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Author Topic:   Rebuttal To Creationists - "Since We Can't Directly Observe Evolution..."
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 49 of 2926 (898037)
09-17-2022 5:29 PM
Reply to: Message 46 by PaulK
09-17-2022 5:09 PM


Re: Video not available
Kleinman:
Diversification in populations is simply a matter of replication. That's because replication gives the chance for mutations to occur.
PaulK:
Diversification is not identical with adaption.

That's correct, the diversification might also be neutral or detrimental.
Kleinman:
It takes energy to replicate and if you force different variants to compete for a limited amount of energy, this will limit the population size of the most fit variant. This slows the diversification (adaptation) of all variants in the given environment. Most or all of the less fit variants end up going extinct.
PaulK:
More accurately then competition is needed for adaption, which is slower than unconstrained drift (which you mistakenly call “adaption”)

Experimental evidence shows you are incorrect. The probability of an adaptive mutation depends on the number of replication a particular variant is able to do. That is why the Lenski variants evolve more slowly than the Kishony variants. Lenski energy limits his populations which slows the growth of the individual variant populations. Kishony's colonies easily achieve population sizes of a billion or more. That size population gives a reasonable probability that all possible mutations will occur on some member of that colony when a mutation rate is 1e-9.

This message is a reply to:
 Message 46 by PaulK, posted 09-17-2022 5:09 PM PaulK has replied

Replies to this message:
 Message 60 by PaulK, posted 09-18-2022 2:05 AM Kleinman has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 51 of 2926 (898041)
09-17-2022 7:56 PM
Reply to: Message 50 by dwise1
09-17-2022 7:23 PM


Re: Video not available
Kleinman:
I'm not trying to bullshit you.
dwis1:
No, that is all that you are doing. That is all that you have to work with.

All that creationists have is bullshit. That is all that you have to offer, to present. That is all that you have ever presented in about 544 messages!

Is that your god? The God of Bullshit?

It is strange that you would think that physics, math, and experimental evidence are bullshit.

This message is a reply to:
 Message 50 by dwise1, posted 09-17-2022 7:23 PM dwise1 has replied

Replies to this message:
 Message 55 by dwise1, posted 09-17-2022 8:15 PM Kleinman has not replied
 Message 73 by ringo, posted 09-18-2022 3:43 PM Kleinman has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 56 of 2926 (898046)
09-17-2022 8:17 PM
Reply to: Message 52 by dwise1
09-17-2022 8:04 PM


Re: Video not available
Kleinman:
I'm not trying to bullshit you. I'm trying to explain to you the physics of Darwinian evolution. Since you are so impatient, just read this:
The Physics of Darwinian Evolution
dwise1:
Whaaaaat??? Two-slightly-plus pages of bullshit????

You need to join forces with MrIntelligentDesign. That guy is a truly a legend in his own mind, just like you. And he publishes his nonsense on vanity sites, just like you. Except his nonsense show a lot more work going into them than ... yours. I mean, he's nuttier than a fruitcake, but at least he shows up ... sometimes. You ... eeh!!

It doesn't take much to explain the physics of Darwinian evolution if you have taken and passed a high school-level physics course. Perhaps you don't understand that it takes energy to replicate?

This message is a reply to:
 Message 52 by dwise1, posted 09-17-2022 8:04 PM dwise1 has not replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 57 of 2926 (898047)
09-17-2022 8:42 PM
Reply to: Message 53 by Percy
09-17-2022 8:06 PM


Re: Video not available
Kleinman:
What fun is physics without math? Think about what the meaning of the carrying capacity of an environment means.
Percy:
Well what are you waiting for? Let's bring on the math and have some fun, Professor Kleinman.

OK, let's start with the math of competition. Haldane's model in his "cost of natural selection" paper is a good starting point. You can find that paper here:
JSTOR: Access Check
Note that Haldane's model has been proven to be a conservation of energy process. You have to modify his model for the particular case. For example, Lenski's experiment includes bottlenecking so you have to modify Haldane model as shown here:
Fixation and Adaptation in the Lenski E. coli Long Term Evolution Experiment
There are a couple of ways to model adaptation. You can use the "at least one rule from probability theory as shown here in this paper:
The basic science and *********** of random mutation and natural selection
Or you can use a Markov chain random walk calculation to compute the probability of an adaptive mutation occurring as show here:
The Kishony Mega-Plate Experiment, a Markov Process
Note that either means of computing the probability of an adaptive mutation occurring gives the same result. Either formulation work for the Lenski or Kishony experiment because they are both single selection pressure experiments.
Percy:
And don't leave me hanging about what the different populations are competing for. Was my guess of lebensraum right?
Populations compete for the energy available in the given environment. That's because it takes energy to survive and replicate. Overcrowding may be a selection condition but in and of itself, it is food (energy) that biological populations compete over.
BTW. is m-thematics now a forbidden word?

