If this is a trillion different functional sequences that is a tiny fraction of the total sequence space. The functional space has to almost equal the total sequence space or evolution fails and there is no evidence that supports this claim across the spectrum of possible proteins.
How many peaks are possible?
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And how many amino acid sequences will produce biological function?
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Based on the evidence of the observed sequences of PRPF8 only a tiny fraction of the total sequence space and there is no evidence of multiple adaptive peaks.
That doesn’t tell you whether there are other peaks. All it says is that current sequences could be on top of one such peak. How do you determine that the current PRPF8 sequences did not evolve from some valley in the fitness landscape, and there’s further peaks elsewhere in the landscape?
To make just one conceivable scenario, take this one:
Here I have suggested that Eukaryotic PRPF8 homologues (red dots), a well-conserved bunch, occupy some peak in the fitness landscape. On an adjacent peak we find PRP8 homologoues (yellow dots) from prokaryote group II self-splicing introns.
How do you know that these did not evolve from the green dots down lower in the landscape and now occupy different adjacent peaks? Explain how you rule out that this scenario can be the case merely from your observation that the red dots are clustered close together?
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You understand that “adaptive peak” is a metaphor; “fitness surface” is a metaphor. But yes, anything subject to selection has one or more adaptive peaks. It can’t be avoided. The main reason I don’t understand your question is that this is so obvious.
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Really? What evidence tells you that interdependence can’t evolve from non-interdependence?
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That’s a bold claim. How would you support it?
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PRPF8 is the only protein with function in the whole of biology?
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Simply that unless PRPF8 has over 20^2000 functional sequences that can fit with the other spliceosome proteins then the mutation will get lost in the search space as it is 20^500 larger than the functional space.
The evidence shows that its functional space is only a tiny fraction of any of these numbers.
You will have to come up with a better model than that, or at least a more fleshed-out one. If I can flesh it out a bit, you seem to be proposing that PRPF8 must start out as a random sequence that must fit into the existing structure. That’s an absurd strawman model and an egregious misunderstanding of evolution.
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When an organism inherits a gene for a protein, is the entire gene sequence shuffled around randomly? If not, your model doesn’t work for biology. You have also failed to show that PRPF8 has to evolve, or that there aren’t other protein sequences with function that could have also evolved. Instead, you are painting the bulls eye around one protein as if that is the only thing that could evolve. That is the Sharpshooter fallacy.
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The question is did the eukaryotic cell evolve or was it a new origin event. I have shown you with only one of its proteins that is most likely a separate origin event. We have not touched on.
-the spliceosome
-chromosome structure
-the cell nucleus
-the nuclear pore complex
etc
Your claim of evolution is a texas sharp shooter fallacy. You are claiming evolution and yet you cannot even make up a viable evidence based story to counter the problems I am surfacing.
Does PRPF8 exist in most eukaryotic organisms? We can talk about the other 169 proteins that make up the spliceosome and they are dependent on working with each other. These are facts not after the fact targets like looking at the eukaryotic cell and claiming evolution.
Just Bill being Bill. 
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Sadly, you have not. You have bloviated upon the subject, but that’s not the same thing.
You appear not to understand the Texas sharpshooter. Best avoid it.
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It is after the fact. You are pointing to the targets that were hit while ignoring all of the other possible targets that were not hit. That is the Sharpshooter fallacy. You are incorrectly assuming that the proteins we see in modern species are the only proteins that could evolve.
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How so?
Let’s use a deck of cards as our example. If we shuffle a deck of cards and then deal out 52 cards in order, that order of cards has a 1 in 8 x 10^67 probability of occurring, and yet it occurred. How do you explain how such an unlikely event is so easy to produce?
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Why do keep asserting these things with zero evidence, Bill?
Well, it just so happens that I am quite familiar with myosin mutants that move function off the peak and (only sometimes) cause disease. There is a vast amount of data showing that the functional peaks for myosin and other sarcomeric proteins are fairly flat, far more (and far better) data than the data from the study by Axe that you seem to be clinging to.
Maybe they are a good system for understanding what you are trying, and failing, to express here.