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Author Topic:   Rebuttal To Creationists - "Since We Can't Directly Observe Evolution..."
Kleinman
Member
Posts: 1492
From: United States
Joined: 10-06-2016


Message 241 of 2383 (898569)
09-26-2022 1:02 PM
Reply to: Message 239 by Taq
09-26-2022 12:20 PM


Re: Apples and oranges
Kleinman:
The correct analogy for your raindrop concept would be, what is the probability of two particular raindrops ending up in the same body of water?
Taq:
A raindrop falls and runs downhill to a small stream. Small streams flow into a larger river. Larger river dumps into ocean. Same body of water.

Sexual reproduction is analogous. Lineages flow into each other and form the larger body of variation that is the population.

If you understood how sexual reproduction works you would be able to figure these things out.​

I get it now! Sexual reproduction works by gravity! I'm impressed by your understanding of the laws of physics.
Kleinman:
And you must model DNA evolution and the accumulation of adaptive mutations in a lineage using the multiplication rule.
Taq:
Not for sexually reproducing populations.

Tell us how you think adaptive alleles are evolved in sexually reproducing populations.

This message is a reply to:
 Message 239 by Taq, posted 09-26-2022 12:20 PM Taq has replied

Replies to this message:
 Message 243 by Taq, posted 09-26-2022 1:33 PM Kleinman has not replied

  
Taq
Member
Posts: 9063
Joined: 03-06-2009
Member Rating: 3.3


Message 242 of 2383 (898572)
09-26-2022 1:28 PM
Reply to: Message 240 by Kleinman
09-26-2022 12:51 PM


Re: Apples and oranges
Kleinman writes:
Are some of the variants more fit than other variants and are they engaged in biological evolutionary competition?
Beneficial mutations on separate genes would not be in competition with each other because they could merge into the same lineage.
You aren't answering my question about whether all 100,000 individuals are on the same evolutionary trajectory.
Yes I am. Because genes move through the population this puts the population on the same trajectory. The only way this could not be the case is if there is an interruption in gene flow between subpopulations.
What is the probability of beneficial alleles in a diverse population recombining in the same descendant?
Your father is homozygous for a beneficial mutation in gene A. Your mother is homozygous for a beneficial mutation in gene B. You have a 25% chance of getting both beneficial mutations. Do you understand this or not?
Added in edit: The probability would actually be 100% if both parents were homozygous. The 25% chance is if both parents were heterozygous for their respective beneficial allele.
How do 20 million possible beneficial mutations end up in the lineages of all humans?
Natural selection drives beneficial genes to fixation, and sexual recombination drives the merger of beneficial alleles into the same genome.
Try reading beyond the abstract:
That is for asexual populations. Primates reproduce sexually.
OK, Haldane's frequency equation for a sex-linked diploid is:
pn^2AA + 2pnqnAa + qn^2aa = 1
Which of the variants fix in the population, AA, Aa, or aa?
That's for a single allele. What about different genes?
It's the number of replications of a particular allele that determines the probability of an adaptive mutation occurring at some site in that allele.
In the Lederberg experiment the mutation rate was the same for all bacteria. Spectinomycin resistance occurred once in every 10 billion divisions and phage resistance occurred once in every 10 million divisions. How do you explain this?

Edited by Taq, .


This message is a reply to:
 Message 240 by Kleinman, posted 09-26-2022 12:51 PM Kleinman has replied

Replies to this message:
 Message 244 by Kleinman, posted 09-26-2022 2:35 PM Taq has replied

  
Taq
Member
Posts: 9063
Joined: 03-06-2009
Member Rating: 3.3


Message 243 of 2383 (898573)
09-26-2022 1:33 PM
Reply to: Message 241 by Kleinman
09-26-2022 1:02 PM


Re: Apples and oranges
Tell us how you think adaptive alleles are evolved in sexually reproducing populations.
Let's use antibiotic resistance as our model.
We have two populations of the same bacterial species. We put one population on a plate that has antibiotic A and another population on a plate with antibiotic B. We get resistant colonies on both plates. We then mix the two populations together in media that has no antibiotic. How many of those bacterial descendants of this mixed population are going to have both mutations for resistance to both drugs? None, if the bacteria are reproducing asexually.
Do the same for a diploid sexually reproducing population. What are the results? Could you find bacterial descendants of the mixed population that has both resistance markers if they are found on different genes? YES!!

