4 posts were split to a new topic: Comments on Hunter: Details of Protein Evolution
It’s a very interesting paper, but Hunter is full of crap as always. His entire post amounts to these few sentence:
Why does a repeating genetic sequence “strongly suggest” that it “evolved from repeated duplications?” What experiment revealed this truth? What evidence gives us this profound principle? The answer, of course, is that there is none. Nowhere do the evolutionists justify this claim because there is no empirical justification.
There is no scientific evidence for it. Zero.
So, is that true? No. So what is the evidence?
This is bona fide evidence:
Gadid phylogeny and AFGP gene/homolog structures.
The phylogenetic tree of Gadidae is a congruent cladogram derived from Bayesian and maximum likelihood trees using complete ND2 gene sequences ( SI Appendix , Fig. S1). Light blue branches indicate lineages of the Gadinae subfamily. The two gadine subclades containing AFGP-bearing species (red vertical bars), their most recent common ancestor (blue dot), and the emergence of the AFGP trait are as indicated. The three AFGP-bearing species (AFGP+) and four AFGP-lacking species analyzed in this paper are shaded in blue and yellow, respectively. The structure of their AFGP gene or nongenic homolog is shown to the right. Gray and purple shaded areas indicate homologous regions. Cyan segments are sequence repeats. The dark blue segment is a repetitive AFGP cds or AFGP-like sequence.
One would have to explain why a phylogeny such as this is evidence, but you’d never succeed in convincing a propagandist like Hunter of that. If he were to ever accept a phylogeny as evidence, all of ID would collapse.
Comments on Hunter: Details of Protein Evolution
We had @Cornelius_Hunter here once, but he did not stick around. Maybe he will come back. At that point, and only at that point, it might be interesting to engage this article.
Well I hate to be the cause of any heartburn out there.
Welcome back @Cornelius_Hunter.
If you so choose, you are welcome to make your case for that article here. And people can engage with you on it if they see fit. Please let the @moderators know if there are any issues that arise.
The phylogenetic reconstruction is not evidence for the claim that: the fact that the TAA sequence is repeating “strongly suggests” that the underlying gene “evolved from repeated duplications of an ancestral 9-nucleotide threonine-alanine-alanine-coding element.” These are different things.
I didn’t know that.
Don’t tell me you’re unfamiliar with the extensive literature on trinucleotide repeat expansions?
Your claim was that the phylogenetic reconstruction serves as evidence for the paper’s claim. That doesn’t make sense to me. As for trinucleotide repeat expansions, you seem to be confusing nucleotides and amino acids.
Really? I don’t think so…
Yes, you are confusing nucleotides and amino acids. Trinucleotide repeat expansions deal with three nucleotides repeating, not three amino acids.
Hi Dr. Hunter,
As far as I can tell, the real issue is “how should scientists infer unobserved events?”
Since we are of course not omniscient, we humans are always inferring unobserved events. The forensic scientist did not observe the defendant pull the trigger–that event is unobserved for the purpose of court proceedings. However, the scientist does note that the murder weapon was recovered at the scene and correctly handled with a chain of custody, that DNA matching the defendant with a very high likelihood was recovered from the weapon, and that gunpowder was on the defendant’s hands when he was arrested 2 minutes after the shooting. Given what we know about human behavior and the way events typically happen, is the conclusion that the defendant committed the crime a “just so story,” or is is probable enough that it should be accepted as the most likely explanation?
In other words, just because a linked set of events was unobserved doesn’t necessarily mean an explanatory narrative is a “just so story.” Would you agree with that generalization?
Just as a forensic scientist makes inferences based on observed “rules” of human behavior and scientific phenomena to unobserved events, a biologist makes inferences based on observed “rules” of genetics. Biologists have identified various kinds of genetic mutations and have at least a rough idea of their probability distribution, for example. And even an ID proponent like Behe concedes that multiple mutations can accumulate (or coincide) in order to produce an important change of function (chloroquine resistance) in Plasmodium falciparum.
You asserted in your blog post (which I read) that Zhuang’s conclusion is a “just so story.” However, to me it seems consistent with observed genetic science in the same way that the forensic scientist’s conclusions in my hypothetical are consistent with well-known human behavior and scientific phenomena. So to me, Zhuang’s conclusion does not seem at all like a Kipling tale about how the giraffe got its neck.
Now if you were to perform a MCMC over Zhuang’s explanation and discover that the probability of reaching the final state was 10e-2500 (for example), that would definitely give me pause. Assertions come easy, but probabilistic analysis takes work and merits a close examination. If you were to perform an MCMC or some similar analysis, I would certainly pay attention to whatever you publish. Without domain expertise, I would of course have to rely on the critical eye of biologists to assess whether your model and probability tables made sense. But I would do my best to give such an analysis a “fair shake.”