This message is a reply to:
 Message 53 by Percy, posted 09-17-2022 8:06 PM Percy has replied

Replies to this message:
 Message 175 by Percy, posted 09-22-2022 10:10 AM Kleinman has replied
 Message 176 by AZPaul3, posted 09-22-2022 10:51 AM Kleinman has not replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 59 of 2926 (898049)
09-17-2022 9:47 PM
Reply to: Message 58 by Percy
09-17-2022 9:11 PM


Re: Video not available
Percy:
Brilliant response, Professor Kleinman. Bravissimo!

There was one part I didn't get. Could you explain this equation from the analysis section:

Thanks a bunch!
Sorry, I do not know how to format the equation in dBCodes, but let's call it equation [3]. Their problem is that they are assuming that biological evolution obeys an exponential (or exponential-like) distribution function. The correct distribution function for biological evolutionary adaptation is the binomial distribution. The random experiment is a replication and the two possible outcomes are does an adaptive mutation occur or does an adaptive mutation not occur. If you go back and read this paper,
The basic science and *********** of random mutation and natural selection
I show how to derive the probability equation for at least one occurrence of that adaptive mutation occurring as a function of mutation rate and the number of replications. Simply go back to first principles and consider the stochastic system and the correct probability distribution becomes apparent.
The advantage of deriving the governing equation by first principles is that you can easily extend the model to multiple simultaneous selection conditions. What you end up having are nested binomial probability problems.
I hope this makes sense to you.

This message is a reply to:
 Message 58 by Percy, posted 09-17-2022 9:11 PM Percy has replied

Replies to this message:
 Message 61 by Percy, posted 09-18-2022 9:34 AM Kleinman has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 62 of 2926 (898065)
09-18-2022 10:54 AM
Reply to: Message 60 by PaulK
09-18-2022 2:05 AM


Re: Video not available
Kleinman:
Experimental evidence shows you are incorrect.
PaulK:
Really? You’ve already misrepresented Lenski once.
Kleinman:
That is why the Lenski variants evolve more slowly than the Kishony variants. Lenski energy limits his populations which slows the growth of the individual variant populations.
PaulK:
That is not what the Lenski paper you quoted says. Lenski argues that in asexually reproducing life, large populations slow adaption because more advantageous mutations are available.
Lenski's Team:
When large asexual populations adapt, competition between simultaneously segregating mutations slows the rate of adaptation and restricts the set of mutations that eventually fix. This phenomenon of interference arises from competition between mutations of different strengths as well as competition between mutations that arise on different fitness backgrounds.




Perhaps I should have include this part of the Lenski's Team statement to put it in better context for you.
Kleinman:
When large asexual populations adapt, competition between simultaneously segregating mutations slows the rate of adaptation and restricts the set of mutations that eventually fix. This phenomenon of interference arises from competition between mutations of different strengths as well as competition between mutations that arise on different fitness backgrounds. Previous work has explored each of these effects in isolation, but the way they combine to influence the dynamics of adaptation remains largely unknown.
I added the bold face. Lenski's Team doesn't understand why competition slows adaptation. That's why I wrote the following and you incorrectly responed:
Kleinman:
Kishony's colonies easily achieve population sizes of a billion or more. That size population gives a reasonable probability that all possible mutations will occur on some member of that colony when a mutation rate is 1e-9.
PaulK:
And, per Lenski that should slow adaption.

The Lenski Team knows that competition slows adaptation, they see that in their experiment, they just don't know why. Do you think that the ability to form larger colony size slows adaptation? Do you think that doubling the population size doubles the probability of an adaptive mutation occurring?

This message is a reply to:
 Message 60 by PaulK, posted 09-18-2022 2:05 AM PaulK has replied

Replies to this message:
 Message 63 by PaulK, posted 09-18-2022 11:20 AM Kleinman has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 64 of 2926 (898068)
09-18-2022 11:21 AM
Reply to: Message 61 by Percy
09-18-2022 9:34 AM


Re: Video not available
Kleinman:
Sorry, I do not know how to format the equation in dBCodes,...
Percy:
Oh, Professor Kleinman, you are so funny. To someone of your intellect dBCodes and Latex equations are mere children's toys.