This message is a reply to:
 Message 241 by Kleinman, posted 09-26-2022 1:02 PM Kleinman has not replied

  
Kleinman
Member
Posts: 1492
From: United States
Joined: 10-06-2016


Message 244 of 2383 (898579)
09-26-2022 2:35 PM
Reply to: Message 242 by Taq
09-26-2022 1:28 PM


Re: Apples and oranges
Kleinman:
Are some of the variants more fit than other variants and are they engaged in biological evolutionary competition?
Taq:
Beneficial mutations on separate genes would not be in competition with each other because they could merge into the same lineage.

So, in your model of human evolution, the fixation of beneficial alleles does not occur?
Kleinman:
You aren't answering my question about whether all 100,000 individuals are on the same evolutionary trajectory.
Taq:
Yes I am. Because genes move through the population this puts the population on the same trajectory. The only way this could not be the case is if there is an interruption in gene flow between subpopulations.

In your model, does every human lineage have equal reproductive fitness? Do any human lineages go extinct?
Kleinman:
What is the probability of beneficial alleles in a diverse population recombining in the same descendant?
Taq:
Your father is homozygous for a beneficial mutation in gene A. Your mother is homozygous for a beneficial mutation in gene B. You have a 25% chance of getting both beneficial mutations. Do you understand this or not?

I don't think you are doing your math correctly on that one. But WRT your model, do all the fathers in your model have beneficial allele A and all the mothers have beneficial alleles B?
Kleinman:
How do 20 million possible beneficial mutations end up in the lineages of all humans?
Taq:
Natural selection drives beneficial genes to fixation, and sexual recombination drives the merger of beneficial alleles into the same genome.

How do you compute the probability that all these beneficial mutations end up in a single lineage in your model?
Kleinman:
Try reading beyond the abstract:
Taq:
That is for asexual populations. Primates reproduce sexually.

Try reading this again:
quote:
This process is also found to a degree in sexual populations (the Hill–Robertson effect) if recombination cannot act quickly enough to place all of the competing mutations on the same genetic background (16).
How do you compute the rapid fixation of 20 million beneficial mutations in your model?
Kleinman:
OK, Haldane's frequency equation for a sex-linked diploid is:
pn^2AA + 2pnqnAa + qn^2aa = 1
Which of the variants fix in the population, AA, Aa, or aa?
Taq:
That's for a single allele. What about different genes?

You have yet to show how you do a fixation calculation for your model for a single genetic loci let alone 20 million genetic loci. Are you ever going to get beyond your simple-minded neutral evolutionary model where you assume that 20 million mutations are beneficial?
Kleinman:
It's the number of replications of a particular allele that determines the probability of an adaptive mutation occurring at some site in that allele.
Taq:
In the Lederberg experiment the mutation rate was the same for all bacteria. Spectinomycin resistance occurred once in every 10 billion divisions and phage resistance occurred once in every 10 million divisions. How do you explain this?

Where did the resistance allele come from that the phage transmits? What if the phage transmitted some other allele besides a resistance allele?
Kleinman:
Tell us how you think adaptive alleles are evolved in sexually reproducing populations.
Taq:
Let's use antibiotic resistance as our model.

We have two populations of the same bacterial species. We put one population on a plate that has antibiotic A and another population on a plate with antibiotic B. We get resistant colonies on both plates. We then mix the two populations together in media that has no antibiotic. How many of those bacterial descendants of this mixed population are going to have both mutations for resistance to both drugs? None, if the bacteria are reproducing asexually.

Do the same for a diploid sexually reproducing population. What are the results? Could you find bacterial descendants of the mixed population that has both resistance markers if they are found on different genes? YES!!

Just as a side note to this comment, Kishony's experiment doesn't work when using two drugs simultaneously. Do you understand why?
And to your comment here, you have assumed that the two subsets of your sexually reproducing population each have fixed their respective resistance alleles so they exist at frequencies of 1 in their respective populations. If we assume both subsets have equal population sizes when you combine the frequencies of the resistance alleles for each drug will be 0.5. What happens if the resistance alleles are not at high frequency in the population? What is the probability of a recombination event for the beneficial alleles if their frequencies are f1, f2, and where the remaining members of the population have frequency f3, i.e., resistance to neither drug? And BTW, combination therapy works for the treatment of malaria which can do sexual reproduction. And the malaria population size for someone with hyperparasithemia can reach 1 trillion.

