I concede that made no sense in that sentence and have removed it.
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Are these really models that could tell us how a de novo flagellum formed? Case re opened 
No, but that’s not what they’re modeling, they’re modeling the exact situation I described, where beneficial mutations rise in frequency in the population, and relative fitness increases, despite the majority of mutations being deleterious. They’re modeling that exact thing, the thing you first responded to by calling it a “nice story” and asking if it can be modeled, and not some new thing you now imagine instead and want to change the subject to.
Case remains closed. You can open your new case if you want, but this one is closed.
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Your model does not support the claim that the flagellum could evolve by proposed evolutionary mechanisms. Showing a fling object can soar to 1000 feet does not show it can fly and land on Mars. New case opened
If I moved the goal posts my bad.
Bill, your estimate of the numbers of possible targets is off by hundreds of orders of magnitude.
As I explained before:
First, instead of proteins, consider a typical 4 base restriction enzyme recognition site. The fraction of all 4-mers that will consist of any given such site will be 1 in 256. However, essentially all 1000-mers will possess such a site; in other words, the relevant fraction is 1, as is the probability of finding such a site in a given collection of 1000-mers.
While protein function is a bit more complicated than this, the same principles apply, and these considerations cast ID proponents’ favorite probability calculations in considerably different light. Thus, as one lengthens a given set of polypeptides to lengths that approximate that required for a particular enzymatic function (and these may be rather small, or modest entities on the order of 50-100 amino acids), the fraction of polypeptides that possess a specific functional motif will reflect the size and sequence of the motif, and will decrease as the size of the motif is larger. However, once the lengths of a population of polypeptides exceeds that of a given functional motif, then the fraction of functional polypeptides in such populations actually increases with polypeptide length.
This means that all of the calculations by ID proponents that scale probability inversely with polypeptide length are wrong.
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This maybe true but showing that ID calculations have issues and showing that known evolutionary mechanisms can build complex adaptions are very different issues.
The preservation argument of gpuccio at UD is a legitimate obstacle as a protein like PRPF8 with north of 2300 amino acids is highly preserved over deep time despite lots of DNA mutations.
-Behe’s irreducibly complexity argument along with the mathematically calculable size of protein sequence space and evidence of preservation is a pretty powerful argument that hard directed sequence change is required if evolution is a real theory.
2 billion is a massive underestimate:
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Except that it isn’t highly conserved, as previously shown. You nor gpuccio have yet to calculate all of the other possible protein sequences that could evolve as part of a spliceosome, or what other genetic system could have evolved in eukaryotes.
The scientific claim is that we can explain evolution with known mechanisms.
It could have happened is not the basis of a real hypothesis.
Modeling the evolution of the spliceosome is the beginning of a scientific hypothesis.
The other guys say that it takes the organization of north of one million nucleotides to create a spliceosome and we know conscious intelligence can create lots of FI. Whether it is a directed mechanism contained in the cell or some other method the overwhelming evidence is that it needs to be directed toward a group of functional sequences. Just as Dawkins modeled it in the blind watchmaker.
Like I said - Size not only doesn’t matter, it is irrelevant.
I don’t know who “the other guys” are, but I am pretty sure they have not directly measured FI. So this remark is pretty meaningless.
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The overarching theory is that life changed through many different evolutionary mechanisms. Where we have sufficient information, we can use that overarching theory to derive specific hypotheses. However, specific hypotheses may not be derived if we lack enough information, such as in the case of the very specific changes that happened billions of years ago.
What evidence are you talking about? Where is the evidence demonstrating that an intelligence is responsible for the FI in a given genome?
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The existence of FI is evidence.
You are begging the question. It’s a bit like claiming that leprechauns create rainbows, and my evidence is the observation of a rainbow.
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This claim need a little more support to make it universal.
I think you understand some of the methods as you demonstrated understanding in your review of Axe’s paper. You appear to be claiming indirect measurements are meaningless. Is this the claim you are making?
That’s relative fitness.
We can show conscious intelligent beings create FI as you have with your above analogy.
Yes. I didn’t mean it any other way. The fitness of descendants compared to ancestors by direct competition. They are getting fitter compared to their ancestors, in that environment.
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Those intelligent designers weren’t around billions of years ago, so you lack a mechanism.
Is there anything other than “relative” fitness? In what way could this be a meaningful or helpful clarification?
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True but others may have been there. Let’s not discount Crick’s panspermia hypothesis. We have established a workable mechanism we just don’t know exactly what it looked like.