You seem to be good at formatting, I'll leave that to you. You do seem to be having some difficulty with physics and math. For example, you seem to think that populations are competing for space. There is plenty of space in the Sahara desert but very little available energy for populations to use (no food).
Kleinman:
...but let's call it equation [3]. Their problem is that they are assuming that biological evolution obeys an exponential (or exponential-like) distribution function.
Percy:
It's a brilliancy. You offered the paper Distribution of fixed beneficial mutations and the rate of adaptation in asexual populations as if supporting your views when it actually is just an example of how not to do it, then tell us the answer is in The basic science and *********** of random mutation and natural selection. Could you please contrast this equation with the one above and explain why this is the proper equation for the probability of a beneficial mutation:

Thank you so much, Professor Kleinman. You're the best!

Percy has posted equation (5) from my paper:
The basic science and *********** of random mutation and natural selection
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
Equation [3] from the Lenski Team paper is a probability distribution equation. Equation (5) from my paper is an "at least one" probability calculation. That is, what is the probability of a particular mutation occurring at least once in a particular population as a function of mutation rate and population size.
Perhaps you should try to figure out what the random trial is and what the possible outcomes are for that equation [3]. I hope that helps clarify the math to you.

This message is a reply to:
 Message 61 by Percy, posted 09-18-2022 9:34 AM Percy has replied

Replies to this message:
 Message 149 by Percy, posted 09-21-2022 10:53 AM Kleinman has not replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 65 of 2926 (898069)
09-18-2022 11:44 AM
Reply to: Message 63 by PaulK
09-18-2022 11:20 AM


Re: Video not available
Kleinman:
I added the bold face.
PaulK:
Which shows the question Lenski is addressing.

They address this question but fail to answer it. If you think they do, feel free to post a quote from their paper that gives the correct explanation and law of physics that justifies their answer. You won't because they didn't.
Kleinman:
Lenski's Team doesn't understand why competition slows adaptation. That's why I wrote the following and you incorrectly responed:
PaulK:
You’re arrogantly blustering without understanding. Adaption is not simply generating mutations.

Don't be silly. I know the difference between modification and adaptation. Not every genetic modification is an adaptation.
Kleinman:
The Lenski Team knows that competition slows adaptation, they see that in their experiment, they just don't know why
PaulK:
You are wrong. Utterly utterly wrong. As you would know if you read the paper. As you would know if you actually understood the quote.

Feel free to post the quote from their paper that explains why competition slows adaptation. You won't because they didn't explain. The reason is very simple. Less fit variants are consuming resources that the more fit variants could use to increase their population size. The more fit variant must first drive the less fit variants to extinction in order for their population to increase in size and improve the probability of an adaptive mutation occurring. It is a simple first law of thermodynamics process and an "at least one" probability problem.
Kleinman:
Do you think that the ability to form larger colony size slows adaptation?
PaulK:
Of course not. I agree with Lenski’s explanation.

Post Lenski's explanation.
Kleinman:
Do you think that doubling the population size doubles the probability of an adaptive mutation occurring?
PaulK:
No, although if the probability is low it will come close.

Good! Do you think that a series of microevolutionary changes add up to a macroevolutionary change?

This message is a reply to:
 Message 63 by PaulK, posted 09-18-2022 11:20 AM PaulK has replied

Replies to this message:
 Message 66 by PaulK, posted 09-18-2022 12:11 PM Kleinman has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 67 of 2926 (898074)
09-18-2022 12:47 PM
Reply to: Message 66 by PaulK
09-18-2022 12:11 PM


Re: Video not available
Kleinman:
They address this question but fail to answer it. If you think they do, feel free to post a quote from their paper that gives the correct explanation and law of physics that justifies their answer. You won't because they didn't.
PaulK:
I fully grant that they don’t make the silly mistake of appealing to the laws of physics when that would only serve to obfuscate the issues.

And I really don’t think that their model is amenable to quoting either.

Of course you won't post their explanation because they have none.
Kleinman:
Don't be silly. I know the difference between modification and adaptation. Not every genetic modification is an adaptation.
PaulK:
You know that adaption requires fixation? Really?

