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Author | Topic: Rebuttal To Creationists - "Since We Can't Directly Observe Evolution..." | |||||||||||||||||||||||||||||||||||||||
Taq Member Posts: 10033 Joined: Member Rating: 5.3 |
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.
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Kleinman Member (Idle past 355 days) Posts: 2142 From: United States Joined: |
Kleinman:Why does it take a billion replications in each of their lineages to accumulate each of their beneficial mutations?
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Taq Member Posts: 10033 Joined: Member Rating: 5.3 |
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.
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Kleinman Member (Idle past 355 days) Posts: 2142 From: United States Joined: |
Kleinman: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: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.
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Taq Member Posts: 10033 Joined: Member Rating: 5.3
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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:
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.
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Kleinman Member (Idle past 355 days) Posts: 2142 From: United States Joined: |
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. How can they make their experiment less stringent? Kleinman: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:The paper in the following link shows you how to do the mathematics of random recombination: Random recombination and evolution of drug resistance
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Taq Member Posts: 10033 Joined: Member Rating: 5.3 |
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.
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Kleinman Member (Idle past 355 days) Posts: 2142 From: United States Joined: |
Kleinman: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: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: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: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.
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vimesey Member (Idle past 93 days) Posts: 1398 From: Birmingham, England Joined:
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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 ?
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Tanypteryx Member Posts: 4409 From: Oregon, USA Joined: Member Rating: 5.4
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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.Stop Tzar Vladimir the Condemned! 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
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Kleinman Member (Idle past 355 days) Posts: 2142 From: United States Joined: |
Kleinman: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.
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Kleinman Member (Idle past 355 days) Posts: 2142 From: United States Joined: |
ringo: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?
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nwr Member Posts: 6409 From: Geneva, Illinois Joined: Member Rating: 5.3 |
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
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Percy Member Posts: 22479 From: New Hampshire Joined: Member Rating: 4.7 |
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?
Percy has posted equation (5) from my paper:
The basic science and mathematics of random mutation and natural selection 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:
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
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Taq Member Posts: 10033 Joined: Member Rating: 5.3 |
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: 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, .
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