Thanks – I downloaded Stegemann & Bock 2006, will read it later today, and compare their data and experimental methods to the antifreeze hypothesis.
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But it’s an observation, not a rationalization. Look at the Lenski experiment. Now, after the fact, each out come is “seemingly unlikely” and “serendipitous”.
Where is natural selection in this analogy?
You don’t seem to really deal with this concept that many more eggs and sperm are produced, and from these a large number but only a fraction develop into eggs, of which many more are born than can possibly survive, and among them are lots of those “junk” mutants, but a few of them actually contribute to survival and reproduction.
And evolution isn’t “searching for Constantinople”, it’s blindly sampling until something that works, is found. You should dispense with this kind of texas sharpshooter fallacy-type thinking.
I could pick out the 600 mutations in one of the LTEE lineages and declare that particular sequence of mutations my “CONSTANTINOPLE”, and invoke all the same arguments you do here for why this couldn’t possibly have evolved.
Of course it should. You have some sort of a priori commitment to the idea that de novo evolution of proteins is too unlikely to happen. But then we find evidence that is most consistent with the model that says this actually happened, and your response is to just stamp your feet and INSIST it’s too unlikely and we must not be understanding the evidence correctly. And then bring up some terrible analogy that has nothing to do with mutations or natural selection.
And your case for this seems to hinge entirely on the fact that one of the authors used the phrase “seemingly unlikely, serendipitous” to describe the series of events that led to this particular outcome. I suppose the key word in that is “seemingly”.
Here’s another point that should cause you to doubt your a priori commitment to the impossibility of de novo protein evolution. There is now mounting historical precedent that putative recently emerged ORFan genes are increasingly discovered to have significantly similar non-coding regions when and if closely related species are sequenced.
This evidence will only continue to increase in the future. As more and more cases like the AFGP study here are published, and key predictions of de novo protein evolution from non-coding DNA is elucidated, your continued resistance will just continue to look ever more absurd and denialistic.
That is a crappy cop out. The kind of evidence we are looking at is what is expected on the hypothesis that ORFan genes evolve de novo from non-coding DNA. There’s no reason to expect that these patterns of similar gene regions should exist at all in closely related fish without this protein coding gene on any other hypothesis.
You can’t just hand wave this away by saying we don’t understand all things about biology. No, we don’t, but we don’t have to understand all things about biology to understand the concept of testing predictions hypothesis by comparing them to data, or by comparing the fit, parsimony, and explanatory power of models, with observed data.
I can only repeat myself:
If the hypothesis is that a a protein coding gene relatively 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 non-coding 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 absence of all these patterns.
What could a design hypothesis even look like here that isn’t just a straight up copy of the expectations on evolution combined with some ridiculous and ad-hoc rationalization that this is just what the designer wanted?
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I see I was scooped.
I suppose.
It also has that lovely bonus of describing the reality we inhabit accurately. The outcome Lenksi experiment is wildly improbable by the same computations used to say the flagella is evolved. Yet it happened. Why then should we trust these calculations with flagella? We shouldn’t.
Rum the argument is not about probability its about using probability to test if the proposed mechanism is a reasonable hypothesis. In the Lenski case the results look completely in line with known evolutionary mechanisms.
The design side would say the origin of the flagellar motor is out of the reach of current evolutionary mechanisms due to probability constraints.
This question may have already been asked, but what exactly would satisfy you (@Cornelius_Hunter and @pnelson) that an event such as the appearance of the antifreeze gene actually happened?
Obviously, describing a step-by-step sequence of mutations is insufficient, because every such sequence can be dismissed as “improbable” by you if it requires more than a couple of steps.
So, are you claiming that any such sequence of mutations renders evolution impossible (or at least extremely improbable)? If not, can you outline for me the evidence that a paper like the one in the OP would have to lay out to convince you?
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If we know the starting sequence, the ending sequence and then can test if there are sequences in the middle that can help cold water survival you could then test for the likelihood that an adaptive path was formed from random genetic change. To really test this is a big job.
It is certainly possible to estimate the probability of a random process with selection finding an irreducible complex structure given the data generated so far in the scientific literature. The problem is getting both side to agree with the assumptions.