OF course, adaptation does not require fixation. The Kishony experiment clearly demonstrates that.
Kleinman:
Feel free to post the quote from their paper that explains why competition slows adaptation.
PaulK:
They don’t make that blanket claim. They only claim that competition between beneficial mutations slows adaption. Which would seem intuitively obvious - which is why their contribution is to produce a better model of the effects.

Do you understand that the beneficial mutation that gives the greatest improve in fitness fixes first, the beneficial mutation that gives the second greatest improvement in fitness fixes second and so on. But each adaptation/fixation cycle requires the most fit variant to drive the less fit variants to extinction before the next beneficial mutation will have a reasonable probability of occurring on that variant. It is all about conservation of energy, the first law of thermodynamics, which apparently obfuscates this process for you.
Kleinman:
Do you think that a series of microevolutionary changes add up to a macroevolutionary change?
PaulK:
I don’t see any reason why it could not.

You understood that the addition rule of probabilities does not apply to complementary events (doubling population size does not double the probability of an adaptive mutation occurring). Now you need to learn that the addition rule of probabilities does not apply to the joint probability of random events occurring. What rule of probability theory applies to the computation of the joint probability of two or more random events occurring?

This message is a reply to:
 Message 66 by PaulK, posted 09-18-2022 12:11 PM PaulK has replied

Replies to this message:
 Message 68 by PaulK, posted 09-18-2022 1:07 PM Kleinman has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 69 of 2926 (898077)
09-18-2022 1:38 PM
Reply to: Message 68 by PaulK
09-18-2022 1:07 PM


Re: Video not available
Kleinman:
Of course you won't post their explanation because they have none.
PaulK:
You are making no sense. The way that Lenski addresses the question of how competition between “mutations of different strengths” interacts with competiton between “mutations that arise on different fitness backgrounds” is to construct a model. Which is what I said. How you can expect this to be an “answer” that is readily quotable I have no idea.

It's really not that complicated. You have a population consisting of a variety of different with different reproductive fitness competing for a limited amount of energy (food). The most effective variant able to reproduce will drive all the rest of the less fit variants to extinction over generations. That's how biological competition works.
Kleinman:
OF course, adaptation does not require fixation. The Kishony experiment clearly demonstrates that.
PaulK:
Of course it will in any practical situation. Even a mega plate has finite resources.

That's probably true. But the carrying capacity of a given environment for bacteria and other microbes will be many orders of magnitude larger than that for say, humans and chimpanzees.
Kleinman:
Do you understand that the beneficial mutation that gives the greatest improve in fitness fixes first, the beneficial mutation that gives the second greatest improvement in fitness fixes second and so on
PaulK:
That is silly. How could that reliably occur?

It's what the Lenski Team measured in their experiment. The number of generations to fixation has been increasing ever since the beginning of the experiment. This shouldn't be surprising to you. Why would a less fit variant fix before a more fit variant? This is about relative reproductive fitness.
Kleinman:
Now you need to learn that the addition rule of probabilities does not apply to the joint probability of random events occurring
PaulK:
That has nothing to do with how a sequence of microevolutionary events can lead to macroevolution.

Are you one of those that think that mutations aren't random occurrences? If so, tell us on which member of Kishony's or Lenski's population the next adaptive mutation will occur.

This message is a reply to:
 Message 68 by PaulK, posted 09-18-2022 1:07 PM PaulK has replied

Replies to this message:
 Message 70 by PaulK, posted 09-18-2022 1:56 PM Kleinman has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 71 of 2926 (898086)
09-18-2022 3:22 PM
Reply to: Message 70 by PaulK
09-18-2022 1:56 PM


Re: Video not available
Kleinman:
It's really not that complicated. You have a population consisting of a variety of different with different reproductive fitness competing for a limited amount of energy (food). The most effective variant able to reproduce will drive all the rest of the less fit variants to extinction over generations. That's how biological competition works.
PaulK:
Quantifying the effects, however, is not so simple - and that was what Lenski said had not been done and what Lenski set out to do.

Here's how you do the math for a single fixation/adaptation cycle
Fixation and Adaptation in the Lenski E. coli Long Term Evolution Experiment
Kleinman:
That's probably true. But the carrying capacity of a given environment for bacteria and other microbes will be many orders of magnitude larger than that for say, humans and chimpanzees.
PaulK:
Which is why adaptive change in the real world relies on fixation.

