful De Novo proteins. I wish I could take your class so I could stand up, challenge you in front of your students then expose your lies. All we see is adaptation by loss of information. Pathetic

Creationists love to assert that there is no mechanism for well understood evolutionary processes. It’s an example of projection, because they have no mechanisms at all for creation, other than that an invisible inaudible impalpable god did it while humans weren’t looking. I replied briefly in a comment.

If you were in my class, I wouldn’t have to say a word: my students would chew you up.
Of course there are known mechanisms that can vary proteins and create them de novo.

Yeah, because he brought up the classic Big Daddy scenario — he thought he knew so much more than a college professor who teaches evolutionary biology that he could raise his hand and clobber me with his cluelessness. He couldn’t. I’ve been in this situation before, with smarter critics than @ThatGuyBuster, and no, they’re usually so ignorant of basic biology that they can’t even begin to address a specific question.

My students wouldn’t be in an evolutionary biology class unless they had taken general chemistry, organic chemistry, cell biology, and molecular biology, with at least an introduction to biodiversity, and some of them would be taking ecology concurrently. They know the science. They might be stunned into silence by such a demonstration of stupidity by a person intruding on a class they are not qualified to take, and by the sheer confident ignorance on display.

But that’s a creationist for you — profoundly stupid and totally unaware of it.

He continues:

Ha Ha Ha…..you can’t debate me. You cannot be this clueless. There is not even an hypothesis that even attempts to explain the mechanism that creates useful De Novo proteins.

I have to repeat that: There is not even an hypothesis that even attempts to explain the mechanism that creates useful De Novo proteins. Not even an hypothesis. Jesus. @ThatGuyBuster hasn’t even tried to look for one, and instead just repeats the bogus claims of numerous creationist preachers and the Discovery Institute.

So I fired up PubMed, searched for “mechanisms of de novo protein evolution”, and 2 seconds later it came back with this 2023 review paper, Evolution and implications of de novo genes in humans, by Broeils and others (its from the Netherlands, I have no idea if I pronounce his name correctly. Sorry.) It was super easy, barely an inconvenience. I sure wish creationists knew how to read.

This is the abstract.

Genes and translated open reading frames (ORFs) that emerged de novo from previously non-coding sequences provide species with opportunities for adaptation. When aberrantly activated, some human-specific de novo genes and ORFs have disease-promoting properties—for instance, driving tumour growth. Thousands of putative de novo coding sequences have been described in humans, but we still do not know what fraction of those ORFs has readily acquired a function. Here, we discuss the challenges and controversies surrounding the detection, mechanisms of origin, annotation, validation and characterization of de novo genes and ORFs. Through manual curation of literature and databases, we provide a thorough table with most de novo genes reported for humans to date. We re-evaluate each locus by tracing the enabling mutations and list proposed disease associations, protein characteristics and supporting evidence for translation and protein detection. This work will support future explorations of de novo genes and ORFs in humans.

To translate: many de novo genes have been identified, thousands of putative sequences in humans, but I should qualify that — relatively few that meet the criteria of regulated, transcribed, and translated genes, and I’ll get to the specific number shortly. We don’t know what most of them do, and it’s quite likely that most of what we’re seeing is likely to be spurious expression that doesn’t do anything, but we do know how they originate. Some of them do modify cellular physiology, and often the changes are associated with disease.

However, they are trivial to generate — the paper estimates over 7000 human ORFs at the time of its publication, but relatively few of them are translated, so they don’t make proteins, and most of them can be expected to decay and disappear over a few generations. Easy come, easy go. @ThatGuyBuster is correct that few of them make useful de novo proteins, but that’s OK, we have a mechanism for that, too. It’s called natural selection.

The most important thing here is that the paper discusses mechanism of origin, that thing that @ThatGuyBuster says we don’t have. Let’s dive into that mechanism, which is nicely illustrated in a diagram.

Here are the mechanisms that drive gene birth in humans…and also in lots of other organisms as well. If you’re not a creationist, you’re probably already familiar with these.

First is gene duplication, where a chunk of a chromosome is accidentally duplicated, producing two copies of a particular gene, freeing one of them to gradually mutate away from its original function. The example I use in class is the antifreeze gene in antarctic fish. A pancreatic enzyme was replicated perhaps 30 million years ago, and while one copy retained its original function as a digestive enzyme, the other copy was only partially expressed, producing a short peptide that was secreted into the circulatory system, where it acted as an antifreeze molecule.

