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# Rebuttal To Creationists - "Since We Can't Directly Observe Evolution..."

Author Topic:   Rebuttal To Creationists - "Since We Can't Directly Observe Evolution..."
Taq
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 Message 136 of 2806 (898215) 09-20-2022 4:35 PM Reply to: Message 135 by Kleinman09-20-2022 4:11 PM

Re: Apples and oranges
Kleinman writes:
Do you understand that mutations are random events? And that accumulation of beneficial mutations on a lineage is a Markov process where the joint probability of beneficial mutations occurring is governed by the multiplication rule of probabilities.
Yes, I understand it just fine.
Where is the problem?
That's why your back-of-the-envelope calculation of humans having 200,000 beneficial mutations is wrong. You are using a simple neutral evolution calculation and assuming that 10% of the mutations are beneficial based on rank speculation.
Wrong on both accounts. I never assumed that all mutations are neutral nor did I claim that 10% of all mutations are beneficial. First, I said that only 10% of fixed mutations would occur in functional DNA which means only 10% of fixed mutations would have a chance of being beneficial (assuming de novo gene production is rare). Of those fixed mutations I said maybe 10% are beneficial as just a guess. 10% of 10% would be 1% of all fixed mutations could be beneficial. Again, I stress the word fixed.
I am not saying that 10% of even 1% of all mutations are beneficial. We are talking about the fixed mutations. And wouldn't you know it, beneficial mutations have a much higher chance of reaching fixation than neutral ones on a one-to-one basis. If you want, we could say that 0.1% or even 0.0001% of fixed mutations between humans and chimps are beneficial in humans, if you want.
You are also edging closer to the Sharpshooter fallacy where you assume that the genomes we get at the end were the only possible outcome. What you ignore is the many different paths that could have been taken. Epistasis is also a very real thing. Interaction between mutations can have a profound effect on what paths evolution can and does take. A seemingly neutral mutation can actually influence the fitness impact of future mutations, making a future mutation either beneficial or detrimental where it would have been neutral without the preceding mutation. There is more than one road that leads to Rome.
Why don't you learn how the Kishony and Lenski experiments work?
I already know how they work.

 This message is a reply to: Message 135 by Kleinman, posted 09-20-2022 4:11 PM Kleinman has replied

 Replies to this message: Message 137 by Kleinman, posted 09-20-2022 4:44 PM Taq has replied

Kleinman
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Joined: 10-06-2016

 Message 137 of 2806 (898216) 09-20-2022 4:44 PM Reply to: Message 136 by Taq09-20-2022 4:35 PM

Re: Apples and oranges
Kleinman:
Why don't you learn how the Kishony and Lenski experiments work?
Taq:
I already know how they work.

Why does it take a billion replications in each of their lineages to accumulate each of their beneficial mutations?

 This message is a reply to: Message 136 by Taq, posted 09-20-2022 4:35 PM Taq has replied

 Replies to this message: Message 138 by Taq, posted 09-20-2022 4:55 PM Kleinman has replied

Taq
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 Message 138 of 2806 (898217) 09-20-2022 4:55 PM Reply to: Message 137 by Kleinman09-20-2022 4:44 PM

Re: Apples and oranges
Kleinman writes:
Why does it take a billion replications in each of their lineages to accumulate each of their beneficial mutations?
Because of the stringency of the fitness landscape. There are only 1 or a few mutations that will allow adaptation to the new conditions. In the Lenski experiment it required a very rare recombination event to evolve aerobic citrate metabolism. In the case of antibiotic resistance there can be as few as 1 mutation that confers resistance. Some adaptations are just harder to come by than others.
On top of that, bacteria are asexual. A lack of recombination in each generation limits the mixing of different mutations and different alleles.

 This message is a reply to: Message 137 by Kleinman, posted 09-20-2022 4:44 PM Kleinman has replied

 Replies to this message: Message 139 by Kleinman, posted 09-20-2022 5:08 PM Taq has replied

Kleinman
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 Message 139 of 2806 (898218) 09-20-2022 5:08 PM Reply to: Message 138 by Taq09-20-2022 4:55 PM

Re: Apples and oranges
Kleinman:
Why does it take a billion replications in each of their lineages to accumulate each of their beneficial mutations?
Taq:
Because of the stringency of the fitness landscape. There are only 1 or a few mutations that will allow adaptation to the new conditions. In the Lenski experiment it required a very rare recombination event to evolve aerobic citrate metabolism. In the case of antibiotic resistance there can be as few as 1 mutation that confers resistance. Some adaptations are just harder to come by than others.