How many fixation/adaptation cycles do you think humans and chimpanzees have done?
Kleinman:
It's what the Lenski Team measured in their experiment. The number of generations to fixation has been increasing ever since the beginning of the experiment. This shouldn't be surprising to you. Why would a less fit variant fix before a more fit variant? This is about relative reproductive fitness.
PaulK:
You are making no sense again. We are talking about clinal reproduction. If the two mutations occur in the same lineage then the one that occurred first should reach fixation first. If they occurred in different lineages the one that fixes the first will have eliminated the other, so the second will never reach fixation.

Do you mean "clonal" not "clinal"? Lenski's experiment operates by the most fit variant with the previous beneficial mutation fixes and as that subset accumulates replications over generations, the probability of the next beneficial mutation occurring on one of its members increases. This occurs in a sequential manner. The probability of two or more adaptive mutations occurring in a non-sequential manner requires many orders larger population than Lenski allows for in his experiment. This is due to the multiplication rule of probabilities.
Kleinman:
Are you one of those that think that mutations aren't random occurrences?
PaulK:
No. But please go on, explain how the fact that “the addition rule of probabilities does not apply to the joint probability of random events occurring” prevents microevolutionary events adding up to macroevolution.
(You won’t.).

Sure I will. This is best demonstrated by the Kishony experiment. Watch this short video.
https://www.youtube.com/watch?v=Irnc6w_Gsas&t=5s&ab_chann...
Kishony correctly recognizes that each adaptive mutation requires about a billion replications. Each time some variant gets an adaptive mutation, it must form a new colony which must achieve a population size sufficient for there to be a reasonable probability for the next adaptive mutation to occur on one of its members. This is due to the multiplication rule of probabilities. I published the math that predicted the behavior of his experiment years before the experiment was performed. Here is that paper:
The basic science and *********** of random mutation and natural selection
Equations (12,13) show how you apply the multiplication rule to compute the joint probability for a lineage to accumulate a set of adaptive mutations. I do not take credit for being the first to understand this fundamental principle of biological evolutionary adaptation. Edward Tatum wrote about this in his 1958 Nobel Laureate Lecture. Edward Tatum wrote this:
Edward Tatum – Nobel Lecture - NobelPrize.org
Edward Tatum:
In microbiology the roles of mutation and selection in evolution are coming to be better understood through the use of bacterial cultures of mutant strains. In more immediately practical ways, mutation has proven of primary importance in the improvement of yields of important antibiotics – such as in the classic example of penicillin, the yield of which has gone up from around 40 units per ml of culture shortly after its discovery by Fleming to approximately 4,000, as the result of a long series of successive experimentally produced mutational steps. On the other side of the coin, the mutational origin of antibiotic-resistant micro-organisms is of definite medical significance. The therapeutic use of massive doses of antibiotics to reduce the numbers of bacteria which by mutation could develop resistance, is a direct consequence of the application of genetic concepts. Similarly, so is the increasing use of combined antibiotic therapy, resistance to both of which would require the simultaneous mutation of two independent characters.

This message is a reply to:
 Message 70 by PaulK, posted 09-18-2022 1:56 PM PaulK has replied

Replies to this message:
 Message 74 by PaulK, posted 09-18-2022 3:50 PM Kleinman has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 75 of 2926 (898094)
09-18-2022 5:07 PM
Reply to: Message 73 by ringo
09-18-2022 3:43 PM


Re: Video not available
Kleinman:
The Physics of Darwinian Evolution
ringo:
I'm curious about why you keep bringing up Darwin. That's like bringing up the Wright Brothers in a discussion about twenty-first-century aviation.

What principles of aeronautical engineering did the Wright Brothers get wrong? Do you think Darwin got biological evolutionary competition and descent with modification wrong? If so, show your physics and math.
Kleinman:
It is strange that you would think that physics, math, and experimental evidence are bullshit.
ringo:
It's the garbage-in, garbage-out principle. Whatever you put into the front end of the bull, the same thing is going to come out the back end.

At least you have some idea of what a conservation principle is. Now, only if you could figure out how to apply it to Darwinian Evolution.