This message is a reply to:
 Message 242 by Taq, posted 09-26-2022 1:28 PM Taq has replied

Replies to this message:
 Message 245 by Taq, posted 09-26-2022 3:40 PM Kleinman has replied

  
Taq
Member
Posts: 9063
Joined: 03-06-2009
Member Rating: 3.3


Message 245 of 2383 (898582)
09-26-2022 3:40 PM
Reply to: Message 244 by Kleinman
09-26-2022 2:35 PM


Re: Apples and oranges
Kleinman writes:
So, in your model of human evolution, the fixation of beneficial alleles does not occur?
Fixation of beneficial mutations does occur in my model. Why you think otherwise is beyond me.
In your model, does every human lineage have equal reproductive fitness? Do any human lineages go extinct?
There would be variation of fitness across individuals just like in any mammalian population.
Do any human lineages go extinct?
The only lineages that actually exist are the y-chromosome and mitochondrial lineages because those are haploid, and those can go extinct.
I don't think you are doing your math correctly on that one. But WRT your model, do all the fathers in your model have beneficial allele A and all the mothers have beneficial alleles B?
The math was wrong. It should be 100% if the father and mother are homozygous.
If a father is homozygous for a beneficial mutation in gene A and a mother is homozygous for a beneficial mutation in gene B, 100% of offspring will have one copy of each beneficial mutation. Do you agree or not?
How do you compute the probability that all these beneficial mutations end up in a single lineage in your model?
If they are all being driven to fixation because of selection then that would be population wide for all of the beneficial mutations. If you are asking for the specific equations, those are found in population genetics:
Population Genetics
How do you compute the rapid fixation of 20 million beneficial mutations in your model?
Fixation wouldn't need to be rapid.
You have yet to show how you do a fixation calculation for your model for a single genetic loci let alone 20 million genetic loci.
quote:
Natural Selection results in change of allele frequency (q) [read as "delta q"]
in consequence of differences in the relative fitness (W)
of the phenotypes to which the alleles contribute.
Fitness is a phenotype of individual organisms.
Fitness is determined genetically (at least in part).
Fitness is related to success at survival AND reproduction.
Fitness can be measured & quantified (see below).
i.e., the relative fitness of genotypes can be assigned numerical values.
The consequences of natural selection depend on the dominance of fitness:
e.g., whether the "fit" phenotype is due to a dominant or recessive allele.
Then, allele frequency change is predicted by the General Selection Equation:
delta q = [pq] [(q)(W2 - W1) + (p)(W1 - W0)] / Wbar
where W0, W1, & W2 are the fitness phenotypes
of the AA, AB, & BB genotypes, respectively
Theory of Natural Selection
The equations are all over the internet. It's not like it's a secret.
Where did the resistance allele come from that the phage transmits? What if the phage transmitted some other allele besides a resistance allele?
Phage resistance doesn't come from the phage genome. It is due to mutations in the gene tonB. I will ask again.
In the Lederberg experiment the mutation rate was the same for all bacteria. Spectinomycin resistance occurred once in every 10 billion divisions and phage resistance occurred once in every 10 million divisions. How do you explain this?
And to your comment here, you have assumed that the two subsets of your sexually reproducing population each have fixed their respective resistance alleles so they exist at frequencies of 1 in their respective populations.
If they didn't have the resistance marker then they wouldn't have grown on the antibiotic plate. 100% of the bacteria on each plate carry the mutation for each antibiotic.
If we assume both subsets have equal population sizes when you combine the frequencies of the resistance alleles for each drug will be 0.5.
Exactly. The two lineages have merged. Half the population has both mutations. If they are now challenged by both antibiotics half of the population will survive, and 100% will have both mutations in the same lineage, and it wouldn't have required iterative mutations.
quote:
And BTW, combination therapy works for the treatment of malaria which can do sexual reproduction.
What would happen if one village used one drug and a village close by used a different drug? Could you have resistance to each drug develop in each village, and then find both resistance markers in the offspring between those two resistant populations? The answer is yes. The same mutations wouldn't have to repeat themselves in each population.

This message is a reply to:
 Message 244 by Kleinman, posted 09-26-2022 2:35 PM Kleinman has replied

Replies to this message:
 Message 246 by Kleinman, posted 09-26-2022 5:23 PM Taq has replied

  
Kleinman
Member
Posts: 1492
From: United States
Joined: 10-06-2016


Message 246 of 2383 (898590)
09-26-2022 5:23 PM
Reply to: Message 245 by Taq
09-26-2022 3:40 PM


Re: Apples and oranges
Kleinman:
So, in your model of human evolution, the fixation of beneficial alleles does not occur?
Taq:
Fixation of beneficial mutations does occur in my model. Why you think otherwise is beyond me.

