Can Mutation Invent?

[Nils]

Especially when the overwhelming majority of observed beneficial mutations degrade or remove genetic information instead of altering (like the malaria examples) or even more infrequently adding genetic information.

Beneficial 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.
Agree?

[/quyou ote]
You didn’t answer my question.
[/quote]
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.

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.

Probably you can find somewhere in the vast literature on evolution something similar.

I haven't been able to find any examples.
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.

However as I write in post #31 I base my conclusion on three presumptions. Is any of these false?

I believe I have already stipulated to those three premises.

If not, the conclusion follows directly without any experiment.

No it doesn't...
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.

The three premises you mention and the conclusion come from post #31. There is nothing about billions of benefical mutations.

We already have one example on the table that contradicts that that presumption.

What are you talking about?

We 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).

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 experiment

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.

[DBowling]

Especially when the overwhelming majority of observed beneficial mutations degrade or remove genetic information instead of altering (like the malaria examples) or even more infrequently adding genetic information.

Beneficial 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.
Agree?

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.

Lenski's thirty year experiment has demonstrated a number of beneficial mutations.
So the issue here is not an absence of beneficial mutations in Lenski's experiments.
The issue that Behe points out is the nature (not quantity) of the beneficial mutations.
The observed nature of Lenski's beneficial mutations overwhelmingly degrades and diminishes genetic information instead of adding new genetic information.

However as I write in post #31 I base my conclusion on three presumptions. Is any of these false?

I believe I have already stipulated to those three premises.

If not, the conclusion follows directly without any experiment.

No it doesn't...
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.

The three premises you mention and the conclusion come from post #31. There is nothing about billions of benefical mutations.

Ok... I'll do it again
I am willing to stipulate to your three premises in post #31.
Fair enough?

We already have one example on the table that contradicts that that presumption.

What are you talking about?

This is what I am talking about...
We agree that malaria's resistance to chloroquine involves two non-beneficial mutations working together to perform a new function.
We have a real live example of two mutations working together that is not formed by two beneficial mutations

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).

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 experiment

No... in the paragraph above I am referring the observed behavior of evolution in malaria's developing resistance to atovaquone and chloroquine.

To summarize...
Lenski's experiments demonstrate that beneficial mutations overwhelmingly remove or degrade genetic information as opposed to adding new genetic information as current evolutionary theory presumes.

The malaria examples demonstrate that coordinated mutations in the real world are not necessarily a function of beneficial mutations.
If coordinated mutations were typically a function beneficial mutations, then we would expect to see 100 million examples of beneficial mutations producing 2 coordinated mutations for every single example of non-beneficial mutations producing 2 coordinated mutations.
Since this is not what we observe in the real world, that draws into question the unverified presumption that coordinated mutations are typically a function of beneficial mutations (instead of non-beneficial mutations).

[Nils]

Especially when the overwhelming majority of observed beneficial mutations degrade or remove genetic information instead of altering (like the malaria examples) or even more infrequently adding genetic information.

Beneficial 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.
Agree?

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.

Lenski's thirty year experiment has demonstrated a number of beneficial mutations.
So the issue here is not an absence of beneficial mutations in Lenski's experiments.
The issue that Behe points out is the nature (not quantity) of the beneficial mutations.
The observed nature of Lenski's beneficial mutations overwhelmingly degrades and diminishes genetic information instead of adding new genetic information.

OK, I have to repeat the quote of Behe about Lemski’s experiment, from post #4: "there were no molecular machines, no new genes and yet it had so many chances evolutionary theory would have predicted you get something really impressive and it wasn't seen". That is Behe’s astonishing statement. What is your comment to this?

- - -

To summarize...
Lenski's experiments demonstrate that beneficial mutations overwhelmingly remove or degrade genetic information as opposed to adding new genetic information as current evolutionary theory presumes.

So what? Even if a great majority of beneficial mutations remove or degrade and that in the long run isn’t beneficial there are some that add information and that is enough. Those will prevail in the long run. Behe has written about this in an article on “The first rule” but this article has been heavily criticised.

The malaria examples demonstrate that coordinated mutations in the real world are not necessarily a function of beneficial mutations.
If coordinated mutations were typically a function beneficial mutations, then we would expect to see 100 million examples of beneficial mutations producing 2 coordinated mutations for every single example of non-beneficial mutations producing 2 coordinated mutations.

