Biola's OrfanID Research

Continuing the discussion from ID Lacks a Punch Line:

This is an important point. Quality computational work is sufficient to as a starting point, in my opinion.

@pnelson, can you please give us a link to this website? I’d love to take a look, but it cannot be found by google. Also, I am a bit confused because OrfanID is a term used by another group on this website:

I am also a bit puzzled, because Taxonomically restricted genes do not actually demonstrate ID in any meaningful way. Yes, I’ve read your paper with Buggs on this matter. Why do you think taxonomically restricted genes are evidence (1) for ID, or (2) against common descent/evolution? I just don’t get it.

Maybe @Agauger or @bjmiller can help clarify.


I have long suspected that there is a massive misunderstanding at the foundation of this debate, the equivocation of the terms gene and genome. Are there genes humans have that chimps do not? It appears that this is the case. However, do chimps have homologous DNA for that human gene? In many of the cases I have looked at, they do.

Genes are transcribed sections of DNA. When we say that humans have genes that chimps do not it means that there are sections of the human genome that are transcribed in humans while the same stretch of the chimp genome is not trascribed. Both species have homologous DNA, with a few mutations differing between them, but only one species may have a gene in that location.

Once you clear up this misunderstanding, many of the ID articles lose a lot of their punch.


Isn’t it obvious? He has a prior theological commitment to the proposition that de novo evolution of functional genes can’t happen. So when he finds evidence of a taxonomically restricted gene, instead of that constituting evidence against his theological commitment, he takes it as disproof of evolution.

Showing that a highly similar but unexpressed genetic locus exists in closely related species, and that a phylogenetic analysis of such sequences in a more diverse group of such closely related species also fits perfectly with the hypothesis that this locus has been incrementally evolving into the expressed locus in the species with an Orfan gene, is dismissed because of that very same prior theological commitment.

Hunches by individuals from past generations of scientists that this can’t happen are invoked as strong arguments in support of the prior theological commitment. Rather than letting the evidence speak for itself, the evidence is all interpreted through the lens of a previously formed belief about what can or can’t happen.

When one is operating by conclusion first, evidence becomes incapable of changing one’s mind. People who think like this have basically become conspiracy theorists. A phylogeny indicating incremental evolution of a de novo protein coding gene from an unexpressed noncoding locus must have been planted by the intelligent designer.

Yeah, sure, it looks like it evolved over time and became a protein coding gene in this species, but that’s just a fatamorgana. Who knows what the designer was thinking? But because I know, I just really really know that this can’t happen, the designer must have just made it look like it by accident, or because he’s got a bit of a sense of humor. Those other species with a similar but unexpressed locus? That’s just there because, well… the designer is a funny guy, and a bit of an artist.

How is this any different from saying that pictures of a round Earth are doctored by NASA?

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Nothing demonstrates ID for you, Josh. You ruled it out categorically a long time ago, and continue to do so. Thus there is little point in me trying to explain the connection. Sorry.

The site is a beta tester for the same authors on the poster (Richard Gunasekera et al.). I don’t think the site is operational at the moment.

I think you misread me @pnelson. Happy to explain further if you like. Remember, I affirm that God created us, and in this sense he designed us all.

Oh, great. Thanks for letting us know.

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Yes, but this is not an empirical finding, in the sense that you want ID’s connection to orphan and taxonomically-restricted genes explained.

I would be curious as to why you find human orphan genes such a problem. Let’s take this hypothetical example:

AAGTTACCGATAATGACTTATGACCTTT  ---transcribed human orphan gene
AAGTTACCGATAAT  CTTATGACCTTT  --orthologous chimp DNA, not transcribed

The two sequences are separated by a two base indel. The human orphan gene shows evidence of function while the orthologous section of the chimp genome is not trascribed, and the orthologous sections of other ape genomes also have similar sequence that is not transcribed and does not show evidence of function.

So how is this a problem for the theory of evolution? It would seem to me that this is extremely obvious and strong evidence for a two base indel creating function in a section of the genome that previously lacked function. Can you tell me why this is wrong?

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It’s not wrong. Unfortunately, as a young research field, the study of orphan and taxonomically restricted genes suffers from ambiguous terminology: one investigator’s orphan may be another’s ortholog. Instances of synteny across species, where one taxon possesses a functional open reading frame (ORF), and the other, a disrupted ORF (as in your example) may still, depending on standards of annotation, be described as “orphans” when they aren’t really orphans at all.

We treat this problem in Chapter 12 of this book; I’d be happy to provide the final version MS to anyone who is interested (contact me at

From what I have read, my example is a real orphan gene because chimps lack that gene. A gene is a contiguous stretch of transcribed DNA, at a minimum. If DNA is not transcribed then it is not a gene. Therefore, two species can lack a shared gene but still share orthologous DNA at that locus. When biologists look for genes they use techniques like RNAseq, not sequenced genomes.

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The main problem with that definition is that most of the human genome is transcribed, though most of it is transcribed rarely. (If nothing else, ENCODE showed this.) I think you have to add something about performing a biological function. And of course it’s also generally supposed that promoters are parts of genes, though they are not generally transcribed.


A post was split to a new topic: I am Open to Design Arguments of a Sort

All good points. I sometimes skip over the important bits, so it is always good to have someone fill in the relevant details. Here is a relevant abstract:

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