The math is way beyond you. 20 million beneficial mutations * 300 generations/fixation = 6 billion generations
Kleinman:
In your model, does every human lineage have equal reproductive fitness? Do any human lineages go extinct?
Taq:
There would be variation of fitness across individuals just like in any mammalian population.

How much variation? And how many different lineages in your population?
Kleinman:
Do any human lineages go extinct?
Taq:
The only lineages that actually exist are the y-chromosome and mitochondrial lineages because those are haploid, and those can go extinct.

So you are claiming that no human lineages have ever gone extinct? What happens to the less fit human lineages when the most fit are fixed in the population?
Kleinman:
I don't think you are doing your math correctly on that one. But WRT your model, do all the fathers in your model have beneficial allele A and all the mothers have beneficial alleles B?
Taq:
The math was wrong. It should be 100% if the father and mother are homozygous.

If a father is homozygous for a beneficial mutation in gene A and a mother is homozygous for a beneficial mutation in gene B, 100% of offspring will have one copy of each beneficial mutation. Do you agree or not?

That's still not quite right. What if both the mother and father are homozygous for gene A or homozygous for gene B?
Kleinman:
How do you compute the probability that all these beneficial mutations end up in a single lineage in your model?
Taq:
If they are all being driven to fixation because of selection then that would be population wide for all of the beneficial mutations. If you are asking for the specific equations, those are found in population genetics:

Population Genetics

Percy likes it when you post from your link. Post the equation you think applies.
Kleinman:
How do you compute the rapid fixation of 20 million beneficial mutations in your model?
Taq:
Fixation wouldn't need to be rapid.

Fixation isn't rapid and Haldane's mathematical estimate of 300 generations/fixation has been verified experimentally. And if you are concerned that Lenski's experiment uses asexual replicators, don't worry, Haldane's math includes that for diploid sexual replicators. 20 million beneficial mutations * 300 generations/fixation. How many generations are in your model?
Kleinman:
You have yet to show how you do a fixation calculation for your model for a single genetic loci let alone 20 million genetic loci.
quote:
Natural Selection results in change of allele frequency (q) [read as "delta q"]
in consequence of differences in the relative fitness (W)
of the phenotypes to which the alleles contribute.

Fitness is a phenotype of individual organisms.
Fitness is determined genetically (at least in part).
Fitness is related to success at survival AND reproduction.
Fitness can be measured & quantified (see below).
i.e., the relative fitness of genotypes can be assigned numerical values.

The consequences of natural selection depend on the dominance of fitness:
e.g., whether the "fit" phenotype is due to a dominant or recessive allele.

Then, allele frequency change is predicted by the General Selection Equation:

delta q = [pq] [(q)(W2 - W1) + (p)(W1 - W0)] / Wbar

where W0, W1, & W2 are the fitness phenotypes
of the AA, AB, & BB genotypes, respectively

Theory of Natural Selection
Taq:
The equations are all over the internet. It's not like it's a secret.


Plug in a selection coefficient and tell us how many generations to fixation. Then you only have 19,999,999 more fixations to go.
Kleinman:
Where did the resistance allele come from that the phage transmits? What if the phage transmitted some other allele besides a resistance allele?
Taq:
Phage resistance doesn't come from the phage genome. It is due to mutations in the gene tonB. I will ask again.

In the Lederberg experiment the mutation rate was the same for all bacteria. Spectinomycin resistance occurred once in every 10 billion divisions and phage resistance occurred once in every 10 million divisions. How do you explain this?

So the resistance allele has to evolve in the bacteria and the phage acquires the gene and transmits it to drug-sensitive bacteria. Are you claiming this is the mechanism that gives humans a reproductive advantage over chimps?
Kleinman:
And to your comment here, you have assumed that the two subsets of your sexually reproducing population each have fixed their respective resistance alleles so they exist at frequencies of 1 in their respective populations.
Taq:
If they didn't have the resistance marker then they wouldn't have grown on the antibiotic plate. 100% of the bacteria on each plate carry the mutation for each antibiotic.

It appears the selection coefficient is extremely high, all the drug-sensitive variants are killed off in a single generation. Is that how your model for human evolution works?
Kleinman:
If we assume both subsets have equal population sizes when you combine the frequencies of the resistance alleles for each drug will be 0.5.
Taq:
Exactly. The two lineages have merged. Half the population has both mutations. If they are now challenged by both antibiotics half of the population will survive, and 100% will have both mutations in the same lineage, and it wouldn't have required iterative mutations.