You haven’t given any clear definition of what you mean by “coordinated”. (Curious word, coordinated by who or what). Is “coordinated” the same as “needed”? What do you mean by beneficial mutations producing 2 coordinated mutations? From where do you get this figure 100 million? How can you compare the number of possible beneficial mutations in a specific DNA with the number of non-beneficial that together produce a beneficial combination? That such a combination exists in malaria doesn’t implicate that a similar combination exists in other DNAs for instance E coli. Also, the number of beneficial possible mutations isn’t a fixed number, it is highly dependent of the environment. Your statement seems confused.

Since this is not what we observe in the real world, that draws into question the unverified presumption that coordinated mutations are typically a function of beneficial mutations (instead of non-beneficial mutations).

Again, “coordinated”? I don't understand.

- - -

And, you didn’t comment, from the previous post:
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 nor 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/ )

[DBowling]

Lenski's thirty year experiment has demonstrated a number of beneficial mutations.
So the issue here is not an absence of beneficial mutations in Lenski's experiments.
The issue that Behe points out is the nature (not quantity) of the beneficial mutations.
The observed nature of Lenski's beneficial mutations overwhelmingly degrades and diminishes genetic information instead of adding new genetic information.

OK, I have to repeat the quote of Behe about Lemski’s experiment, from post #4: "there were no molecular machines, no new genes and yet it had so many chances evolutionary theory would have predicted you get something really impressive and it wasn't seen". That is Behe’s astonishing statement. What is your comment to this?

Well... I wouldn't personally have expected fully functional molecular machines...
Allowing for some hyperbole on Behe's part, I agree with Behe's basic sentiment.

To create the tree of life would require billions of certain types of beneficial mutations (specifically substitutions and more importantly adds).
I personally wouldn't expect to see a fully developed molecular machine, but the path to creating new molecular machines would have to at least start with multiple adds and substitutions 'working together' to create some sort of new function.
Instead or multiple adds creating new functions, we see just the opposite. The beneficial mutations in Lenski's mutations don't add new information, they overwhelmingly do just the opposite. They degrade existing genetic information.

So we see that the behavior of random mutation in Lenski's experiments (degrading existing genetic information) is inconsistent with the anticipated behavior required to create the tree of life (adding adding new genetic information).

Again the issue here is the nature of observed beneficial mutations not the quantity of beneficial mutations.

The malaria examples demonstrate that coordinated mutations in the real world are not necessarily a function of beneficial mutations.
If coordinated mutations were typically a function beneficial mutations, then we would expect to see 100 million examples of beneficial mutations producing 2 coordinated mutations for every single example of non-beneficial mutations producing 2 coordinated mutations.

You haven’t g coiven any clear definition of what you mean by “coordinated”. (Curious word, coordinated by who or what). Is “coordinated” the same as “needed”? What do you mean by beneficial mutations producing 2 coordinated mutations? From where do you get this figure 100 million? How can you compare the number of possible beneficial mutations in a specific DNA with the number of non-beneficial that together produce a beneficial combination? That such a combination exists in malaria doesn’t implicate that a similar combination exists in other DNAs for instance E coli. Also, the number of beneficial possible mutations isn’t a fixed number, it is highly dependent of the environment. Your statement seems confused.

Since this is not what we observe in the real world, that draws into question the unverified presumption that coordinated mutations are typically a function of beneficial mutations (instead of non-beneficial mutations).

Again, “coordinated”? I don't understand.

I use the term 'coordinated' to refer to multiple specific and separate mutations working together to perform a unique specific function.

The real world example of coordinated mutations that we have been discussing is Malaria's resistance to chloroquine.
Both mutations are required (ie working together) to provide a single function (resistance to chloroquine) that is independent from functions that the individual mutations alone provide.

And, you didn’t comment, from the previous post:
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 nor 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/ )

From what I saw in that link, I didn't see anything involving the observed behavior and capability of random mutations.

Behe's issue concerns whether or not the observed behavior of random mutation in nature and in the lab is capable of generating the complex code that we see in the DNA of life today and in the fossil record.

I don't think that link even addresses the observed behavior of random mutation.

[DBowling]

In my previous post I neglected to address this issue...

The malaria examples demonstrate that coordinated mutations in the real world are not necessarily a function of beneficial mutations.
If coordinated mutations were typically a function beneficial mutations, then we would expect to see 100 million examples of beneficial mutations producing 2 coordinated mutations for every single example of non-beneficial mutations producing 2 coordinated mutations.

From where do you get this figure 100 million? How can you compare the number of possible beneficial mutations in a specific DNA with the number of non-beneficial that together produce a beneficial combination? That such a combination exists in malaria doesn’t implicate that a similar combination exists in other DNAs for instance E coli.

The 100 million comes from comparing the frequency of beneficial mutations and non beneficial mutations creating a new function in malaria.