It certainly is, and you wouldn’t be convinced until this experiment is performed for all functional differences between all species?
I am leaning toward this being a Darwinian adaption but to be fully convinced requires experimental validation.
Were not in the game of proving negatives. Is the evolutionary scenario reasonable based on the observed evidence?
I was asking about accepting unguided evolution in general, not for this specific example. Would you require literally every functional change to be validated in the way you describe before you would be satisfied that ID is unjustified?
It’s not proving a negative to supply an accurate probability. It’s basic probability theory which you seem unaware of also.
Of course it is with all the consilient evidence taken it total. Is your personal incredulity based solely on your scientific ignorance a reasonable position?
The more data the higher confidence. As I said there is an untested hypothesis that this is a Darwinian adaption. I would not doubt that it is testable and true but I only have moderate confidence in this conclusion until I see the data. If the starting and ending sequence only were separated by 2 mutations my confidence would be a lot higher.
It’s not untested. You just refuse to accept the supporting evidence due to your religious beliefs. Face it Bill, nothing short of a time machine letting you watch every mutation in every generation would convince you, and even then you’d find some excuse to make.
Explain the test in your own words.
Rumraket already did above. Not our problem you refuse to learn.
Several contributors to this thread have invoked the biasing role of natural selection to raise the probability of this scenario. I would encourage them to look again at the original paper (open access, link in OP), in particular, this summary of the hypothesis:
Gadid AFGP Evolved from Entirely Nongenic DNA.
Fig. 4 summarizes the forgoing deductions on the noncoding origins of the essential AFGP sequence components and the possible molecular steps in the evolutionary transformation of these components into a complete new functional AFGP. The AFGP founder structure (Fig. 4A) existed in the gadid ancestor as a short noncoding genomic sequence comprising a segment (∼240 nt) with latent-coding exons (bronze segments) that have the potential to form a peptide sequence with properties for a secretory signal. The adjoining 27-nt GCA(Ala)-rich sequence (cyan segment) contained multiple nested 9-nt elements, any of which could become the three codons for the AFGP tripeptide (Thr-Ala-Ala) building block through a 1-nt substitution. Chance duplications of this ancestral 27-nt GCA-rich sequence produced four tandem copies (Fig. 4B). One of the 9-nt AFGP tripeptide-coding elements in the midst of the four copies likely underwent microsatellitelike duplications producing a budding ORF for the repetitive AFGP tripeptide cds, which began spreading the two pairs of 27-nt GCA-rich duplicates apart to the flanking positions (Fig. 4C). A putative translocation event in the last common ancestor of AFGP-bearing gadids moved the hitherto unexpressed AFGP precursor to a new genomic location that fortuitously contained a TATA motif thereby enabled transcription (Fig. 4D). Concurrently or subsequently, a 1-nt frameshift deletion in the second 5′ 27-nt duplicate likely occurred and served to link the latent cds for the SP and the downstream AFGP (Thr-Ala-Ala)n repeats in a single read-through ORF. Expression and secretion of the nascent antifreeze protein became possible (Fig. 4E). The smallest (and often the most abundant) functional AFGP isoform (AFGP8) comprises only four tripeptide repeats (10), which could be achieved through only two tandem duplications. The fledgling antifreezing protection could, therefore, augment fitness in the individual at the onset of northern hemisphere marine glaciation. Subsequent intensification of environmental selection pressures likely drove the intragenic (Thr-Ala-Ala)n cds expansion forming large AFGP polyprotein genes (Fig. 4F) as well as ad- ditional whole gene duplications. The result manifests in the multigene family of AFGP polyproteins (SI Appendix, Fig. S3) and the robust antifreeze activities the AFGP-bearing gadids possess today (10, 13).
Until step 4E, no selectable function exists. (How the cod were surviving in freezing seas prior to this raises a separate question, but, as is typically the case for post hoc selective scenarios, the environment can be invoked deus ex machina as needed.)
Thus every event prior to step 4E must count on genetic drift – i.e., chance. Zhuang et al. indicate this by their word choices, which I have noted in bold in the cited passage.
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For the anti freeze protein? Why don’t you just put your own words around it and show you have at least some comprehension of these arguments.
Nice dodge.