That's the problem, physicians have been taught for years an incorrect way of using antimicrobial agents and it has resulted in multidrug-resistant microbes. Doctors have been taught to use antimicrobial agents as single drug therapy. When one drug fails, go onto the next, and the next, and the next,... Microbiologists need to do a better job teaching physicians how drug resistance evolves. Do you know any microbiologists that know how drug resistance evolves?
Kleinman:
And BTW, combination therapy works for the treatment of malaria which can do sexual reproduction.
Taq:
What would happen if one village used one drug and a village close by used a different drug? Could you have resistance to each drug develop in each village, and then find both resistance markers in the offspring between those two resistant populations? The answer is yes. The same mutations wouldn't have to repeat themselves in each population.

The probability of that happening depends on the frequency of the different resistance alleles in the population. I'm still waiting for you to figure out that math. I'll even give you a couple of hints. It is the same math as a random card drawing problem except you only have 3 different kinds of cards in the deck. Call one card "A" for the first resistance allele, a second card "B" for the second resistance allele, and the third card "C" for members of the population that have neither the "A" nor "B" resistance alleles. Assume all the members of the population are homozygous at the respective genetic loci to make the math a bit easier and you have nA members in the population, nB members in the population, and nC members so that nA + nB + nC = n, the total population size. What's the probability of drawing an A and B parents to give an AB offspring?

This message is a reply to:
 Message 245 by Taq, posted 09-26-2022 3:40 PM Taq has replied

Replies to this message:
 Message 247 by Taq, posted 09-26-2022 6:05 PM Kleinman has replied

  
Taq
Member
Posts: 9063
Joined: 03-06-2009
Member Rating: 3.3


Message 247 of 2383 (898595)
09-26-2022 6:05 PM
Reply to: Message 246 by Kleinman
09-26-2022 5:23 PM


Re: Apples and oranges
Kleinman writes:
The math is way beyond you. 20 million beneficial mutations * 300 generations/fixation = 6 billion generations
The neutral fixation rate in diploid organisms is essentially the mutation rate, which is 50 mutations per generation. Beneficial mutations would fix at a higher rate than neutral mutations.
How much variation? And how many different lineages in your population?
Every time you ask for lineages in a sexually reproducing population you demonstrate you don't know what you are talking about.
So you are claiming that no human lineages have ever gone extinct? What happens to the less fit human lineages when the most fit are fixed in the population?
I am saying that asking for lineages in a sexually reproducing population makes no sense because of the intermingling of alleles and mutations.
What happens to the less fit human lineages when the most fit are fixed in the population?
If the most fit are fixed in the population then there is no less fit. They are all equally fit.
That's still not quite right.
It is. Father is AAbb, mother is aaBB. All offspring will be AaBb. 100% of offspring will have the beneficial mutation for both gene A and gene B.
Fixation isn't rapid and Haldane's mathematical estimate of 300 generations/fixation has been verified experimentally.
The difference is that in sexually reproducing species you can have more than one mutation moving towards fixation at a time. They are moving towards fixation in parallel.
Plug in a selection coefficient and tell us how many generations to fixation.
You don't even understand how sexual reproduction works. Why don't you start there.
So the resistance allele has to evolve in the bacteria and the phage acquires the gene and transmits it to drug-sensitive bacteria.
No. I am simply acting as if bacteria were suddenly diploid and sexually reproducing. Phage is not moving any genes around. In one population you get antibiotic resistance through mutation. In another you get phage resistance through mutation (not through any transport of DNA from phage). When you bring the two bacterial diploid sexually reproducing populations you get offspring with both antibiotic and phage resistance.
Do you know any microbiologists that know how drug resistance evolves?
This microbiologist does understand it just fine.
The probability of that happening depends on the frequency of the different resistance alleles in the population.
That's not what happens in the Lenski and Kishony experiments, is it?

This message is a reply to:
 Message 246 by Kleinman, posted 09-26-2022 5:23 PM Kleinman has replied

Replies to this message:
 Message 248 by Kleinman, posted 09-26-2022 7:32 PM Taq has replied

  
Kleinman
Member
Posts: 1492
From: United States
Joined: 10-06-2016


Message 248 of 2383 (898598)
09-26-2022 7:32 PM
Reply to: Message 247 by Taq
09-26-2022 6:05 PM


Re: Apples and oranges
Kleinman:
The math is way beyond you. 20 million beneficial mutations * 300 generations/fixation = 6 billion generations
Taq:
The neutral fixation rate in diploid organisms is essentially the mutation rate, which is 50 mutations per generation. Beneficial mutations would fix at a higher rate than neutral mutations.