This message is a reply to:
 Message 73 by ringo, posted 09-18-2022 3:43 PM ringo has replied

Replies to this message:
 Message 77 by dwise1, posted 09-18-2022 9:32 PM Kleinman has replied
 Message 82 by ringo, posted 09-19-2022 11:43 AM Kleinman has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 76 of 2926 (898095)
09-18-2022 5:16 PM
Reply to: Message 74 by PaulK
09-18-2022 3:50 PM


Re: Video not available
Kleinman:
How many fixation/adaptation cycles do you think humans and chimpanzees have done?
PaulK:
I think that sexual reproduction significantly complicates the issue. There is no need for mutations to occur in the same lineage,

It doesn't complicate it as much as you think. You can do the math for recombination using a trinomial distribution. If you do the math correctly, you will understand why recombination does not defeat the use of combination therapy for the treatment of HIV.
Kleinman:
Do you mean "clonal" not "clinal"? Lenski's experiment operates by the most fit variant with the previous beneficial mutation fixes and as that subset accumulates replications over generations, the probability of the next beneficial mutation occurring on one of its members increases. This occurs in a sequential manner.
PaulK:
Yes, I meant clonal. And the auto “correct” feature insisted on changing it to “clinal”.

However your reply has nothing to do with your assertion that the most beneficial mutation would fix first, followed by the second most beneficial.

That's what Lenski's experiment shows. Some member of the most fit variant sub-population gets an adaptive mutation and that new variant ultimately drives the now less fit variants to extinction. The probability that the new variant gets another adaptive mutation depends on the number of replications it does. The probability that any particular variant gets two adaptive mutations before fixation in that experiment is very low because of the low population sizes being used.
It's the same math as if two selection conditions are used simultaneously. For example, Kishony's experiment doesn't work when he uses two drugs simultaneously. Some member of the population has to get two adaptive mutations before it can grow in the next higher drug-concentration region. In order to have resonable probabilities for that to happen, Kishony would need a much much larger mega-plate. The colony size would have to reach about a trillion. If you are interested, here's a paper that shows how to do the math:
The mathematics of random mutation and natural selection for multiple simultaneous selection pressures and the evolution of antimicrobial drug resistance
Kleinman:
Kishony correctly recognizes that each adaptive mutation requires about a billion replications. Each time some variant gets an adaptive mutation, it must form a new colony which must achieve a population size sufficient for there to be a reasonable probability for the next adaptive mutation to occur on one of its members. This is due to the multiplication rule of probabilities.
PaulK:
That seems to have more to do with clonal reproduction. And even then it only tells us that a sequence of microevolutionary events will take time. Not that they cannot add up to a macro evolutionary event.

It works the same empirically with sexually reproducing organisms. Common empirical examples of this are the use of combination herbicides and combination pesticides when dealing with weeds and insects in agriculture, both of which are sexually reproducing organisms. Likewise, HIV does recombination but it does not defeat the use of combination therapy. You should learn how to do the math of random recombination. If you can't figure it out, I'll show you how to do the math. Only in very specific instances will recombination lead to variants with beneficial alleles recombining to give offspring with multiple adaptive alleles. You still have the multiplication rule when considering biological adaptive evolution in sexually reproducing organisms.
Kleinman:
Equations (12,13) show how you apply the multiplication rule to compute the joint probability for a lineage to accumulate a set of adaptive mutations.
PaulK:
Your equations do not seem to offer any reason why a number of microevolutionary events cannot add up to macroevolution.

These equations give the mathematica! reason why it takes a billion replications for each adaptive transition in a single selection pressure evolutionary process. When the probability of success for an adaptive mutation occurring in a single replication is the beneficial mutation rate, you will need a large number of replications to have a reasonable probability of at least one of those events occurring. Here's a simple analogy to help you understand:
Consider if for your family to survive that your family needs to win two lotteries. And the probability of winning one lottery is 1 in a million, and the probability of winning the other lottery is 1 in a million. For you to win both lotteries, that probability is 1 in a million times 1 in a million equals 1 in a trillion, a very low probability indeed. But let's say, you win one of those lotteries. And because of this, you are a very wealthy man and you can raise a very large family. And all your descendants start buying tickets to the second lottery. As soon as you have enough descendants, there will be a high probability that one of your descendants wins that second lottery for your family.
The probability of an adaptive mutation occurring on some variant in a population depends on the number of replications that variant does and the mutation rate, nothing else. There are lots of factors that affect that variant from doing the necessary number of replications for the next adaptive mutation. Competition is one of those factors. It is also possible that a single adaptive mutation does not exist for the given selection conditions. But it all comes down to the fact that the number of replications and the mutation rate determine that probability. And adaptive evolutionary events don't add, they are linked by the multiplication rule as are your chances of winning two lotteries are.

