You going to retract your demonstrated lie that I’ve documented with screenshots? Or are you going to keep being a liar?
Your call.
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I rest my case.
I now reviewed the discussion and admit you did not move the goal posts. I apologize for this error.
I will continue tomorrow if you agree not to commit other logical fallacies and not make accusations of dishonesty which requires understanding intent.
Declare victory and go home ending with a quote mine, 
Ahh no, now I rest my case.
He didn’t take the challenge. He’s now obfuscating to avoid admitting.
He’s a liar and will never stop being a liar.
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When you continue, you should consider how many events are required to explain the difference between mouse and human, the number of generations separating those two lineages, and the rate at which different events occur. Ideally, considering both the average rate and the extreme ends of the confidence interval for each value. Multiply these numbers together, and see what you get.
I will here stress that you should already know the types of events possible, and their respective rates. If you don’t, then you can’t have excluded the possibility mathematically and you were just making stuff up. Asking me, or anyone else, either about the possible events to include or the numbers to use for the rates, is an admission you hadn’t done your homework prior to making the claim.
So good luck with that.
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More than anything, he has to stop with the Texas sharpshooter fallacy. Time to fixation of any particular mutation is irrelevant when a tiny fraction of all mutations end up becoming fixed. We see only those that happen to have been fixed, and the prior probability of any one of them doing that is minuscule. It’s only the sheer quantity of mutations that gives us what we see now. This is something Bill has never understood, always ignored.
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Some find new function.
Some become fixed.
By both advantage and chance, the life around us succeeded. Obviously, we will never know the many many variations which did not succeed due to disadvantage and chance. Mutation and fixation is going on all the time. The tree of life around us is one of an infinitude of possibilities. Somebody has to win the lottery, even if the odds for a particular ticket are long.
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Life clearly shows evidence of purpose not advantage and chance. You are counting on a theory based on lucky accidents. This is not a real theory. A real theory has a high probability of being right,
The models are not talking about any particular mutation they are talking about a group (two or more) mutations that can form a biological function.
How would you distinguish an advantageous trait from purposeful trait?
Chance events happen. Many are unlucky. Some are lucky. Both are inevitable.
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Doesn’t matter.
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We know how long ago the common ancestor of any two given species would have lived.
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We know how many differences there are between the genomes of these species.
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We know how long it would have taken for these differences to have arisen and become fixed according to models of population genetics.
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The result of (3) is consistent with (1).
Common ancestry explains these observations.
No model that denies common ancestry can.
That’s the bottom line.
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What parameter in the models determines how many mutations can form a biological function? And is that some particular function or any function?
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Still waiting for:
- Number of events to be explained
- Processes able to produce those events
- Rate at which those processes are known to occur (per generation)
- Number of generations involved
I’ll get you started: In the Howe diagram between mouse and human, there are 189 & 226 genes ‘lost’ from human and mouse respectively, and 2963 & 2596 genes ‘gained’ in human and mouse respectively.
So… what are the processes that can add or remove genes? How often is each known to occur? And what numbers do you get if you multiply that rate by the number of generations?
Come on Bill, show your math!
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If only you knew how to calculate anything, much less probabilities. How do you calculate the probability of some particular gene being intelligently designed?
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Below are the parameters. The second parameter ^ , the 4th P and the 5th parameter o will determine how many mutations will be required to get a likely functional mutations. The functions in the model are disulfide bonds and ligand binding functions.
| N | Number of organisms/duplicate genes in the population |
|---|---|
| λ | Number of initially incompatible nucleotide loci in a duplicate gene that must be changed to form the selectable, multiresidue feature |
| v | Point mutation rate per nucleotide per generation |
| ρ | Ratio of the number of possible mutations of the original duplicated gene that would produce a null allele to the number of possible mutations of the original duplicated gene that would yield a compatible residue. Neutral mutations, such as those that produce synonymous codons, are disregarded. |
| ϕ | Fraction of a particular nucleotide position that is in the incompatible state. (1 - ϕ) is the fraction in the compatible state. |
| t | Time, in generations |
| Tf | Time in generations to the first occurrence of a particular multiresidue, selectable features |
| Tfx | Time in generations to fixation in the population of a particular multiresidue, selectable feature |
| s | Selection coefficient |
Your copy-paste skills are about average. Less can be said about your calculations.
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Behe’s math is still irrelevant, try again.
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And here we see the Texas sharpshooter fallacy.
What counts is the time until first occurrence of any novel function(assuming new duplicate genes are required to have novel functions to stick around, which we already know they aren’t) with a positive effect on fitness.
By the way with regards to the gene gains from the Howe diagram, how many of those have novel functions Bill? I know you don’t know, the question is rhetorical.
So once again, you see the Howe diagram, see it implies gene gains, fail to understand the vast majority of those are just duplicate genes, you then bring in Behe’s crap paper because you’ve flat out invented in your own head the idea they are required to have novel functions, and that they’re required to have evolved them by the sequential fixation of multiple mutations each of which are individually deleterious (like Behe does). You then, based on Behe’s absurd scenario, conclude the duplicate genes in the Howe diagram don’t have time to evolve.
And round and round we go, trying to get you to understand how you both misunderstand the Howe diagram (they’re mostly just duplicate genes, zero evidence any of them have novel functions), and for any of them that might have novel functions, there’s zero reason to think those could only evolve according to the physically unrealistic scenario Behe has concocted.
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