That is hilarious.
Kleinman:
How much variation? And how many different lineages in your population?
Taq:
Every time you ask for lineages in a sexually reproducing population you demonstrate you don't know what you are talking about.

Taq had no parents, he is a product of a population.
Kleinman:
So you are claiming that no human lineages have ever gone extinct? What happens to the less fit human lineages when the most fit are fixed in the population?
Taq:
I am saying that asking for lineages in a sexually reproducing population makes no sense because of the intermingling of alleles and mutations.

All that intermingling of alleles and mutations and still they fix at a rate of greater than 50/generation. The Mexican Salamander has a genome length of 32 billion base pairs. Does that replicator fix 500 mutations/generation?
Kleinman:
What happens to the less fit human lineages when the most fit are fixed in the population?
Taq:
If the most fit are fixed in the population then there is no less fit. They are all equally fit.

That's fitting, the less fit aren't fit for life anymore.
Kleinman:
That's still not quite right.
Taq:
It is. Father is AAbb, mother is aaBB. All offspring will be AaBb. 100% of offspring will have the beneficial mutation for both gene A and gene B.

How did all the fathers end up AAbb and all the mothers aaBB?
Kleinman:
Fixation isn't rapid and Haldane's mathematical estimate of 300 generations/fixation has been verified experimentally.
Taq:
The difference is that in sexually reproducing species you can have more than one mutation moving towards fixation at a time. They are moving towards fixation in parallel.

Do you think that Haldane was wrong when he wrote this:
Haldane:
It is suggested that, in horotelic evolution, the mean time taken for each gene substitution is about 300 generations. This accords with the observed slowness of evolution.
Haldane posts data from sweet peas in his paper. Sweet peas do sexual replication. And do you have any experimental data that shows that fixation can occur more rapidly in sexual replicators than in asexual replicators?
Kleinman:
Plug in a selection coefficient and tell us how many generations to fixation.
Taq:
You don't even understand how sexual reproduction works. Why don't you start there.

Taq, I've taken multiple biology courses and even 2 years of microbiology. I know how meiosis works. So show us how you use the equations you posted to compute the number of generations to fixation for a single allele.
Kleinman:
So the resistance allele has to evolve in the bacteria and the phage acquires the gene and transmits it to drug-sensitive bacteria.
Taq:
No. I am simply acting as if bacteria were suddenly diploid and sexually reproducing. Phage is not moving any genes around. In one population you get antibiotic resistance through mutation. In another you get phage resistance through mutation (not through any transport of DNA from phage). When you bring the two bacterial diploid sexually reproducing populations you get offspring with both antibiotic and phage resistance.

Why should it surprise you when a scientist puts an agent into a population that transfers a resistance allele? This is simply a breeding program with a phage with a known allele and a population of bacteria. Are you claiming that the human reproductive advantage came about due to breeding?
Kleinman:
Do you know any microbiologists that know how drug resistance evolves?
Taq:
This microbiologist does understand it just fine.

Tell us how the Kishony experiment works. And show your math.
Kleinman:
The probability of that happening depends on the frequency of the different resistance alleles in the population.
Taq:
That's not what happens in the Lenski and Kishony experiments, is it?

You still haven't figured out the difference between DNA evolution, biological evolutionary competition, and recombination. Don't worry, I'll be patient with you till you get it.

This message is a reply to:
 Message 247 by Taq, posted 09-26-2022 6:05 PM Taq has replied

Replies to this message:
 Message 250 by Taq, posted 09-27-2022 10:40 AM Kleinman has replied

  
Kleinman
Member
Posts: 1492
From: United States
Joined: 10-06-2016


Message 249 of 2383 (898611)
09-27-2022 9:45 AM
Reply to: Message 175 by Percy
09-22-2022 10:10 AM


Re: Video not available
Further response to Percy's Message 175
Percy, I tried to write the matrix equations using Latex. They appear correctly in the Latex editor I used but don't appear correctly here.
Picking up the discussion on computing the probability of a particular mutation occurring using a Markov Process
Kleinman:
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
Percy:
Again, instead of providing a link to a paper, please describe the model adaptation process yourself and use the link as a supporting reference.
Kleinman:
Note that either means of computing the probability of an adaptive mutation occurring gives the same result.
Percy:
Please show us your work where the same result is produced.