The single beneficial mutation required to create the beneficial mutation required to give malaria resistance to atovaquone occurs at an observed rate of around 1 in 10^12.
Using your premises that would mean that 2 beneficial mutations should be able to create some sort of new function at an estimated rate of around 1 in 2X10^12.
Would you agree?

We agree that malaria's resistance to chloroquine involves two non-beneficial mutations working together. The observed rate of this non-beneficial coordinated mutation is around 1 in 10^20.

So if we compare the frequency of beneficial and non-beneficial mutations we see that two beneficial mutations should produce a new function at a rate that is 10^8 more rapidly than two non beneficial mutations could typically produce a new function.
Or to put it another way...
Two beneficial mutations should produce approximately 100 million (10^8) new functions for every single new function that two non-beneficial mutations are able to to produce.

A significant issue here is not just the difference, but the enormous scope of the difference, around 100 million.
And 100 million (or even 1 million for that matter) should be observable somewhere... somehow.
But it isn't.
That frequency for two coordinated beneficial mutations (or anything remotely close) is just not what we see in nature and in the lab.

So again we see that evolution rates in nature and in the lab are inconsistent with the unverified premise that beneficial mutations are able to produce new complex genetic code at a rate that is orders of magnitude faster than non-beneficial mutations.

We have agreed that it is beyond the capability of all life that has ever existed on earth for 5 or 6 non-beneficial mutations to create a new function.
If the observed frequency of 2 beneficial mutations ability to produce a new function is not orders of magnitude faster than the observed frequency of 2 non-beneficial mutations creating a new function, then it is also beyond the capability of all life that has ever existed on earth for billions of mutations (beneficial or non-beneficial) to create a new function.

[Nils]

In my previous post I neglected to address this issue...

The malaria examples demonstrate that coordinated mutations in the real world are not necessarily a function of beneficial mutations.
If coordinated mutations were typically a function beneficial mutations, then we would expect to see 100 million examples of beneficial mutations producing 2 coordinated mutations for every single example of non-beneficial mutations producing 2 coordinated mutations.

From where do you get this figure 100 million? How can you compare the number of possible beneficial mutations in a specific DNA with the number of non-beneficial that together produce a beneficial combination? That such a combination exists in malaria doesn’t implicate that a similar combination exists in other DNAs for instance E coli.

The 100 million comes from comparing the frequency of beneficial mutations and non beneficial mutations creating a new function in malaria.

The single beneficial mutation required to create the beneficial mutation required to give malaria resistance to atovaquone occurs at an observed rate of around 1 in 10^12.
Using your premises that would mean that 2 beneficial mutations should be able to create some sort of new function at an estimated rate of around 1 in 2X10^12.
Would you agree?

No, only if you include an assumption that there exists two possible beneficial mutations that have never occurred before! This assumption is completely unjustified. If there were a (or two) possible beneficial mutation in E coli it (they) would have occurred millions of years ago (the E coli is more than one hundred million year old). Only if the environment is changed, as in Lempski’s experiment, you would expect to see a new mutation, a mutation that adapts the E coli to the new environment, and one such mutation was found.
Do you agree?

We agree that malaria's resistance to chloroquine involves two non-beneficial mutations working together. The observed rate of this non-beneficial coordinated mutation is around 1 in 10^20.

So if we compare the frequency of beneficial and non-beneficial mutations we see that two beneficial mutations should produce a new function at a rate that is 10^8 more rapidly than two non beneficial mutations could typically produce a new function.
Or to put it another way...
Two beneficial mutations should produce approximately 100 million (10^8) new functions for every single new function that two non-beneficial mutations are able to to produce.

A significant issue here is not just the difference, but the enormous scope of the difference, around 100 million.
And 100 million (or even 1 million for that matter) should be observable somewhere... somehow.
But it isn't.
That frequency for two coordinated beneficial mutations (or anything remotely close) is just not what we see in nature and in the lab.

So again we see that evolution rates in nature and in the lab are inconsistent with the unverified premise that beneficial mutations are able to produce new complex genetic code at a rate that is orders of magnitude faster than non-beneficial mutations.

We have agreed that it is beyond the capability of all life that has ever existed on earth for 5 or 6 non-beneficial mutations to create a new function.
If the observed frequency of 2 beneficial mutations ability to produce a new function is not orders of magnitude faster than the observed frequency of 2 non-beneficial mutations creating a new function, then it is also beyond the capability of all life that has ever existed on earth for billions of mutations (beneficial or non-beneficial) to create a new function.

All these conclusions are erroneously, based on a false statement.

I will comment post #49 later.

[DBowling]

In my previous post I neglected to address this issue...

