Then why have you asked for examples of high FI proteins being produced in modern lab experiments?
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What’s to explain? A new genetic sequence must first arise in a single individual before it can be fixed in the entire population. Surely you understand that, don’t you?
Go on.
“Go on”? That’s it. A new functional sequence cannot be fixed in the population before it arises in a single individual. So the odds of the new sequence arising (in a single individual) is not affected at all by the odds of its being fixed. Do you disagree with this? I hope not.
You want to compare apples and oranges? I thought we were discussing gpuccio’s method.
Bill dodges the question yet again. What a surprise.
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@colewd You never answered the above question, so this is just a friendly reminder. TIA.
It seems to me that this is a really key question @colewd, do you care to respond to it?
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How does a mutation remain in a bacteria long enough to accumulate 10^10 trials? Unless the mutation gets fixed in the population is gets eliminated from the population. How do you think mutations collect in a individual bacteria?
10^10 divided by the mutations per generation.
That question, as worded, is nonsense. What does it mean for a mutation to “accumulate trials”?
Ultimately. But until that happens, it hangs around in the population at varying levels of prevalence. Which can go on for a long time.
Again, pretty basic stuff, Bill.
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This is a change of subject or movement of the goal posts.
I don’t want to butt in to this part of the conversation too much, but are you really suggesting that there are only 2 options: fixation or elimination? Mutations can remain in the population in intermediate frequencies for quite a while - each mutation doesn’t have to be fixed before the next mutation can occur.
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I agree and this can be part of a model.
Huh. Let’s try this with specific numbers.
Let’s use the example of the 1000 litres of pond water that contains 10^12 bacterial cells.
Each cell undergoes a single replication, to produce a new generation of 10^12 bacteria.
If there are .003 mutations per cell per generation, how many mutations are there in this first generation that were not present in the original population?
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Ok, so explain how this ultimately gets a protein fixed in the population?
Good. So you admit you were wrong. Progress.
why? It has nothing to do with the odds of a novel functional protein arising.
OK - I’m late to the discussion and haven’t even attempted to get caught up on the discussion, but is seems like a summary would be really useful. Can you:
- State Gpuccio’s claim in a way the @colewd (or @Gpuccio himself) would agree to?
- State any points of agreement about Gpuccio’s claim (there must be something?).
- What assumptions are necessary for Gpuccio’s method to work as intended?
- Which of these assumptions are justifiable?
and he [Colewd??] is not able to defend the model he is suggesting.
Let’s be more careful with this. Bill’s troubles defending Gpuccio follow if the method has no merit, but not the other way around.
I’m on your side here, but here you have an opportunity to really nail down this argument. You should use it!
It’s not enough to claim the other side is “unwilling or unable”; break the argument down into smaller and smaller pieces until it can’t get any simpler. Then the real source of disagreement is revealed.
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This is wrong. There is a trend toward more complexity in evolution, with organisms displaying more cell types over time.