Why don't you tell Lenski and Kishony how to make their experiments perform more rapidly? And there are multiple different mutations that give antibiotic resistance. Each must take their own evolutionary trajectory. Read this:
JSTOR: Access Check
Taq:
On top of that, bacteria are asexual. A lack of recombination in each generation limits the mixing of different mutations and different alleles.
Why doesn't recombination defeat combination therapy for the treatment of HIV? Why don't you tell us the mathematics which describes random recombination if you can? I'll even give you a hint. You do that math using the trinomial distribution.

 This message is a reply to: Message 138 by Taq, posted 09-20-2022 4:55 PM Taq has replied

 Replies to this message: Message 140 by Taq, posted 09-20-2022 5:17 PM Kleinman has replied

Taq
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 (2)
 Message 140 of 2806 (898219) 09-20-2022 5:17 PM Reply to: Message 139 by Kleinman09-20-2022 5:08 PM

Re: Apples and oranges
Why don't you tell Lenski and Kishony how to make their experiments perform more rapidly?
I don't see why the speed of the experiment matters.
Why doesn't recombination defeat combination therapy for the treatment of HIV?
It does.
quote:
Human immunodeficiency virus (HIV) is a diploid virus: each virion carries two complete RNA genomic strands. Homologous recombination can occur when a cell is coinfected with two different but related strains. Naturally occurring recombinant HIV strains have been found in infected patients in regions of the world where multiple genotypic variants cocirculate. One recombinant HIV strain has spread rapidly to millions of persons in Southeast Asia. Recombination is a mechanism whereby high level and multidrug-resistant strains may be generated in individual treated patients. Recombination also poses theoretical problems for the development of a safe HIV vaccine. Certain features of HIV replication, such as syncytium formation and transactivation, may be best understood as components of a sexual reproductive cycle. Recombination may be an important HIV evolutionary strategy.
Recombination in HIV: an important viral evolutionary strategy. - PMC
Why don't you tell us the mathematics which describes random recombination if you can? I'll even give you a hint. You do that math using the trinomial distribution.
Mathematics is meaningless unless you understand the process you are applying it to. From what I can see, you simply don't understand how evolution or biology works.

 This message is a reply to: Message 139 by Kleinman, posted 09-20-2022 5:08 PM Kleinman has replied

 Replies to this message: Message 141 by Kleinman, posted 09-20-2022 5:38 PM Taq has replied

Kleinman
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From: United States
Joined: 10-06-2016

 Message 141 of 2806 (898221) 09-20-2022 5:38 PM Reply to: Message 140 by Taq09-20-2022 5:17 PM

Re: Apples and oranges
Kleinman:
Why don't you tell Lenski and Kishony how to make their experiments perform more rapidly?
Taq:
I don't see why the speed of the experiment matters.

You are claiming that the stringent standards of the experiment are what is causing it to take a billion replications for each beneficial mutation. How can they make their experiment less stringent?
Kleinman:
Why doesn't recombination defeat combination therapy for the treatment of HIV?
Taq:
It does.
quote:
Human immunodeficiency virus (HIV) is a diploid virus: each virion carries two complete RNA genomic strands. Homologous recombination can occur when a cell is coinfected with two different but related strains. Naturally occurring recombinant HIV strains have been found in infected patients in regions of the world where multiple genotypic variants cocirculate. One recombinant HIV strain has spread rapidly to millions of persons in Southeast Asia. Recombination is a mechanism whereby high level and multidrug-resistant strains may be generated in individual treated patients. Recombination also poses theoretical problems for the development of a safe HIV vaccine. Certain features of HIV replication, such as syncytium formation and transactivation, may be best understood as components of a sexual reproductive cycle. Recombination may be an important HIV evolutionary strategy.
Recombination in HIV: an important viral evolutionary strategy. - PMC

You and the people who wrote your 1997 reference need to come up to date on the empirical evidence. 3 drug combination therapy for the treatment of HIV works successfully despite the fact that the virus does recombination. If you understood the mathematics of random recombination, you would know why.
Kleinman:
Why don't you tell us the mathematics which describes random recombination if you can? I'll even give you a hint. You do that math using the trinomial distribution.
Taq:
Mathematics is meaningless unless you understand the process you are applying it to. From what I can see, you simply don't understand how evolution or biology works.