The malaria examples demonstrate that coordinated mutations in the real world are not necessarily a function of beneficial mutations.
If coordinated mutations were typically a function beneficial mutations, then we would expect to see 100 million examples of beneficial mutations producing 2 coordinated mutations for every single example of non-beneficial mutations producing 2 coordinated mutations.

From where do you get this figure 100 million? How can you compare the number of possible beneficial mutations in a specific DNA with the number of non-beneficial that together produce a beneficial combination? That such a combination exists in malaria doesn’t implicate that a similar combination exists in other DNAs for instance E coli.

The 100 million comes from comparing the frequency of beneficial mutations and non beneficial mutations creating a new function in malaria.

The single beneficial mutation required to create the beneficial mutation required to give malaria resistance to atovaquone occurs at an observed rate of around 1 in 10^12.
Using your premises that would mean that 2 beneficial mutations should be able to create some sort of new function at an estimated rate of around 1 in 2X10^12.
Would you agree?

No, only if you include an assumption that there exists two possible beneficial mutations that have never occurred before! This assumption is completely unjustified.

Actually my statement was based on the following

if M1 is beneficial, the population of individuals the have the mutation M1 will spread and finally reach almost the total population. Then the number of generations until M2 occurs will be about the same magnitude as G1. If the time for spreading is Gs, the total time will very approximatively be G1 + Gs + G1. If G1 is a big number 2xG1+Gs is much smaller than G1xG1.

The main point being that based on this assumption, we should be able to observe two beneficial mutations producing a new function at a frequency that is orders of magnitude faster than rate at which we are able to observe two non-beneficial mutations are able to produce a new function.

I just don't see the observable empirical evidence that two beneficial mutations can produce a new function orders of magnitude faster than two non-beneficial mutations can produce a new function.

Only if the environment is changed, as in Lempski’s experiment, you would expect to see a new mutation, a mutation that adapts the E coli to the new environment, and one such mutation was found.

I'm not sure that is totally accurate.
From Wikipedia's article on Lenski's experiments...

The data once again fit the proposed power law model, and, indeed, fit within predictions of the model from earlier data. These results suggest that, contrary to previous thinking, adaptation and adaptive divergence can potentially increase indefinitely, even in a constant environment

But to get back to Behe's point, I don't think we have seen any coordinated beneficial adds creating a new function in Lenski's experiments. However, we have seen lots of beneficial mutations in Lenski's experiments that degrade existing genetic information.

[Nils]

In five different posts in this thread I have argued that in an old species as E coli and with a stable environment there will be no (or very few) beneficial mutations. You have never commented that statement! Instead you have continued to say things as:
Post #49

I personally wouldn't expect to see a fully developed molecular machine, but the path to creating new molecular machines would have to at least start with multiple adds and substitutions 'working together' to create some sort of new function.

Post #50

Two beneficial mutations should produce approximately 100 million (10^8) new functions for every single new function that two non-beneficial mutations are able to to produce.

Post #51

The main point being that based on this assumption, we should be able to observe two beneficial mutations producing a new function at a frequency that is orders of magnitude faster than rate at which we are able to observe two non-beneficial mutations are able to produce a new function.

Now you quote Wikipedia's article on Lenski's experiments:

The data once again fit the proposed power law model, and, indeed, fit within predictions of the model from earlier data. These results suggest that, contrary to previous thinking, adaptation and adaptive divergence can potentially increase indefinitely, even in a constant environment

It’s nice that you finally acknowledges this. The consequence is that the mutation rate in E coli in the long run is very low (as long as there is no change in the environment).
To explain:
A few lines earlier in the Wikipedia reference it says:

All populations showed a pattern of rapid increase in relative fitness during early generations, with this increase decelerating over time. By 20,000 generations the populations grew approximately 70% faster than the ancestral strain.[11] This increase and deceleration in increase has continued in subsequent generations.

my underline

Thus, the fitness got higher but the increase decelerated. The experiment have lasted only 30 years and the deceleration has been clearly visible, so much that it can related to a power law. From that follows that in the next million or even thousand year the increase will become very low, probably not measurable. That means that the mutation frequency will be very low or zero. Therefore it is wrong to expect a high rate of beneficial mutations in E coli as you do (assuming a constant environment as in Lenski’s experiment).

[DBowling]

The experiment have lasted only 30 years and the deceleration has been clearly visible, so much that it can related to a power law. From that follows that in the next million or even thousand year the increase will become very low, probably not measurable. That means that the mutation frequency will be very low or zero. Therefore it is wrong to expect a high rate of beneficial mutations in E coli as you do (assuming a constant environment as in Lenski’s experiment).

As I mentioned before, we get one type of data from Lenski's experiments in the lab, and a different type of data from the behavior of malaria in the real world.

