Depends on the protein and how it is measured.
From your link
Summary
To summarize, the claims that have been and will be made by ID proponents regarding protein evolution are not supported by Axe’s work. As I show, it is not appropriate to use the numbers Axe obtains to make inferences about the evolution of proteins and enzymes. Thus, this study does not support the conclusion that functional sequences are extremely isolated in sequence space, or that the evolution of new protein function is an impossibility that is beyond the capacity of random mutation and natural selection.
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Why don’t you read the hole paper.
“hole” paper.
I did. Why don’t you try reading it and then explain why the author’s summary is wrong. You linked to the article without reading it, now you’re mad because it contradicts your claims.
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I agree with him that Axe’s paper alone is not enough to make the conclusion. If you add the other studies in the paper, gpuccio’s work, durstons work, mercers work and apply the numbers to eukaryotic cellular structures you can make the conclusion.
You need to support this claim.
Especially because gpuccios “work” is based on Durston’s work, and that has been discussed at length here: Durston: Functional Information.
Fair enough.
Similar but gpuccio uses a different method.
gpuccio uses essentially the same math and makes use of essentially same assumption. Consider inviting him here to make his case if you doubt it.
He is not very active right now if I see him on UD I will invite him. I think one main difference is he does not add any substitutability to a sequence if its position changed from the human equivalent.
If what you are saying is the correct, his approach is worse than Durston’s.
Are you saying an entirely new catalytic anti body can arise from a totally random sequence of random length, or that a new catalytic anti-body can arise from random variation of a pre existing form of a catalytic anti-body. There is a difference in the scenarios being described.
There would be no precursors because without helicase or something equivalent, the cell lineage is dead. If the cell lineage is dead, therefore no more evolution. That’s why I chose it as an example.
One could postulate something allowed evolution of helicase to take place, but that is an appeal to a mechanism with details that are unknown, unseen, untestable, undescribable – which makes it then pretty much equivalent to a theological belief. The only difference is that it is accepted on faith that it operates according to ordinary principles of chemistry and physics, but that is a faith belief too.
What is apparent is spontaneous generation in the present day, doesn’t happen, and it is consistent with the predictions of the difficulty of chemically creating cellular replicators from scratch. Abiogenesis is not solved by evolutionary theory, even by admission of evolutionary biologists. The problems facing spontaneous generation are many of the same problems facing abiogenesis. It’s a matter of pure faith that the conditions in the past were different enough to make abiogenesis feasible. But as James Tour pointed out, abiogenesis research hasn’t solved the problem it claims to solve. I’ve offered theoretical considerations why this is like trying to solve the emergence of a 747 jetliner by appealing to tornadoes passing through a junkyard as a mechanism. It just isn’t expected to work just based on mechanical feasibility.
We could appeal to God’s providence, however. Abiogenesis is not beyond that.
Exactly! But it seems that some of our friends here have difficulties to grasp this point.
I would love to have gpuccio here for he is a very insightful and articulate scientist. He would bring a lot to the conversation.
I thought he was a physician, not a scientist.
Possible. I don’t know.
If there were 10125 possibly winning combinations, someone would surely win.
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