OK. First, for those readers that don't know what a Markov Chain is, here's a definition from Wikipedia:
Markov chain - Wikipedia
quote:
A Markov chain or Markov process is a stochastic model describing a sequence of possible events in which the probability of each event depends only on the state attained in the previous event.[1][2][3] Informally, this may be thought of as, "What happens next depends only on the state of affairs now."
The first application of a Markov Chain model to DNA evolution was done by Jukes and Cantor and is called the Jukes-Cantor model. The way one does such a calculation is first to draw a state transition diagram of the system of interest. The state transition diagram for a single site in a genome looks as follows:
In this instance, the only possible mutations are base substitutions, no insertions or deletions. The circles represent the possible states, one for each possible base. The P's with the subscripts that label the arrows are the probabilities for the possible state transitions. An AC subscript means an A base has mutated to a C base, a GT subscript means a G base has mutated to a T base, an AA subscript means that no mutation has occurred, and so on for the other transition probabilities.
Then, a transition matrix can be written to describe the evolutionary change in time t is = (pij) where the pij gives the probabilities of change from the state Ei to Ej at time t + Δt where Δt is a replication. If we neglect insertions, deletions, transpositions, and other types of mutations (that is substitutions only), the transition matrix would look as follows:
P (t)=( pAA pAC pAG pAT
pCA pCC pCG pCT
pGA pGC pGG pGT
pTA pTC pTG pTT )

\left[ {\begin{array}
p_{AA} & p_{AC} & p_{AG} & p_{AT}\\
p_{CA} & p_{CC} & p_{CG} & p_{CT}\\
p_{GA} & p_{GC} & p_{GG} & p_{GT}\\
p_{TA} & p_{TC} & p_{TG} & p_{TT}\\
\end{array} } \right
\][/latex]-->
If one assumes that the mutation rates are constant and have the same value for DNA transitions and transversion, we obtain the Jukes-Cantor model.
P (t)=[1−μ μ/3 μ/3 μ/3
μ/3 1−μ μ/3 μ/3
μ/3 μ/3 1−μ μ/3
μ/3 μ/3 μ/3 1−μ]

\left[ {\begin{array}{cccc}
1−μ & μ/3 & μ/3 & μ/3\\
μ/3 & 1−μ & μ/3 & μ/3\\
μ/3 & μ/3 & 1−μ & μ/3\\
μ/3 & μ/3 & μ/3 & 1−μ\\
\end{array} } \right]
[/latex]-->
The Jukes-Cantor model implicitly assumes a population of one. If one wants to compute the frequency distribution of different variants as a population grows "N", it is done as follows:
P (t)=[1−μ/N μ/(3∗N) μ/(3∗N) μ/(3∗N)
μ/(3∗N) 1−μ/N μ/(3∗N) μ/(3∗N)
μ/(3∗N) μ/(3∗N) 1−μ/N μ/(3∗N)
μ/(3∗N) μ/(3∗N) μ/(3∗N) 1−μ/N)]