The paper in the following link shows you how to do the mathematics of random recombination:
Random recombination and evolution of drug resistance

 This message is a reply to: Message 140 by Taq, posted 09-20-2022 5:17 PM Taq has replied

 Replies to this message: Message 142 by Taq, posted 09-20-2022 5:48 PM Kleinman has replied

Taq
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 Message 142 of 2806 (898222) 09-20-2022 5:48 PM Reply to: Message 141 by Kleinman09-20-2022 5:38 PM

Re: Apples and oranges
Kleinman writes:
You are claiming that the stringent standards of the experiment are what is causing it to take a billion replications for each beneficial mutation.
I am claiming that the beneficial mutations for the adaptation they are studying are rare. That is the stringency I am talking about.
For the Lenski experiment, they had no idea how long it would take which was part of the experiment. It could have taken just a few days, but it didn't. In the case of the Kishony experiment they would have known the rate of adaptation for the conditions they put the bacteria under so that they could get the results they wanted within the experimental design. The same can be said for classical experiments like the Luria-Delbruck fluctuation experiment and the Lederbergs' plate replica experiment.
3 drug combination therapy for the treatment of HIV works successfully despite the fact that the virus does recombination. If you understood the mathematics of random recombination, you would know why.
What does that have to do with human evolution?
To use an analogy, you are pretending that the odds of winning the lottery can be applied to flipping a coin.

 This message is a reply to: Message 141 by Kleinman, posted 09-20-2022 5:38 PM Kleinman has replied

 Replies to this message: Message 143 by Kleinman, posted 09-20-2022 6:58 PM Taq has replied

Kleinman
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Joined: 10-06-2016

 Message 143 of 2806 (898223) 09-20-2022 6:58 PM Reply to: Message 142 by Taq09-20-2022 5:48 PM

Re: Apples and oranges
Kleinman:
You are claiming that the stringent standards of the experiment are what is causing it to take a billion replications for each beneficial mutation.
Taq:
I am claiming that the beneficial mutations for the adaptation they are studying are rare. That is the stringency I am talking about.

The probability of any mutation occurring, not just beneficial mutations are rare. They occur at a frequency of about 1/(mutation rate) replications. There is nothing you can do to change that mathematical fact of life.
Taq:
For the Lenski experiment, they had no idea how long it would take which was part of the experiment. It could have taken just a few days, but it didn't. In the case of the Kishony experiment they would have known the rate of adaptation for the conditions they put the bacteria under so that they could get the results they wanted within the experimental design. The same can be said for classical experiments like the Luria-Delbruck fluctuation experiment and the Lederbergs' plate replica experiment.
What Lenski found is that it took billions of replications for each beneficial mutation to occur on his most fit lineage and Kishony found that it requires a colony size of a billion for a beneficial mutation to occur. This should not have been a surprise since beneficial (and all) mutations occur at a frequency of about 1/(mutation rate) replications.
Kleinman:
3 drug combination therapy for the treatment of HIV works successfully despite the fact that the virus does recombination. If you understood the mathematics of random recombination, you would know why.
Taq:
What does that have to do with human evolution?

The mathematics of random recombination works the same for all replicators. The probability of a particular random recombination event occurring will be low unless the frequency of the two alleles is high in the population. You should try to do the math yourself.
Taq:
To use an analogy, you are pretending that the odds of winning the lottery can be applied to flipping a coin.
If you are talking about whether an adaptive mutation will occur or not, it is similar to a coin tossing problem. The difference is that coin tossing is symmetric with a probability of 0.5 for each outcome. The outcomes for whether an adaptive mutation occurs or not is highly asymmetric with a probability of the beneficial mutation rate and 1-(the beneficial mutation rate). When it comes to getting two or more adaptive mutations, it's like winning two or more lotteries. That math is governed by the multiplication rule.

