How do those new components support your claim?
That’s a rather easy problem to solve. Bird species that are not chickens but are ancestral to chickens passed on the trait of egg laying.
How is that evidence?
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This is just insane. Reality tells us that in very complex systems, such as cardiac muscle, increased function can cause death.
The peak is not necessarily the place to be. We’re just trying to get you to acknowledge that there’s a mountain or hill, while you’re pretending that the peak is some sort of spike.
Would you like to look at reality, Bill? It will blow all of your unstated assumptions to smithereens.
All negative “science can’t explain this to my satisfaction” arguments. Where is the positive evidence eukaryotic cells were intelligently designed?
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If it’s a separate origin event (whatever that means) why are mitochondria descended from alpha proteobacteria? Why are parts of the nuclear genome clearly related to particular archaeal groups, while other parts are clearly related to eubacterial groups? Does that fit your concept of an “origin event”?
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And you employ an argument about the PRPF8 protein to advance the conclusion that eukaryotes cannot share common descent with prokaryotes because you think the PRPF8 protein could not have evolved. So how did you determine that PRPF8 is not just one among many similar, well-connected peaks in the fitness landscape or protein sequence space?
PRPF8 is a key component of the spliceosome which is a mission critical part of the eukaryotic cell. I don’t rule adaptive peaks but they are indeed not important unless the total sequence space is small enough that they have a chance to be found from a random search.
So how do you know how frequent such peaks are, or whether they were connected to some other primordial function? How do you know PRPF8 did not evolve from some other primordial protein, or ultimately from non-coding DNA?
We are also talking about one of 170 proteins that perform a function where adaptive peaks are very hard to ascribe to an individual protein in the complex.
Why would it be any different just because there are a collection of proteins contributing to the system?
Bill do you even understand what the landscape metaphor is about? Please explain to me in your own words what the metaphor of a peak in the landscape describes.
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No, he’s absolutely correctly describing your argument. If he’s not correctly describing your argument, then your argument does not even make sense and I have to wonder what it is you think you are trying to say when you bring up the PRPF8 protein. If he’s not correctly describing your argument, then I doubt that even you yourself understand what the heck you are trying to argue.
I’ll try to recap how I understand your argument:
You argue that common descent can’t be the case, because if it were the case then PRPF8 would have to have evolved somehow. And you argue it couldn’t because something about the size of sequence space, and the rarity of functional sequences in that space.
You invoke, as a point that should cause us to think that protein sequences with PRPF8-like functions are exceedingly rare and isolated in that space, the fact that the PRPF8-like proteins in the eukaryotic clade are highly conserved.
This is where we step in to get you to explain how the degree of conservation of PRPF8 in the eukaryote clade establishes that proteins with PRPF8-like functions are rare and isolated in protein sequence space.
This is where you (hopefully) try to explain how it is you think the degree of conservation of PRPF8 shows that proteins with that function are too rare and isolated in protein sequence space to have evolved. So, back to you.
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New components require new designs. They are evidence of a new origin event.
The chicken and egg problem is about PRPF8 which requires splicing requires the protein complex it is part of the produce itself.
New code that codes for functional proteins is evidence of an original design.
In general there are a lot of unique features in the eukaryotic cell that support the new origin hypothesis.
How do you know they didn’t evolve? How did you exclude that option?
Why could it not have evolved from the Prp8 protein encoded by group II self-splicing introns found in prokaryotes?
How do you rule out that they didn’t just evolve?
Bill you are just claiming they’re evidence of design. You’re not explaining WHY they’re evidence of design.
Here’s why you should think PRPF8 in eukaryotes is actually evidence for evolution. It has a significant degree of sequence similarity to a protein encoded in prokaryotic group II self-splicing introns and those sequences show a highly significant degree of nesting hierarchical structure. Which strongly implies they are truly homologous sequences, aka derive from a common ancestor.
Think about it. If evolution were true, and the PRPF8 gene sequence which itself contains intronic sequences that need to be spliced out, which is a process it is itself involved in, actually evolved, then it would have had to evolve from some sort of simpler system where it could self splice.
Well wouldn’t you know it, there is actually such a system in a particular clade of prokaryotes, which have a Prp8 protein that his clearly homologous to the PRPF8 protein in eukaryotes. Introns that can splice themselves out, called group II self-splicing introns, actually encode a Prp8 homologue (usually just referred to as an IEP, intron encoded protein) in prokaryotes. And the gene sequences that encode these prokaryotic and eukaryotic proteins together exhibit highly significant degrees of nesting hierarchical structure, which we have explained to you over and over before simply does not make sense on design and only makes sense on common descent.
Even further, the α-proteobacterial ancestors of mitochondria belong to the very clade of bacteria known to contain group II self splicing introns. Even further, recent discoveries in archaeal domain diversity have uncovered the likely clade from which the proto-eukaryotic host derives, as simpler homologoues of several key eukaryotic organelles and cytosolic structures have been found in these archaeal species. Just to point out another “coincidence” completely consistent with the evolution of eukaryotes through endosymbiosis; isn’t it funny that the discovered putative ancestors of mitochondria (the α-proteobacteria), and the putative ancestors of the eukaryotic host (the archaeal species) both belong to prokaryotic clades containing members specializing in living in hydrothermal vents? So they’re actually species known to live alongside each other in the same environment. Just another funny coincidence the designer decided on to make it look like evolution happened?
