[/quyou ote]Nils wrote: ↑Sun Sep 19, 2021 2:16 pmBeneficial mutations are indeed very uncommon. Especially when the environment isn’t changing. It’s not a law that there always are possible mutations that are beneficial. That’s why Behes statement in the OP is so astounding. The e coli bacteria has existed in more than one hundred million years. How could there be a lot of beneficial mutations that have never occurred long time ago appearing now in Lemski’s thirty year experiment.
You didn’t answer my question.
You didn’t answer my question this time either.
The question is related to the question I posed in post #4 which you didn’t answer. Why don’t you answer. It is an important question and relates to what you write now, see below.
The three premises you mention and the conclusion come from post #31. There is nothing about billions of benefical mutations.DBowling wrote: ↑Sun Sep 19, 2021 6:11 pmI haven't been able to find any examples.Nils wrote: ↑Sun Sep 19, 2021 2:16 pmProbably you can find somewhere in the vast literature on evolution something similar.DBowling wrote: ↑Sun Sep 19, 2021 5:40 am
We have a real life example on the table of two mutations working together to form a new function in malaria's resistance to chloroquine.
Due to the exponential nature of the two mutations occurring, you presume that this particular example involves two non-beneficial mutations working together to perform a specific function.
And for the sake of argument I will stipulate to your presumption that malaria's resistance to chloroquine involves two non-beneficial mutations.
You also presume that two beneficial mutations will work together to perform a new function more rapidly and more frequently than two non-beneficial mutations working together to perform a new function.
I am asking for empirical evidence of this presumption. I am not saying it doesn't exist. I just want to see an example, so we can compare the rate at which two beneficial mutations produce a new function with the rate at which two non-beneficial mutations produce a new function.
We would start by finding a new function of some sort that requires two mutations working together (similar to malaria's resistance to chloroquine).
Then we would see if there is a midpoint where either of those two mutations produces a beneficial function by itself.
- If one of those two mutations provides a beneficial function by itself.
- And then a second mutation works together with that first mutation to provide a different beneficial function.
==> Then we will have our example and we can determine the rate at which two beneficial mutations are able to produce a new function.
And based on the malaria examples of resistance to atovaquone (1 in 10^12) and chloroquine (1 in 10^20), somewhere around 10^8 (or 100 million) examples of two beneficial mutations working together to provide a new function should have been produced within the timeframe that two non-beneficial mutations produced resistance to chloroquine.
I believe I have already stipulated to those three premises.However as I write in post #31 I base my conclusion on three presumptions. Is any of these false?
No it doesn't...If not, the conclusion follows directly without any experiment.
You still have the unverified presumption that the complex code found in the DNA of life today can be created by billions of single beneficial mutations.
What are you talking about?We already have one example on the table that contradicts that that presumption.
I’m sorry, I can’t follow your argument. Are you discussing Lemski’s experiment or are you talking generally? Perhaps you are making the same error as Behe does in the OP and which I discuss in the beginning of this post. It is not possible to estimate the frequency of beneficial mutations in Ecoli from Lemski’s experimentWe agree that malaria's resistance to chloroquine involves two non-beneficial mutations working together to perform a new function.
And if your presumption was true, there should be around 100 million examples of two beneficial mutations working together to provide a new function
for every single example of two non-beneficial mutations working together to provide a new function.
Since we have yet to see a single example of two beneficial mutations working together to provide a new function (where we would expect to see millions of examples), that demonstrates that the path to producing new functions with multiple mutations does not typically involve multiple beneficial mutations.
In fact... The only example we have on the table at the moment involves multiple non-beneficial mutations (not multiple beneficial mutations).
A general comment. You assume that there is no study of multiple beneficial mutations described in any of the thousands of articles on mutations and evolutionary biology because neither you or I can’t find any. Isn’t that a bit overhasty. (You didn’t comment the reference I gave in #42 https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4429600/ )
I think that we should finish this discussion before starting a discussion about Behe’s Intelligent Design argument.