Lenski's experiments have generated a number of beneficial mutations, so we have enough information to accurately evaluate the typical behavior of beneficial mutations. And from Lenski's experiments we have discovered that beneficial mutations overwhelmingly degrade and diminish genetic information. And this behavior is inconsistent with the beneficial mutations required to build the tree of life. To generate the tree of life, beneficial mutations would hypothetically need to add new complex genetic information instead of constantly degrading existing genetic information that we see in Lenski's experiments.

Malaria's adaptation to different drugs gives us insight into the rate at which random mutation is able to generate coordinated mutations (ie... multiple mutations working together to perform a new function). Based on malaria's adaptation to atovaquone and chloroquine we see an exponential relationship between 1 beneficial mutation creating a new function, and 2 beneficial mutations creating a new function.
And by extrapolating the exponential nature of malaria's adaptation to chloroquine we have agreed that it is beyond the capability of all life that has ever existed on this planet for 5 or 6 coordinated non-beneficial mutations to create a new function.

The unverified premise is that multiple beneficial mutations can create new functions orders of magnitude faster than multiple non-beneficial mutations.
With malaria we have one *observable example of two non-beneficial mutations creating a new function.
If beneficial mutations are truly orders of magnitude faster non-beneficial mutations at creating new functions, then where are the millions of observable examples of two beneficial mutations creating a new function.

The lack of observable examples of 2 beneficial mutations creating new a new function in nature, draws into doubt the unverified premise that the multiple single beneficial mutations are a feasible path for creating the complex code that we see in the DNA of life today.

Lenski's experiments tell us that the observed behavior of beneficial mutations overwhelmingly degrades genetic information (as opposed to adding new genetic information).
Malaria's example in nature gives us a real world example of an exponential rate for two coordinated mutations, which is inconsistent with the premise that coordinated mutations are a function of a path of single beneficial mutations.

[Nils]

#54
quote=DBowling post_id=252852 time=1633450017 user_id=10713]

The experiment have lasted only 30 years and the deceleration has been clearly visible, so much that it can related to a power law. From that follows that in the next million or even thousand year the increase will become very low, probably not measurable. That means that the mutation frequency will be very low or zero. Therefore it is wrong to expect a high rate of beneficial mutations in E coli as you do (assuming a constant environment as in Lenski’s experiment).

1.This is about your argument that we should expect lot of beneficial mutations in the e coli experiment, which I deny. Do you agree or not to the last sentence and my reasoning in post # 53 (see above) ? If you don’t respond to my arguments it’s not meaningful to discuss.

Besides, we can’t discuss the issue 1, and all the issues below at the same time. Some of them are complex and will probably need repeated rounds to come to an end. It would be helpful if you choose one so we can discuss that in detail.

As I mentioned before, we get one type of data from Lenski's experiments in the lab, and a different type of data from the behavior of malaria in the real world.

Yes, of course.

2.

Lenski's experiments have generated a number of beneficial mutations, so we have enough information to accurately evaluate the typical behavior of beneficial mutations.

Who says that this is typical. It’s about a bacteria that is hundred of millions year old and the experiment is using a fixed environment. This says nothing about the speed of development in more complex species using sexual reproduction and in a changing environment,

3.

And from Lenski's experiments we have discovered that beneficial mutations overwhelmingly degrade and diminish genetic information.

Who cares as long as there are some beneficial mutation as in Lenski’s experiment.

4.

Malaria's adaptation to different drugs gives us insight into the rate at which random mutation is able to generate coordinated mutations (ie... multiple mutations working together to perform a new function). Based on malaria's adaptation to atovaquone and chloroquine we see an exponential relationship between 1 beneficial mutation creating a new function, and 2 beneficial mutations creating a new function.
And by extrapolating the exponential nature of malaria's adaptation to chloroquine we have agreed that it is beyond the capability of all life that has ever existed on this planet for 5 or 6 coordinated non-beneficial mutations to create a new function.

OK

5

The unverified premise is that multiple beneficial mutations can create new functions orders of magnitude faster than multiple non-beneficial mutations.

I need to know more to be able to comment,

6

With malaria we have one observable example of two non-beneficial mutations creating a new function.
If beneficial mutations are truly orders of magnitude faster non-beneficial mutations at creating new functions, then where are the millions of observable examples of two beneficial mutations creating a new function..

The lack of observable examples of 2 beneficial mutations creating new a new function in nature, draws into doubt the unverified premise that the multiple single beneficial mutations are a feasible path for creating the complex code that we see in the DNA of life today.

I don’t have knowledge of the total evolution literature and experiments. Do you?