These are puzzle pieces, and evolution makes absolutely perfect sense of them. On design you are forced to just conjure up some vacuous ad-hoc declaration that “well that’s just what the designer wanted it to look like”. Which is absolutely absurd.
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Demonstrably false as we know how unintelligent natural evolutionary processes give rise to new components.
Ignorance based personal incredulity as we know how unintelligent natural evolutionary processes can produce IC systems.
Demonstrably false as we know how unintelligent natural evolutionary processes give rise to new genetic sequences producing new functional proteins.
0 for 3 there Bill. Looks like your bluster about having positive evidence for Design was just that - empty bluster.
The evidence of preservation and size of sequence space is conclusive to me. This just a small part of the transition required. You have lots of pieces as you mentioned and some existed in prokaryotic cells but there is no logical reason they plus dramatic new innovations came together with blind and unguided processes. The eukaryotic cell is a highly sophisticated integrated system that is substantially more complex than the prokaryotic cell.
Type 2 introns are not sufficiently functional inside a eukaryotic nucleus due to Mg2 plus levels.
I don’t think you can make any reasonable case for evolution here given the current set of facts.
Have you considered that the analogy implies its own solution? The chicken and the chicken-egg co-evolved, thus avoiding the chicken/egg problem. Now apply to the spliceosome.
You just can’t provide any of this conclusive evidence to anyone else. I’m sure your ignorance based “I don’t believe in evolution so it must be false” is conclusive to you.
So, in fact, your argument has been correctly portrayed throughout this thread.
Glad we got this settled.
Now you can proceed to explain HOW the degree of preservation of PRPF8, and the total size of sequence space for proteins of that length, conclusively settles that it could not have evolved? You have mentioned these before, and I am still left wondering how they lead to your conclusion.
Premise 1: RPPF8 is highly conserved. Check!
Premise 2: Sequence space for proteins of that length is 20^L, which is a very large number. Check!
Premise 3-?: …
Conclusion: Therefore it is highly doubtful, or impossible, that PRPF8 could have evolved.
Fill in the missing premises in that argument please.
Premise 3 is that the conservation is evidence that the total number of functional sequences is less than the total sequence space. The substitutability would have to be exceeding high (greater than 50% of the available AA’s) for evolution to work and there is no evidence this is the case.
Once again you confuse the peak with the mountain.
But that premise does not entail, nor even imply the conclusion. Bill you have yet to connect the dots.
I would agree the total number of functional sequences is less than the total sequence space. But how does that lead to the conclusion?
The substitutability would have to be exceeding high (greater than 50% of the available AA’s) for evolution to work
Why?
Let’s fill in your premise three:
Premise 1: PRPF8 is highly conserved. Check!
Premise 2: Sequence space for proteins of that length is 20^L, which is a very large number. Check!
Premise 3: The total number of functional sequences is less than the total sequence space. Check!
Conclusion: Therefore it is highly doubtful, or impossible, that PRPF8 could have evolved.
Oops, that conclusion still doesn’t follow.
You have yet to connect the premises to the conclusion. I invite you to fill in premise 4-?, however many it takes.
Rum your separating two sentences that work together and that is confusing you. The substitutability is the issue. The preservation is strong evidence against very high substitutability.
In the very aggressive case relative to the evidence that 50% of the amino acids work in every location your functional space is 2^-2500. No trial and error search has a prayer here.
How is it evidence of that? And why is “>50%substitutability”(which I am still not sure what means) required for PRPF8 to have evolved?
Why is it not compatible with the hypothesis that extant eukaryotic PRPF8 homologues just occupy some adaptive peak, and that sequences further downhill are still functional, but have comparatively lower fitness and therefore are selected against in the organism’s present state?
Why could this example not be the case?
Here sequences further down the hill would have lower fitness, which explains why we don’t see them. That means they would work, they would be functional, but in so far as a mutant crops up that moves the organism further downhill, it is quickly outcompeted by other cells without that mutation.
How do you rule out this alternative interpretation of conservation?
In the very aggressive case relative to the evidence that 50% of the amino acids work in every location your functional space is 2^-2500.
I have no idea what this even means. What does it mean to say that “50% of amino acids work in every location”? That sentence does not parse meaningfull into english for me. Put more words on it, flesh it out in more detail please.
No trial and error search has a prayer here.
So you keep saying, but keep failing to show. Go back to the argument, fill in the missing premises.
Premise 1: PRPF8 is highly conserved. Check!
Premise 2: Sequence space for proteins of that length is 20^L, which is a very large number. Check!
Premise 3: The total number of functional sequences is less than the total sequence space. Check!
Premise 4: [something about substitutability that you will have to express more clearly]
Premise 5-?: [Whatever premise is needed to lead to the conclusion]
Conclusion: Therefore it is highly doubtful, or impossible, that PRPF8 could have evolved.
Please continue expanding this argument until the conclusion actually follows.
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Based on what evidence?
Where did you show that this has always been the case through the entire history of eukaryotes?
How so?
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