 This message is a reply to: Message 142 by Taq, posted 09-20-2022 5:48 PM Taq has replied

 Replies to this message: Message 144 by vimesey, posted 09-20-2022 10:53 PM Kleinman has replied Message 150 by Taq, posted 09-21-2022 10:55 AM Kleinman has replied

vimesey
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 (1)
 Message 144 of 2806 (898225) 09-20-2022 10:53 PM Reply to: Message 143 by Kleinman09-20-2022 6:58 PM

Re: Apples and oranges
The probability of a particular random recombination event occurring will be low unless the frequency of the two alleles is high in the population.
There we have it - the Texas sharpshooter fallacy.

Could there be any greater conceit, than for someone to believe that the universe has to be simple enough for them to be able to understand it ?

 This message is a reply to: Message 143 by Kleinman, posted 09-20-2022 6:58 PM Kleinman has replied

 Replies to this message: Message 146 by Kleinman, posted 09-21-2022 8:05 AM vimesey has not replied

Tanypteryx
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 (1)
 Message 145 of 2806 (898226) 09-20-2022 11:32 PM Reply to: Message 123 by ringo09-20-2022 1:36 PM

Re: Video not available
So it's hard to figure out what you're trying to accomplish here.
It looks like he's trying to generate traffic on his papers. He doesn't have many reads or citations.

What if Eleanor Roosevelt had wings? -- Monty Python

One important characteristic of a theory is that is has survived repeated attempts to falsify it. Contrary to your understanding, all available evidence confirms it. --Subbie

If evolution is shown to be false, it will be at the hands of things that are true, not made up. --percy

The reason that we have the scientific method is because common sense isn't reliable. -- Taq

 This message is a reply to: Message 123 by ringo, posted 09-20-2022 1:36 PM ringo has seen this message but not replied

 Replies to this message: Message 147 by Kleinman, posted 09-21-2022 8:07 AM Tanypteryx has replied

Kleinman
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 Message 146 of 2806 (898230) 09-21-2022 8:05 AM Reply to: Message 144 by vimesey09-20-2022 10:53 PM

Re: Apples and oranges
Kleinman:
The probability of a particular random recombination event occurring will be low unless the frequency of the two alleles is high in the population.
vimesey:
There we have it - the Texas sharpshooter fallacy.

Vimsey thinks that an Australian Aborigine with a beneficial allele and an Arctic Eskimo with a different beneficial allele will meet, have children and recombine those two beneficial alleles. They must have done it on recombination.com. Quite a sharp argument you have there.

 This message is a reply to: Message 144 by vimesey, posted 09-20-2022 10:53 PM vimesey has not replied

Kleinman
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 Message 147 of 2806 (898231) 09-21-2022 8:07 AM Reply to: Message 145 by Tanypteryx09-20-2022 11:32 PM

Re: Video not available
ringo:
So it's hard to figure out what you're trying to accomplish here.
Tanypteryx:
It looks like he's trying to generate traffic on his papers. He doesn't have many reads or citations.

Why not, it's working. However, that's not what motiviated me to start posting here again. One of your administrators sent me an email with a list of topics and this was one of them. Perhaps this administrator was trying to generate traffic on what is a pretty boring discussion. Anyway, I like teaching biologists the physics and mathematics of biological evolution. But I have to keep the discussion at a beginner's level because of their minimal training and very biased understanding of the subject. It's hard to teach the physical and mathematical facts of life about biological evolution when all the student knows is what is taught in his fossil tea-leaf reading courses. Why so few transitional fossils (are there really any?) when it takes a billion replications for each transitional adaptational step in the Kishony and Lenski experiments?

 This message is a reply to: Message 145 by Tanypteryx, posted 09-20-2022 11:32 PM Tanypteryx has replied

 Replies to this message: Message 148 by nwr, posted 09-21-2022 10:52 AM Kleinman has replied Message 151 by Tanypteryx, posted 09-21-2022 12:24 PM Kleinman has not replied Message 157 by ringo, posted 09-21-2022 3:08 PM Kleinman has replied

nwr
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 Message 148 of 2806 (898233) 09-21-2022 10:52 AM Reply to: Message 147 by Kleinman09-21-2022 8:07 AM

Re: Video not available
One of your administrators sent me an email with a list of topics and this was one of them.
I think that was just a test mailing. See Message 53.