Lenski's experiments tell us that the observed behavior of beneficial mutations overwhelmingly degrades genetic information (as opposed to adding new genetic information).

See 3 above

7

Malaria's example in nature gives us a real world example of an exponential rate for two coordinated mutations, which is inconsistent with the premise that coordinated mutations are a function of a path of single beneficial mutations.

I don’t understand. How do you define “coordinated” and “function”? I asked before but didn’t get any answer.

As I say before. It is impossible to discuss all these seven issues at the same time.

[DBowling]

#54
quote=DBowling post_id=252852 time=1633450017 user_id=10713]

The experiment have lasted only 30 years and the deceleration has been clearly visible, so much that it can related to a power law. From that follows that in the next million or even thousand year the increase will become very low, probably not measurable. That means that the mutation frequency will be very low or zero. Therefore it is wrong to expect a high rate of beneficial mutations in E coli as you do (assuming a constant environment as in Lenski’s experiment).

1.This is about your argument that we should expect lot of beneficial mutations in the e coli experiment, which I deny. Do you agree or not to the last sentence and my reasoning in post # 53 (see above) ? If you don’t respond to my arguments it’s not meaningful to discuss.

I have responded to this argument... repeatedly... and I did so in my last post above.

I am not looking to Lenski's experiments to provide data regarding the 'rate' of beneficial mutations in nature.
However, I am paying close attention to the 'nature' of beneficial mutations in Lenski's experiments.
Such as...
what is the nature of beneficial mutations in Lenski's experiments?
Do beneficial mutations typically add genetic information?
Or... Do beneficial mutations typically degrade existing genetic information?

Lenski's experiments have generated a number of beneficial mutations, so we have enough information to accurately evaluate the typical behavior of beneficial mutations.

Who says that this is typical. It’s about a bacteria that is hundred of millions year old and the experiment is using a fixed environment. This says nothing about the speed of development in more complex species using sexual reproduction and in a changing environment.

Behe has actually spent quite a bit of time looking at this question

Behe's book Darwin Devolves

Demonstrates how beneficial mutations overwhelmingly degrade existing genetic information in nature as well as in Lenski''s lab experiments.

Behe discusses the nature of beneficial mutations in nature and in the lab in this lecture
https://www.youtube.com/watch?v=24t2eCjPbq4

And from Lenski's experiments we have discovered that beneficial mutations overwhelmingly degrade and diminish genetic information.

Who cares as long as there are some beneficial mutation as in Lenski’s experiment.

As has been mentioned before, there is no doubt that beneficial mutations do in fact occur... both in nature and in Lenski's experiments.

The question at hand is... do beneficial mutations typically add new genetic information, or do beneficial mutations typically degrade existing genetic information?
And the empirically observed answer from both nature and the lab is that beneficial mutations overwhelmingly degrade existing genetic information.

With malaria we have one observable example of two non-beneficial mutations creating a new function.
If beneficial mutations are truly orders of magnitude faster non-beneficial mutations at creating new functions, then where are the millions of observable examples of two beneficial mutations creating a new function..

The lack of observable examples of 2 beneficial mutations creating new a new function in nature, draws into doubt the unverified premise that the multiple single beneficial mutations are a feasible path for creating the complex code that we see in the DNA of life today.

I don’t have knowledge of the total evolution literature and experiments. Do you?

Nope
But I do know enough about gathering data to know that if "B" is orders of magnitude more frequent than "A".
Then "B" will be observed at a rate that is also orders of magnitude more frequently than "A" is observed.

Malaria's example in nature gives us a real world example of an exponential rate for two coordinated mutations, which is inconsistent with the premise that coordinated mutations are a function of a path of single beneficial mutations.

I don’t understand. How do you define “coordinated” and “function”? I asked before but didn’t get any answer.

Actually I have answered that question... repeatedly...

Most recently from post 49

I use the term 'coordinated' to refer to multiple specific and separate mutations working together to perform a unique specific function.

The real world example of coordinated mutations that we have been discussing is Malaria's resistance to chloroquine.
Both mutations are required (ie working together) to provide a single function (resistance to chloroquine) that is independent from functions that the individual mutations alone provide.

[Nils]

#54
quote=DBowling post_id=252852 time=1633450017 user_id=10713]

The experiment have lasted only 30 years and the deceleration has been clearly visible, so much that it can related to a power law. From that follows that in the next million or even thousand year the increase will become very low, probably not measurable. That means that the mutation frequency will be very low or zero. Therefore it is wrong to expect a high rate of beneficial mutations in E coli as you do (assuming a constant environment as in Lenski’s experiment).