Another kind of gene duplication is retroposition, where a gene is copied to a new location in the genome. This can also be a means to introduce evolutionary novelty, and it also has the possibility of putting the gene into a novel regulatory environment, changing its pattern of expression. A curious feature of retroposition is that the majority of genes identified as originating by this mechanism is that they are expressed in the testis. The testis is a hotbed of exploratory variation, which I promise I’ll return to.

The third mechanism in the diagram is gene fusion. This is a process that adds new capabilities to a gene. The example I use in class is the receptor tyrosine kinase, RTK — it’s a protein that couples a tyrosine kinase, an enzyme that phosphorylates and dephosphorylates proteins, with a cell surface receptor, so it can act as a key component in a signaling cascade. RTKs evolved about a billion years ago in the ancestor to all animals, and is not found in plants and bacteria, so it was an important evolutionary step.

The final mechanism is de novo birth. This one is easy to do — most of the human genome is junk, so a great big scrapyard of nearly random sequences and pseudogenes. All it takes is, on the left under transcription first, the spurious transcription of DNA sequences, to produce a pool of RNAs that might have useful activity. Or, on the right under ORF first, a mutation that produces a start codon in the junk (all that takes is a methionine triplet) with an associated stop codon. This is an elementary chance event that can happen spontaneously. As you might expect, most of these ORFs are useless, so they are not positively selected, and most of them will be lost, eventually. If any of them have an advantageous effect, they may be retained.

The paper mentions that there are over 7000 of these ORFs known so far, but only a handful that have demonstrated function. A number of them have a deleterious function, and that’s where the testis comes in.

During spermatogenesis, the organism is trying to pump out a large number of copies of this special cell type, and cells are dividing rapidly and also being processed in a long and complex process. One aspect of sperm maturation is that the cells’ chromatin is opened up — it’s like you’ve got a car assembly line, and you leave the hoods open wide for a prolonged time because so many mechanics have to get in there and add their special tweaks. What this means is that sperm cells are even more prone to spurious expression, and some of the proteins expressed may be beneficial to the sperm, if they prevent apoptosis and promote cell survival. At this stage of development, all the organism cares about is generating more gametes. The testis may be expressing more ORFs as a kind of “hail Mary” process to amplify gamete production, or just as a chance product of less regulated gene expression.

The downside, though, is that changes that increase sperm production and survival may not be so beneficial in the adult organism, where stability and uniformity are more important. Patterns of gene expression that inhibit apoptosis or promote cell division can enhance cancer cell survival, too.

So we do have hypotheses that explain the creation of useful De Novo proteins — even better, we have observations, measurements, and experiments that demonstrate where they come from and how they work. @ThatGuyBuster strikes out.

He had to throw out one last comment, demonstrating his delusional vision of how his appearance in an evolutionary biology class would go, and this one is even more ridiculous than his prior fantasies. It’s also derivative and routinely debunked.

I would stand up and say simply that a 100 amino acid protein has 20^100 possible configurations and one works. There is no mechanism that can randomly get the correct length and configuration. And you would stammer and melt down….Creation Myths can’t do it either. I say you apologize to your classes for telling them lies

Oh man, that is so familiar. I think I first heard a version in the 1980s (I feel so old).

Look, there is no one configuration for a protein, nor is there a “correct” length. Would you tell a class full of writing students that the correct length of a paragraph is 100 words, and there is only one correct subject and verb for each sentence? Therefore writing new books is impossible? Nonsense.

I’ll just refer you to Ian Musgrave’s article on Lies, Damned Lies, Statistics, and Probability of Abiogenesis Calculations, in which he dissected the fallacies in creationist statistical reasoning.

That was published in 1998. I wouldn’t melt down if a creationist tried that argument on me…I’d just laugh. I’m confident that Creation Myths would be unfazed by that tired old stupidity, too.

Anyway, that’s it for @ThatGuyBuster. I haven’t blocked him on YouTube, since he’s so predictably silly and wrong, he’ll probably be back with more laughable excuses. I might appreciate him more if he signed up for my Patreon — patreon.com/pzmyers. But only cool people sign up for that, like these named supporters.

Subscribers to my patreon get occasional spider photos and accounts of the shenanigans in my lab, which are unfortunately rare lately while I’m focused on convalescence. I’m getting better, though, as you can see from this short adventure when I wandered into my yard during a midwestern rainstorm. I can walk, sort of! We’ve got monarchs growing all over the place!

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Luuk A. Broeils, Jorge Ruiz-Orera, Berend Snel, Norbert Hubner & Sebastiaan van Heesch (2023) Evolution and implications of de novo genes in humans. Nature Ecology & Evolution volume 7, pages804–815 (2023)