(except that, here on Peaceful Science, it never went away)
The article does not characterize the argument properly. A version of the probability argument convinced me that Darwin’s original claim 'universal common descent" was not viable.
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Please do relate to us the proper probability argument which disproves UCD. Provide your calculations and don’t forget to justify any assumptions you may make.
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Time for bingo? Key words tornado, junkyard, 747, 150 amino acids, number of atoms in the universe. Not sure what else.
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So if it convinced you, presumably you understand their argument and should be able to present the argument to us.
What is the probability argument that convinced you?
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Go on.
Can you explain the argument and what about Axe’s argument that convinced you?
Since you are convinced by it, you should be able to enunciate to us the argument.
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The problem with Axe (2004): Sought a specific target protein, calculated it’s likelihood, and extrapolated that to all proteins.
The assumptions embedded in that are…wow. For starters, assumed there is one way, and one way only, to accomplish some biochemical process. Assumed there is no selection for intermediate states. Assumed no recombination.
That stuff alone is sufficient to invalidate his work. It just isn’t relevant to how evolutionary processes work in reality.
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One assumes, since these arguments are based on proteins, that you fully accept then the common descent of all animal life? Ignoring, of course, the fact that the probability arguments are all flawed to the point of absurdity.
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It was not Axe’s argument. It was his experiment that showed the possibility given certain conditions that specific protein function is sequence dependent and in some cases highly sequence dependent.
Except that all of his assumptions were wrong, and his conclusion was wrong. By ~70 orders of magnitude.
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Axe did no such experiment.
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I did not make a claim about his methods. Here is your claim which you reviewed with Doug.
“Axe (2004) has performed site directed mutagenesis experiments on a 150-residue protein-folding domain within a B-lactamase enzyme. His experimental method improves upon earlier mutagenesis techniques and corrects for several sources of possible estimation error inherent in them. On the basis of these experiments, Axe has estimated the ratio of (a) proteins of typical size (150 residues) that perform a specified function via any folded structure to (b) the whole set of possible amino acids sequences of that size. Based on his experiments, Axe has estimated his ratio to be 1 to 10^77. Thus, the probability of finding a functional protein among the possible amino acid sequences corresponding to a 150-residue protein is similarly 1 in 10^77.”
I don’t know enough in the field to interpret it, but did read that paper. Here’s a direct link for anyone keen to do likewise: https://www.sciencedirect.com/science/article/pii/S0022283604007624?casa_token=I1Hf0uk7pSMAAAAA:SiJLUqWGQ32ihUTFDCsj9p_Zh5S0oGui5vdLYoUN2xkPdO8_unFJJiZSUH5o3yc2PhENNq6fCQ
Okay.
So can you explain to me how his experiment demonstrates 1 in 10^77.
For our 1 in 1x10^9 figure, it is very easy to see how we reached it.
Phage display of 2-3 billion different antibodies demonstrated 5 have beta lactamase ability.
Did Axe make 10^100 proteins, and figure out 10^23 of those showed beta lactamase ability, or something along these lines??
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Let’s assume for arguments sake that your 10^9 is right in certain applications. How do you account for the origin of ATP synthase given these odds for a single 100AA protein?
Did you just chuck out a red herring?
But let’s humor you for a sec.
The current idea for how it evolved is that it is thought to have come about from two functionally independent subunits which became associated and mutated to gain a new function.
There is another thread where a paper by Thornton et al demonstrates that the mutations causing association of proteins is favorable from a natural selection point of view, making them more mutable without loss of function, and able to have synergistic beneficial mutations.
The two subunits thought to have associated and gained new functionality together was the combination of V-ATPase with a DNA helicase.
It is supposed that glycolysis first produced ATP, then oxidative phosphorylation and ATP synthase evolved afterwards to make use of waste products of glycolysis to increase efficiency.
That all said and done, I am not ashamed to admit that whether or not abiogenesis is true, if it did occur, we may not know or ever know how it happened.
Abiogenesis is not a prerequisite for evolution to be true.
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Sorry @colewd but this excerpt doesn’t match your description. If you got from this that “ his experiment that showed the possibility given certain conditions that specific protein function is sequence dependent and in some cases highly sequence dependent.”, then I believe you are misunderstanding Axe’s work. You may want to reconsider your position, given that you have not properly grasped the argument that brought you there.
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I don’t see a problem with my statement and I believe you are misinterpreting it. It is certainly as I intended it supported by your claims in the paper of various probabilities given different experimental methods. If there are probabilities of function dependent on sequence then by definition the protein is sequence dependent. That does not mean only one sequence will perform the function.
I understand and if ATP synthase was required for first life then this point is valid, I however only am showing that the low end probability estimates are problematic for protein complexes with multiple proteins and long AA chains. These appear through long time scales and new animal origin events