1.This is about your argument that we should expect lot of beneficial mutations in the e coli experiment, which I deny. Do you agree or not to the last sentence and my reasoning in post # 53 (see above) ? If you don’t respond to my arguments it’s not meaningful to discuss.

I have responded to this argument... repeatedly... and I did so in my last post above.

I am not looking to Lenski's experiments to provide data regarding the 'rate' of beneficial mutations in nature.
However, I am paying close attention to the 'nature' of beneficial mutations in Lenski's experiments.
Such as...
what is the nature of beneficial mutations in Lenski's experiments?
Do beneficial mutations typically add genetic information?
Or... Do beneficial mutations typically degrade existing genetic information?

Why do you not answer my question: Do you agree that "it is wrong to expect a high rate of beneficial mutations in E coli as you do (assuming a constant environment as in Lenski’s experiment)." ? (see post # 53 for your statements)

How you use Lenski's experiment is another issue. Regarding that it's not of an important interest whether beneficial mutation "typically" decrade information or not. What is of interest is if it ever happens that they add information.

Referring to Behi without quouting him is meaningless. Do you really think I should read him trying to extract what YOU think is important.

[DBowling]

#54
quote=DBowling post_id=252852 time=1633450017 user_id=10713]

The experiment have lasted only 30 years and the deceleration has been clearly visible, so much that it can related to a power law. From that follows that in the next million or even thousand year the increase will become very low, probably not measurable. That means that the mutation frequency will be very low or zero. Therefore it is wrong to expect a high rate of beneficial mutations in E coli as you do (assuming a constant environment as in Lenski’s experiment).

1.This is about your argument that we should expect lot of beneficial mutations in the e coli experiment, which I deny. Do you agree or not to the last sentence and my reasoning in post # 53 (see above) ? If you don’t respond to my arguments it’s not meaningful to discuss.

I have responded to this argument... repeatedly... and I did so in my last post above.

I am not looking to Lenski's experiments to provide data regarding the 'rate' of beneficial mutations in nature.
However, I am paying close attention to the 'nature' of beneficial mutations in Lenski's experiments.
Such as...
what is the nature of beneficial mutations in Lenski's experiments?
Do beneficial mutations typically add genetic information?
Or... Do beneficial mutations typically degrade existing genetic information?

Why do you not answer my question: Do you agree that "it is wrong to expect a high rate of beneficial mutations in E coli as you do (assuming a constant environment as in Lenski’s experiment)." ? (see post # 53 for your statements)

Let me be very explicit...
I do not expect a high rate of mutations in either the lab or in nature
I do not expect a high rate of beneficial mutations in either the lab or in nature
Therefore ==> I think it is "wrong" to expect a high level of beneficial mutations in either the lab or in nature.

And since the overwhelming majority of beneficial mutations that do occur in nature and in the lab degrade genetic information
I think it is even more "wrong" to expect a high rate of beneficial mutations to add genetic information.

Referring to Behe without quoting him is meaningless. Do you really think I should read him trying to extract what YOU think is important.

Whether or not you check out the Behe links I provided is totally your decision.

The purpose of the links was to provide source material for anyone who might want to fact check my claims that beneficial mutations in nature and in the lab do not typically add new genetic information.
In fact the observed behavior of beneficial mutations in nature and in the lab overwhelming degrade existing genetic information.

[Nils]

Let me be very explicit...
I do not expect a high rate of mutations in either the lab or in nature
I do not expect a high rate of beneficial mutations in either the lab or in nature
Therefore ==> I think it is "wrong" to expect a high level of beneficial mutations in either the lab or in nature.

This way of reasoning seems a bit circular, you “think it is wrong to expect a high level ..." because you “do not expect high rate...”. Is there a differece between "rate" and "level"? Besides, from where did you get the information of mutation levels in nature?

I interpret your statement as you think that Lenski showed that there isn’t a high rate of E Coli beneficial mutations in the experiment.

And since the overwhelming majority of beneficial mutations that do occur in nature and in the lab degrade genetic information
I think it is even more "wrong" to expect a high rate of beneficial mutations to add genetic information.

