Another day, another round of Bill repeating the same demand he’s already seen answered several dozen times. Ho-hum.
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gpuccio explicitly told us the reason of these 400 millions years. Here what he said on this issue at his first post here at PC:
« How long must the time window be so that sequence homology may be considered a good estimator of FI? I would say at least 200 – 400 million years. Better if 400. Why? Because that’s more or less the time window that is usually associated with “saturation” of synonymous sites, IOWs with the more or less complete loss of any detectable homology in neutral sequences. »
Now the question is why you have wrongly asserted that neither gpuccio nor anyone else offered any justification for these 400 million years? Did you even bother to read gpuccio?
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Are you? That is not at all clear. Is it just me, or does anyone actually understand how Bill is coming up with the numbers he keeps mentioning?
It makes it more likely that functional sequences remain in the population, in order for further mutations to occur that increase the amount of FI. This is presuming that we are using a definition of FI that accurately measures information in a protein or genetic sequence that is necessary for a function to be performed. It seems there is considerable doubt that you are doing so.
I agree natural selection can contribute to the preservation of the functional information.
Good. So you won’t be asking this same question hundreds of more times as if it has never been answered.
Thanks for bringing that to my attention, as I have completely missed that. I apologize for asserting he never answered this now that I see he did “answer” that. Nevertheless, that is a completely useless explanation for why 400 million years is the magic number for determining FI. That simply makes no logical sense.
What does the detectability of homology in DNA sequences have to with functional information in protein amino acid sequences? Just because the DNA sequences have changed so much they can no longer be inferred to be homologous doesn’t somehow mean the protein sequences have stopped changing, or can’t change further.
Do you think this is a good explanation, @Giltil?
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Has someone made this claim?
That’s not an answer to my question. Do you think the LCA was newly created with that protein? Was the protein sequence inserted de novo into the LCA’s genome? No gradual evolution at all? It was absent one minute, then there the next?
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If that is not the implicit claim when Gpuccio brings up detection of homology in DNA, as an explanation for why we need to wait 400 million years, then why does he even bring it up? What possible relevance does it have otherwise?
Do you ever think about the things Gpuccio say, or do you just accept that “he said something” and then you stop bothering to determine if it even makes sense? Do you even read what Gpuccio says? Is it enough for you that he merely says something, and you don’t even care whether it makes logical sense? As long as he gives the pretense of a response, you are then satisfied?
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There is a difference between a claim of resistance to change versus “can’t change”. He is observing resistance to change which is evidence of functional constraint.
The evidence appears to show two trees or two origin events. One tree starts with prokaryotes and one with eukaryotes. The answer is yes eukaryotes started with the ability to splice out introns inside its nucleus. Without this capability a eukaryotic cell could not generate proteins.
How do you know that the first eukaryotes spliced their genes? We don’t know. How do you?
A judgement based on the evidence of the differences between prokaryotes and eukaryotes. The rest is speculation based on the simple to complex model.
What in the world are you smoking to dream up an incredibly ridiculous claim like that?
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The vast differences between the two structures.
https://previews.123rf.com/images/marcopolo/marcopolo0802/marcopolo080200010/2567617-cross-section-diagram-of-prokaryotic-and-eukaryotic-cells.jpg
Thanks Bill for showing something science has known for almost a century. Probably new to you though, right?
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Science is assuming a material cause I am not. This is a case where the material cause does not appear to fit the evidence. Do you think we really had this evidence 100 years ago?
Let me understand your latest claim: Your “Designer” some time in the past designed and manufactured both prokatyotic and eukaryotic cells independently? Then turned them both loose in the world to evolve? How does that fit in with ID’s “Cambrian explosion” design claims?
Do you think you guys can get your story straight at least once in our lifetimes?
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But nobody thinks there are no constraints operating on functional proteins, so the mere reality of constraint is an uninteresting factoid that does not establish how much, or that no function exists elsewhere in sequence space. Even in 400 million years, an infinitesimal fraction of that space has been sampled.
So we are still left with Gpuccio’s 400 million-year-rule being completely unable to establish any basis for calculating the FI in a known protein. And his “explanation” for why we must wait 400 million years specifically, is completely useless as it says nothing about what the rest of sequence space is like. All it says is it is likely that most codons in the protein have mutated at least once. Which doesn’t tell us the difference between deleterious or nonfunctional, and says nothing about whether there are other functional sequences further away which are very dissimilar to the one that mutates.
As I explained in the other thread, even for a 150 aa protein we are left with having sampled an almost infinitesmial fraction of sequence space. For a huge protein like Prpf8 it is much worse by many orders of magnitude.
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Let’s see this.
Imagine a given protein in the common ancestor of vertebrates about 400 millions years ago. Imagine that at the time, 70% of its sequence was absolutely required for its function and that the other 30% were neutral positions. How this protein would have looked like say 10 millions years later in the different vertebrate species of that time. Obviously, the 70% required for its function would have remained unchanged. As for the 30 % neutral part, only a small fraction of the positions would have changed through the action of neutral drift. IOW, 10 millions years later, the homology signal of the neutral part of the protein would have remained very strong.
Now, what about this same protein 100 millions years later in the different vertebrate species of the time? Well, whereas the constrained part (70%) would have remained unchanged, a large fraction of the neutral positions would have changed. However, a sufficient number of neutral positions would still have remained unaffected by the effect of drift, so that a homology signal for the neutral part of the protein would still be detectable.
But 400 millions years later, whereas the constrained part would still be there unchanged, the homology signal of the neutral part would no longer be detectable.
The bottom line here is that the homology signal corresponding to the neutral part of a protein decreases with time until a point P where it becomes undetectable, whereas the homology signal corresponding to the constrained part of the protein remains constant with time. This is why it is only when P is reach that one can safely conclude that all the homology signal observed for a given protein belong necessarily to the constrained, functional part of it. IOW, far from being useless, P is a crucial element of the reasoning for determining FI.