Behe and the venn diagram is connected in Bill’s head through some sort of gymnastics he has never been able to put into words. The new genes in Howe et al’s diagram can ONLY evolve through Behe’s scenario. According to what? Bill’s fantasy world.
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So we’re already talking about a couple of particular functions, not any function. Note again that Tf and Tfx are also referring to a particular feature. What exactly do “compatible” and “incompatible” mean here?
Bill how many of the gained genes in the Howe diagram have novel disulfide bonds and/or novel ligand binding functions? I know you don’t know, the question is once again rhetorical.
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Compatible means in a state the can produce a functional amino acid relative to a disulfide bond or a ligand. In compatible means in a state that won’t produce a functioning amino acid.
Word salad again. By “functional amino acide relative to a disulfide bond” do you mean “a cysteine”? This also seems like a highly artificial, two-state model in which a character (whatever it is) either is functional or non-functional, with no room for degrees of function.
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That is indeed Behe’s model. He also assumes roughly half of alternative amino acid substitutions are nonfunctional. Not just deleterious(there is no degree of fitness in Behe & Snoke)*, nonfunctional.
- Edit I see I misremember. They do model the selection coefficient of the novel function-creating gene (not any intermediate mutations), just to include the probability that they’re lost before fixation.
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This is an area where both Behe and Lynch’s models are in agreement.
It is not, lol. ROFL.
First of all Lynch models a bunch of scenarios, ranging from only 2 residues can produce the function of interest, to ones where 5, 10, or 50 can. There’s this nice figure in Lynch that shows how this difference alone makes an exponetial difference.
Then there’s the fact that Lynch models alternative substitutions to be neutral, rather than outright nonfunctional. You know we can actually read, right?
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Neither of which are relevant to the subject at hand. Again:
I already gave you (1), what are the rest? Come on Bill, it’s time for math…
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quote=“CrisprCAS9, post:112, topic:15676”]
I already gave you (1), what are the rest? Come on Bill, it’s time for math
[/quote]
Number 1 you can read off the Venn.
If you can discover a modeled and tested mechanism for number 2 a Nobel prize awaits you.
Until your Nobel is delivered the single origin model is obsolete based on this evidence.
And yet you couldn’t manage it, and needed me to do it for you. Bill, if you can’t add a few numbers together, what chance do you have with the rest?
No Bill, you said you’d already reviewed them, and mathematically excluded them! Yet now you can’t even name them!?
Were you lying? Again? Sounds like it!
So come on, what are the proposed mechanisms that you reviewed and mathematically excluded?
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Please connect the Venn diagram to Behe’s model.
How many of those gained genes have novel disulfide bonds or ligand binding functions(give some examples), and how many of those had to evolve through the specific scenario Behe describes?
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Gene duplication and divergence. It does not come close to explaining the pattern.
Behe has shown that the mechanism takes too many generations for for just a few changes. How in the world is it going to work for thousands of changes?
You are a Graduate student in evolutionary biology. You need to have realistic assessment of the theory you are studying. The theory can estimate changes in existing populations it cannot in most cases inform us about the origin of those populations.
What is the rate of gene duplication?
Nothing of relevance to the question at hand. Every time you reference Behe, you’re automatically wrong. Stop doing it.
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Connect that to the Howe diagram please. Find examples of genes that do what Behe models and had to evolve in the manner he described.
Surely he didn’t just model some absurd scenario you can find no example of, right? He wouldn’t do that would he?
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He has a PHD from Penn in biochemistry I know him and trust him. Where are you studying?
Credentialism isn’t an argument, try again.
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He is a respected professional biochemistry professor who makes conservative claims. You are an anonymous person on the internet who does not make conservative claims and will not disclose his name or the institution that is indoctrinating him
The same anonymous person who asserts not to listen to a distinguished biochemist professor who I have known and interacted with for 5 years.
You need to make more conservative claims as Dr Harshman does.
More credentialism is still not an argument, try again. With an actual argument, this time.
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