Fundamentalism - the anti-American, anti-Christian branch of American Christianity

 This message is a reply to: Message 147 by Kleinman, posted 09-21-2022 8:07 AM Kleinman has replied

 Replies to this message: Message 152 by Kleinman, posted 09-21-2022 12:41 PM nwr has seen this message but not replied

Percy
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 Message 149 of 2806 (898234) 09-21-2022 10:53 AM Reply to: Message 64 by Kleinman09-18-2022 11:21 AM

Re: Video not available
We've had an Internet outage, landscaper dug up the cable.
Kleinman writes:
You seem to be good at formatting, I'll leave that to you.
Oh, Professor Kleinman, you are too funny, talking of math while presenting no equations. I get it. You want us to create the equations ourselves.
You do seem to be having some difficulty with physics and math.
Oh, yes, Professor Kleinman, I have many problems with physics and math. In the mathemacian/physicist/engineer jokes, I was the engineer who proceeded half the distance to the beautiful woman on each strike of the clock, and I was the mathematician who let the fire burn once he knew there was a solution, and I was the physicist who thought that 9 not being a prime number could be experimental error.
For example, you seem to think that populations are competing for space.
I am so embarrassed about my wrong guess that you meant lebensraum. Are they maybe competing for poker chips?
That would be this equation:
And wants to know the difference between that equation and equation [3] from the Lenski team paper.
Distribution of fixed beneficial mutations and the rate of adaptation in asexual populations
That would be this equation:
${\mathbf{\color{cyan} p(s) = \frac{1}{\sigma} \frac{{e^{-(s/\sigma)}}^\beta}{\Gamma(1+\beta^{-1})}}}$
You implied this equation was wrong when you said, "Their problem is that they are assuming that biological evolution obeys an exponential (or exponential-like) distribution function," in Message 59. But your equation has exponentials, too. You didn't provide any equations yourself, so first tell me if I've chosen the right equations, because it is very difficult to tell which equations you mean you when just post a link to a paper and do not specify which equation. If I selected the wrong equations then please post the correct ones.
And if I selected the correct equations then why don't they appear comparable, since one is probability for a single mutation and the other is just a distribution of probabilities across multiple mutations. Except for the distribution aspect, shouldn't these equations be very similar?
--Percy

 This message is a reply to: Message 64 by Kleinman, posted 09-18-2022 11:21 AM Kleinman has not replied

 Replies to this message: Message 153 by dwise1, posted 09-21-2022 12:45 PM Percy has replied

Taq
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Posts: 9301
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 Message 150 of 2806 (898236) 09-21-2022 10:55 AM Reply to: Message 143 by Kleinman09-20-2022 6:58 PM

Re: Apples and oranges
Kleinman writes:
What Lenski found is that it took billions of replications for each beneficial mutation to occur on his most fit lineage and Kishony found that it requires a colony size of a billion for a beneficial mutation to occur. This should not have been a surprise since beneficial (and all) mutations occur at a frequency of about 1/(mutation rate) replications.
You are again assuming all adaptations are the same. They aren't. Let's take a look at a classic paper, the Lederbergs' plate replica paper:
quote:
The culture is fully sensitive to the phage T-1, as well as to streptomycin, and like most E. coli strains gives rise to resistant mutants at rates of approximately 10^-7 and 10^-10 per division, respectively.
REPLICA PLATING AND INDIRECT SELECTION OF BACTERIAL MUTANTS - PMC
That's a thousand fold difference between beneficial mutation rates for different adaptations.
The mathematics of random recombination works the same for all replicators.
The mathematics are different for each species and each fitness landscape. That's what you can't seem to understand. For some adaptations there might only be a handful of beneficial mutations possible. For a different adaptation there may be thousands of possible beneficial mutations.
Added in edit: How many possible evolutionary pathways are there for an arboreal ape to adapt to an open savanna? I would think there are many, many, many possible pathways. Wouldn't you agree?
The difference is that coin tossing is symmetric with a probability of 0.5 for each outcome.
So it would be incorrect to say that the mathematics for calculating a winning lottery ticket does not apply to the odds of flipping heads?
This same thing applies to different adaptations.

Edited by Taq, .

 This message is a reply to: Message 143 by Kleinman, posted 09-20-2022 6:58 PM Kleinman has replied

 Replies to this message: Message 156 by Kleinman, posted 09-21-2022 1:21 PM Taq has replied

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