It goes farther. Have we ever “observed” a mutation by the criteria @Cornelius_Hunter expects? In every case I know about, we are always inferring mutation after the fact, from experimental data that is far short of a “direct” observation. This includes, for example, in Lenski’s experiments.
Actually I said nothing of the sort, and you still seem to be confused about the problem. So let me explain again. The paper makes the claim that observation A is strong evidence for conclusion B, where:
A = The TAA sequence is repeating (many times).
B = The underlying gene “evolved from repeated duplications of an ancestral 9-nucleotide threonine-alanine-alanine-coding element.”
The paper then builds on that assumption, from there on, and it is fundamental to the results. It is easy to see from a little molecular biology knowledge, that this claim is false. A does not make B compelling. It is not strong evidence for B. In fact, it is a bit of a stretch, though certainly not impossible. There is a big difference between (i) strong evidence, and (ii) a possibility. This claim is motivated by evolutionary thinking. In other words, what is being claimed as an obvious, compelling, conclusion is in fact theory-laden.
I’m not counting on much agreement here, but the fact that something as basic and fundamental as this is causing confusion is very important.
Because that’s how you gather evidence for an evolutionary hypothesis about past events. If the hypothesis is that a a protein coding gene sufficiently recently evolved from non-coding DNA, then a key prediction of this hypothesis is that if there are closely related species without this protein coding gene, they should have a highly similar non-coding region to the ORF in the species with the protein coding gene.
Furthermore, if this evolutionary and mutational emergence of a protein coding gene happened gradually in some particular clade, then it should be possible to find that related species derived from increasingly more basal branch points also have increasingly dissimilar noncoding regions.
This is exactly what is found and which we can see in the elucidated phylogeny. And we could have found the opposite, or the absense of all these patterns.
If you have a hypothesis that fits this distribution of data better, let’s hear it. Why is it the designer keeps designing new genes that look suspiciously like noncoding regions in closely related species?
As for trinucleotide repeat expansions, you seem to be confusing nucleotides and amino acids.
Yes I should have said simple sequence repeats, aka micro/mini-sattellite DNA. These kinds of repetitive DNA stretches, such as 9-nt regions are very prone to tandem duplications both by strand slippage and unequal crossover by homologous recombination, not to mention prone to suffering SNP’s. That’s why they’re used in paternity testing after all. Again this fits very well with the observed variable lengths between individual fish species carrying both the ORF for the AFGP and the related species carrying the non-coding region.
All of this is evidence that a protein coding gene evolved de novo from non-coding DNA.
Agreement is not the goal. Understanding is the goal. If you move us forward this way, many of us would be thrilled.
@Chris_Falter I hope you can help us too.
Yes it is. It actually is. This kind of microsattelite DNA is established as very prone to duplication, so much so that it often varies from parents to offspring.
Additionally, the fact of it’s significant variability in length between closely related fish species just lends additional support to this phenomenon.
Also, this is just one piece of the evidence. This evidence is for how the repeat sequence grew in size between different species. The evidence for the ORF’s origin in non-coding DNA is the phylogeny of similar sequences in closely related fish species, and it’s increasing dissimilarity with distance of relatedness.
If this isn’t evidence for the historical emergence of a de novo protein from non-coding DNA, then what the hell would such evidence even have to look like?
What should closely related species DNA actually look like on that hypothesis, if not something like this?
Can you even answer such questions, or are you just stuck in “I don’t know what it would look like but I just know this isn’t it”?
Just as a forensic scientist’s inferences from observed data (DNA on the gun handle, gunpowder on the hands, proximity to the crime scene in time and space) to an unobserved event (the defendant committed the crime) are theory-laden.
You are missing the point. You are arguing from evolution. The paper doesn’t do that. Instead, it makes a much broader, more important, claim, and that is the point. Quote:
The paper goes on to make more of these claims. As for your argument from evolution, you offer supporting reasons for it. Fine, but that is a different claim, with its own problems. Regarding AFGP, it leads to teleology and enormous serendipity, as displayed in the paper. For example, it states that AFGP is an example of “evolutionary ingenuity.”
In the press release Cheng admits that AFGP evolution “occurred as a result of a series of seemingly improbable, serendipitous events.” For “not just any random DNA sequence can produce a viable protein.” Furthermore, in addition to the gene itself, “several other serendipitous events occurred.” The DNA was “edited in just the right way,” and “somehow, the gene also obtained the proper control sequence that would allow the new gene to be transcribed into RNA.”
Serendipity/Just-So is prevalent in evolutionary thinking. It is a monumental problem.
Now you are walking back the claim. Sure all of that is “evidence,” of course. It is also a meaningless claim.