A figure completely irrelevant to the claim you go on to make. Apparently only put in your post so that you can feel like you’re saying something science-looking. A veritable Chewbacca-defense.
Blind assertion. They can. Nothing says the same protein can’t diverge by hundreds of differences and retain functions. They can, demonstrably, effortlessly given enough time. Remember Douglas Axe’s experiment indicates that at least 10115 different protein sequences are capable of adopting the same fold as TEM-1 beta-lactamase and catalyzing the same reaction.
They don’t have to be all neutral.
Stop saying things already known to be false.
Based on what?
Except direct observation of gene gains by duplication, insertion, etc.
What new function? All of them are receptor binding proteins. The function is the same. You have no idea whether any of the protein in question have any new functions.
And what the heck does “lack of explanatory power finding new function” even mean?
Mutations accumulate, they change the protein’s biophysical properties, some of these can affect it’s function.
So the explanatory power is just fine. If mutations (neutral or not) cannot “explain finding new function”, then neither can design, because both are just how the changes are made. Whether those changes affect function or not is immaterial to what is causing them to occur.
If a designer can pick and choose changes to make to a protein and then make them occur, and these changes can alter the function of the protein, then so can mutations similarly do the same. No “explanatory power” is lacking.
No, it shows no such thing. Literally not a single point of those assertions is shown in anything you have linked or posted here anywhere.
You now agree this is beyond neutral mutations? Do you realize this claim pushes the model toward Behe and away from Lynch.
I agree I don’t see this as a reasonable conclusion for a process that initiates with random changes given the current level of available evidence. I have not claimed anything is impossible as science is always tentative.
You will have to explain why these are problems, and what they may have to do with the Venn diagrams. But I don’t think you know.
You have been appealing to neutral mutations explaining the Venn.
The problems with functional changes to a population are explained in the Behe Lynch discussion.
The problems with finding new function in a sequence have been discussed several times including Rum’s post above. The weakness in Rums argument is as follows.
-Beta Lactamase is not a conserved protein.
-Even if there are 10^115 different sequences able to adopt the fold the total sequence space is 10^490 so there are 10^385 sequences that do not adopt the fold. These numbers are unimaginably large.
Learning about Cricks discovery that DNA is a code and that DNA and proteins depend on a certain level sequence integrity is what started me doubting the theory. There is no real counter argument to the sequence problem given the current level of empirical evidence. Given this how are new genes formed by a process that is initiated by random change?
Ah, backpedalling. But why don’t you see it as a reasonable conclusion? Just what model shows you that?
Gibberish again.
More gibberish. Crick didn’t discover that DNA is a code. DNA in fact is not a code. I have no idea what “certain level sequence integrity” means. As expected, you don’t know.
What is the sequence problem, and what happened to the waiting time problem?
He takes the size of the sequence space for (I assume) the wnt-4 protein (about 350 amino acids long), divides it by Axe’s estimate of the total number of functional beta-lactamase proteins (a protein about 150 amino acids long), this gets him a huge number that corresponds to nothing real.
He doesn’t seem to understand it’s the total space of functional sequences and how they are connected that matter to how much proteins can diverge over time. It is irrelevant how large the space of presumed nonfunctional sequences is. We are talking divergence of protein sequence, not de novo discovery. How can he have failed to fathom this?
I have never seen Bill attempt a calculation that wasn’t instantly doomed to failure.
The first sentence of that paper points out the falsehood you are deliberately perpetuating:
Wnt proteins are a family of secreted glycoproteins that are essential for organogenesis, tissue regeneration, and cell growth. They bind to Frizzled receptors…
I would suggest that if WNT proteins were designed, then the various different proteins would be different within species but corresponding proteins would be identical between species. No reason mouse WNT4 should be different from human WNT4, since they do exactly the same thing in both species. Bill, could you check out the data on that prediction?
Actually he’s subtracting it, and getting an answer which would be wrong even if he was using the right method for subtracting exponents, which he isn’t.
There are two mistakes in the maths even without looking at the context which, as you point out, includes at least two more.
Yet he expects us to believe his mathematical intuition is worth considering.
Okay, just to clarify why everyone else is laughing at you for this. Here are a few points you failed to consider in your… “calculation”, even taking the numbers you put in at face value:
With these in mind I second Roy’s puzzlement. You fail at basic arithmetic three times in a single line of text. Please, explain what hope you think there is that anything you feel about the plausibility of various timescales, probailities, or any other quantifiable parameters in any model is due any consideration whatsoever. Please, explain how on earth it is that you feel you can trust your own intuitions when it comes to such things, let alone that anyone else would be well advised to.
I’m pretty sure what Bill did is to go to uniprot, look up the length of wnt4 or a similar protein for the family, in mice, and then just do 20length to get 10490. (Edit: If not, I have no idea where he gets that 10^490 number). It’s what he does next, and what he thinks that means, that’s gibberish.
I cannot for the life of me imagine why he would do (10^115)^4 and then get it wrong too. What does the 4 represent? Bill is not all there but even that is… well, perhaps I underestimate incompetence.
But 10490-115does equal 10490 / 10115
But he probably did it 490-115 in his head to get 385 where he should have got 375. Okay, I can forgive those 10 orders of magnitude because they’re not really what’s important in this instance.
One problem is that 10115 comes from an entirely different protein than wnt4 (it follows from Axe’s 2004 study of beta lactamase). Okay, I’m the one who brought it up but that was to illustrate the point that even if functional variants of a protein are supposed to be extremely rare in sequence space, that still leaves an unfathomably large space for functional divergence. Ironically Bill is underestimating the sizes.
The real problem is he thinks the total size of the nonfunctional space tells him something about how much functional variants of a protein can diverge. He thinks the 10385 number somehow matters when mutations accumulate. It’s this basic error he should have realized if he could think.
To put it another way, he assumes that a new protein is a random draw from the universe of all possible proteins, and he further assumes that while there is no target sequence there is a target function.
Or to put it in yet another way: When you walk from your house to the store, the odds of where your next step will land is determined by the length of your stride. The odds that your next step will land you two feet from where you are now are not the same as the odds that it will land you somewhere in the Andromeda Galaxy. Is that the sort of error @colewd is making?
I’m not sure I like the analogy for a couple of reasons. Your walk to the store has a clear target, and the path is intelligently designed. But the part about Andromeda seems to be the sort of thing Bill assumes. And your analogy can be recruited to point out another problem. Bill is using this argument against common descent, but if it’s anything it’s an argument against unguided evolution. If you make it to the store it isn’t an argument against movement and in favor of teleportation.