if we will need several mutations at once (for say a language) then it cant happen by known mutational mechanisms.
If. That’s the problem for you.
If design is true then genes breaking a nested hierarchy should be the rule, not the exception. There are a few mechanisms for HGT in eukaryotes, but they only occur extremely, extremely rarely. The overwhelming signal is vertical inheritance which isn’t what we should see from design.
Every human is born with around 75 mutations, so I don’t see how this is a problem.
Here is a debate on the subject at Sand Walk.
That’s the Sharpshooter fallacy. What you need to show is how many possible beneficial adaptations there are that require multiple mutations in any given genome. Simply pointing to when they happen says nothing of how many possible multi-mutation adaptations there are.
I am going to name this the any function will do fallacy ![]()
If you can’t show how many possible functions there are, then you can’t make any claims about the improbability of a function emerging. It’s really that simple.
With all due respect this statement is not biologically relevant. Proteins are interdependent. You cannot make the claim that any function will do. Since function is restricted based on the evidence we can estimate.
@scd,
Could you at least tell me WHERE above?
I haven’t been reading your postings in quite some time …
You can not make the claim that what has evolved is the only thing that can evolve. You need to find all combinations of mutations that will produce adaptive function in a given genome. You haven’t done that.
This is your claim not mine. Once evolution starts if the theory is right then now proteins need to work with what’s already in the cell. This restricts it to new functions that can help the cell.
Are you trying to assert that if Evolution is right … then it is wrong?
Sometimes mutations happen to spare sets of genes … genes that are switched off because they are duplicates. This spare baggage makes it possible for helpful things to appear without getting in the way of ongoing necessary protein work,
I am showing that new proteins are functionally restricted to what exists in the cell. Therefor you can estimate probability that random mutation was the cause of what you are observing.
So, if God guided a mutation for a brand new protein … one that wasn’t needed yet … you would say that it is impossible for that to happen?
God or mind would be a deterministic mechanism and a viable explanation for complex adaptions.
Some mutations are random though and can cause minor change. We can estimate the probability that what we are observing is from random change.
I’m going to call this the Bill Cole ignores selection again fallacy. ![]()
Do you think God left things to be random when he created Adam? Do you think there was any part of the creation of Adam where God said: “Let’s just close our eyes and see what happens?”
If God takes eons to make a creation by Evolution, why do you think God would be any less precise with all that time to do it exactly as he requires?
The Behe analogy of the Billiards Ball Shot emphasizes precision … not probabilities.
How exactly do you “estimate the probability” of something being random … instead of exactly what God intentionally did?
And the ones that work with those proteins are not the only possible proteins that could work with them.
And catalytic antibodies give us a fine minimum estimate that you ignore.
Catalytic antibodies are not restricted to “new functions that can help the cell.”
Catalytic antibodies completely falsify your claim.
Catalytica antibodies provide a lower bound. Why do you ignore them, Bill?