This message is a reply to:
 Message 74 by PaulK, posted 09-18-2022 3:50 PM PaulK has replied

Replies to this message:
 Message 80 by PaulK, posted 09-19-2022 12:24 AM Kleinman has replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 78 of 2926 (898101)
09-18-2022 11:10 PM
Reply to: Message 77 by dwise1
09-18-2022 9:32 PM


Re: Video not available
Kleinman:
What principles of aeronautical engineering did the Wright Brothers get wrong?
dwise1:
The same number that they got right: none!

dwise1 thinks that the inventors of powered flight knew nothing about aeronautical engineering. When is dwise1 going to give us his explanation of the physics and math of Darwinian evolution? That really won't fly.

This message is a reply to:
 Message 77 by dwise1, posted 09-18-2022 9:32 PM dwise1 has replied

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 Message 79 by dwise1, posted 09-18-2022 11:32 PM Kleinman has not replied

  
Kleinman
Member (Idle past 335 days)
Posts: 2142
From: United States
Joined: 10-06-2016


Message 83 of 2926 (898139)
09-19-2022 2:38 PM
Reply to: Message 80 by PaulK
09-19-2022 12:24 AM


Re: Video not available
Kleinman:
It doesn't complicate it as much as you think. You can do the math for recombination using a trinomial distribution. If you do the math correctly, you will understand why recombination does not defeat the use of combination therapy for the treatment of HIV.
PaulK:
So you think that HIV reproduces sexually,

Aside from that sexual reproduction does away with the need for your cycles so it is still an important factor.


HIV does recombination. If you want, I'll provide you with links to papers where they show this.
As for recombination reducing cycles, it doesn't when producing adaptive alleles. What I think you are trying to point out that in some population, you will have one parent with a beneficial allele (call that allele A) at one locus and the other parent having a beneficial allele (call that allele B) at a different locus and when those parents breed, they can produce an offspring with both beneficial alleles A and B. Let's put this into the context of a real situation. One farmer uses a herbicide on his field that selects for allele A and a different farmer uses a different herbicide on a different field that selects for allele B. Both farmers are treating the same weed. So, some of the weeds have allele A, other weeds have allele B, and the remaining weeds have neither allele A nor allele B (call those allele C). What is the probability distribution function that describes this problem and compute the probability that you will get an A parent and a B parent giving an AB offspring as a function of population size, and frequencies of A, B, and C members.
Kleinman:
That's what Lenski's experiment shows.
PaulK:
No, it doesn’t. It doesn’t show that the second mutation to be fixed has to be less adaptive than the first or more adaptive than any other mutations in the wider population.

Read this paper by Lenski:
https://royalsocietypublishing.org/...10.1098/rspb.2015.2292
Lenski:
A recent study showed that fitness trajectories of Escherichia coli populations over 50 000 generations were better described by a power-law model than by a hyperbolic model. According to the power-law model, the rate of fitness gain declines over time but fitness has no upper limit, whereas the hyperbolic model implies a hard limit. Here, we examine whether the previously estimated power-law model predicts the fitness trajectory for an additional 10 000 generations. To that end, we conducted more than 1100 new competitive fitness assays. Consistent with the previous study, the power-law model fits the new data better than the hyperbolic model.
Kleinman:
It works the same empirically with sexually reproducing organisms. Common empirical examples of this are the use of combination herbicides and combination pesticides when dealing with weeds and insects in agriculture, both of which are sexually reproducing organisms.
PaulK:
Haldane showed that a combination of selective pressures would work decades ago, for other reasons.

And, of course, you can’t generalise a special case to a more normal situation.

There are no empirical examples that show that a population evolves more rapidly as they are subject to multiple simultaneous selection pressures.
Kleinman:
These equations give the mathematica! reason why it takes a billion replications for each adaptive transition in a single selection pressure evolutionary process
PaulK:
You’d have to put numbers to them to get that answer. The equations alone won’t do that.

And you still haven’t explained how microevolutionary events can’t add up to macroevolution, just as I predicted.

The only numbers you need to use are the mutation rate and population size.
The reason why microevolutionary events don't add is they random events. You must compute the joint probability of random events occurring using multiplication, not addition.

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 Message 80 by PaulK, posted 09-19-2022 12:24 AM PaulK has replied

Replies to this message:
 Message 85 by PaulK, posted 09-19-2022 3:08 PM Kleinman has replied

  
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