That seems reasonably as long as you talk about Lemski’s E Coli populations. It may be true in many cases in nature but from what I read about evolution there is an enormous difference in speed between e.g. E coli that has evolved little over hundred million years and higher animals with sexual reproduction in rapidly changing environment. Even if many (or most) beneficial mutations don’t add information some do and that is enough. (I said that a few times but you never commented)

So what you stated in post #54 is apparently wrong (my italics) :
“Lenski's experiments have generated a number of beneficial mutations, so we have enough information to accurately evaluate the typical behavior of beneficial mutations. And from Lenski's experiments we have discovered that beneficial mutations overwhelmingly degrade and diminish genetic information.”
Overwhelmingly perhaps but not totally. You continue:
“ And this behavior is inconsistent with the beneficial mutations required to build the tree of life. To generate the tree of life, beneficial mutations would hypothetically need to add new complex genetic information instead of constantly degrading existing genetic information that we see in Lenski's experiments.”
First Lenski’s experiment doesn’t show that there are no beneficial mutations that add genetic information. Secondly, even if it were so, that doesn’t show that this is the case generally. As I have said repeatedly, E coli hasn’t changed much over one hundred million year. That implies that there have been very few beneficial mutations. E coli is a special case, not a general case. Certainly, if evolution generally were as slow as it is for E coli neither you nor I would exist.

Referring to Behe without quoting him is meaningless. Do you really think I should read him trying to extract what YOU think is important.

Whether or not you check out the Behe links I provided is totally your decision.

The purpose of the links was to provide source material for anyone who might want to fact check my claims that beneficial mutations in nature and in the lab do not typically add new genetic information.
In fact the observed behavior of beneficial mutations in nature and in the lab overwhelming degrade existing genetic information.

Ok, I thought you were debating with me. However, I would not recommend Behe’s writings. It’s highly contentious, and sometimes clearly false, see my post #4. Besides, as I say above, the question isn’t if most beneficial mutation add information overwhelmingly or not but if there are any beneficial mutations that do and that issue Behe doesn’t say anything about.

[DBowling]

Let me be very explicit...
I do not expect a high rate of mutations in either the lab or in nature
I do not expect a high rate of beneficial mutations in either the lab or in nature
Therefore ==> I think it is "wrong" to expect a high level of beneficial mutations in either the lab or in nature.

This way of reasoning seems a bit circular, you “think it is wrong to expect a high level ..." because you “do not expect high rate...”. Is there a differece between "rate" and "level"? Besides, from where did you get the information of mutation levels in nature?

I interpret your statement as you think that Lenski showed that there isn’t a high rate of E Coli beneficial mutations in the experiment.

I think you must have misunderstood me somewhere...

I have never claimed that there was a high level or rate of beneficial mutations in Lenski's experiments.
What the data shows is that an overwhelming majority of the beneficial mutations that did occur in Lenski's experiments degraded existing genetic information.

And the behavior of beneficial mutations in Lenski's experiments is consistent with the observable behavior of beneficial mutations in the real world.

And since the overwhelming majority of beneficial mutations that do occur in nature and in the lab degrade genetic information
I think it is even more "wrong" to expect a high rate of beneficial mutations to add genetic information.

That seems reasonably as long as you talk about Lemski’s E Coli populations. It may be true in many cases in nature but from what I read about evolution there is an enormous difference in speed between e.g. E coli that has evolved little over hundred million years and higher animals with sexual reproduction in rapidly changing environment. Even if many (or most) beneficial mutations don’t add information some do and that is enough. (I said that a few times but you never commented)

You've asserted that a few times but I am unaware of any empirically observed mutation rate data to support that assertion.

One of the reasons I provide links to my sources is so that my assertions can be checked against scientific sources.
So far you have not provided any empirically observed data to support your "some do and that is enough" assertion.

On the other hand, the exponential difference between malaria developing resistance to atovaquone (1 mutation) and chloroquine (2 mutations) demonstrates that empirically observed rate at which "some do" is nowhere near enough.

First Lenski’s experiment doesn’t show that there are no beneficial mutations that add genetic information. Secondly, even if it were so, that doesn’t show that this is the case generally. As I have said repeatedly, E coli hasn’t changed much over one hundred million year. That implies that there have been very few beneficial mutations. E coli is a special case, not a general case. Certainly, if evolution generally were as slow as it is for E coli neither you nor I would exist.

You're actually getting pretty close here...

If evolution generally is as slow as it is for E coli, this demonstrates that (unguided) evolution in and of itself is an inadequate explanation for why you and I do in fact exist.

The purpose of the links was to provide source material for anyone who might want to fact check my claims that beneficial mutations in nature and in the lab do not typically add new genetic information.
In fact the observed behavior of beneficial mutations in nature and in the lab overwhelming degrade existing genetic information.

Ok, I thought you were debating with me. However, I would not recommend Behe’s writings.

Oh I am debating with you...
And this has been enjoyable and beneficial to me as this discussion has pushed me to deep dive some topics that I had not previously looked in to.

However since we are on a public board, I think it is beneficial to post source material links for anyone else who may be following this discussion.
And I even hold out some hope that you might even take a look into some of Behe's work... even if your goal is to somehow prove him wrong