\left[ {\begin{array}{cccc}
1−μ/N & μ/(3∗N) & μ/(3∗N) & μ/(3∗N)\\
μ/(3∗N) & 1−μ/N & μ/(3∗N) & μ/(3∗N)\\
μ/(3∗N) & μ/(3∗N) & 1−μ/N & μ/(3∗N)\\
μ/(3∗N) & μ/(3∗N) & μ/(3∗N) & 1−μ/N\\
\end{array} } \right]
[/latex]-->
The initial state of the system is written:
E0 = (A0, C0, G0, T0)
and the state of the system a time ti is:
Ei = (Ai, Ci, Gi, Ti)
and the state of the system going from state Ei to state Ei+1 is computed by simple matrix multiplication.
Ei+1 = Ei [P]
For the Jukes-Cantor model one obtains the equations:
Ai+1 = Ai(1-μ) + Ci*μ/3 + Gi*μ/3 + Ti*μ/3
Ci+1 = Ai*μ/3 + Ci(1-μ) + Gi*μ/3 + Ti*μ/3
Gi+1 = Ai*μ/3 + Ci*μ/3 + Gi(1-μ) + Ti*μ/3
Ti+1 = Ai*μ/3 + Ci*μ/3 + Gi*μ/3 + Ti(1-μ)
And for the variable population model:
Ai+1 = Ai(1-μ/N) + Ci*μ/(3*N)+ Gi*μ/(3*N) + Ti*μ/(3*N)
Ci+1 = Ai*μ/(3*N) + Ci(1-μ/N) + Gi* μ/(3*N)+ Ti*μ/(3*N)
Gi+1 = Ai*μ/(3*N) + Ci*μ/(3*N) + Gi(1-μ/N) + Ti*μ/(3*N)
Ti+1 = Ai*μ/(3*N) + Ci*μ/(3*N) + Gi*μ/(3*N) + Ti(1-μ/N)
Note that A,C,G, and T are frequencies of the particular variants with that particular base at that site. If you multiply any of these frequencies by N, you will get the number of members in the population with that given base at that site.
Then, assume that in the initial condition that the base at that site is T but the beneficial mutation is A. The initial condition is written:
E0 = (A0, C0, G0, T0) = (0,0,0,1)
And do lots of matrix multiplications.
For the Jukes-Cantor model and mutation rate 1e-9, one obtains the following frequency curves:
For the variable population transition model and mutation rate 1e-9, one obtains the following frequency curves:
And for comparison, the probability curves for the "at least one" calculation for a beneficial mutation to occur as a function of population size:
Comparing these 3 graphs shows that the Jukes-Cantor model reaches equilibrium at about 3e9 replications. The variable population size model gets an expected number of A variants equal to 1 at about 1.5e8 and the "at least one" calculation for mutation rate 1e-9 gives a rapidly rising probability at about 1.5e8.
Percy:
And don't leave me hanging about what the different populations are competing for. Was my guess of lebensraum right?
Kleinman:
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.
Percy:
One might even say they're competing for resources.


That's right, but ultimately, I think resources are just individual components of the environment that make the energy in the environment available to the replicator. For example, plants need water to convert the energy from the sun to produce sugar. That's why drought and dehydration is a selection pressure.
So tell me Percy, is the physics and math that I've presented get us into the ballpark on how biological evolution works?

This message is a reply to:
 Message 175 by Percy, posted 09-22-2022 10:10 AM Percy has replied

Replies to this message:
 Message 272 by Percy, posted 09-28-2022 10:34 AM Kleinman has not replied

  
Taq
Member
Posts: 9063
Joined: 03-06-2009
Member Rating: 3.3


Message 250 of 2383 (898619)
09-27-2022 10:40 AM
Reply to: Message 248 by Kleinman
09-26-2022 7:32 PM


Re: Apples and oranges
Kleinman writes:
That is hilarious.
You think this is hilarious?
quote:
For a diploid population of size N and neutral mutation rate u , the initial frequency of a novel mutation is simply 1/(2N), and the number of new mutations per generation is 2Nu. Since the fixation rate is the rate of novel neutral mutation multiplied by their probability of fixation, the overall fixation rate is (2Nu)x(1/2N) = u. Thus, the rate of fixation for a mutation not subject to selection is simply the rate of introduction of such mutations.
Fixation - Wikipedia(population_genetics)
All that intermingling of alleles and mutations and still they fix at a rate of greater than 50/generation.
Generation 1 there are 5 beneficial mutations that occur in the population and they fix at generation 51. In generation 2 there are another 5 beneficial mutations, and they fix at generation 52. In generation 3 there are another 5 beneficial mutations and they fix at generation 53. See a pattern here?
That's fitting, the less fit aren't fit for life anymore.
I see you are just blabbering now.
How did all the fathers end up AAbb and all the mothers aaBB?
Why would all the fathers need to be AAbb in order for at least one father to be AAbb? Same for mothers.
Do you think that Haldane was wrong when he wrote this:
Generation 1 there are 5 beneficial mutations, and in generation 301 they are fixed. In generation 2 there are 5 beneficial mutations, and in generation 302 they are fixed. See a pattern?
Why should it surprise you when a scientist puts an agent into a population that transfers a resistance allele?
Phage do not transfer phage resistance in the Lederberg experiment. The phage in the experiment binds to the gene product of tonB. Mutations in the tonB gene prevent phage from binding to the bacteria.
I will ask again. Why does spectinomycin resistance occur once every 10 billion replications in E. coli and phage resistance occurs once every 10 million replications? Why is there a 1,000 fold difference?
Tell us how the Kishony experiment works.
Read the Kishony experiment. What you fail to understand is that the Kishony experiment is largely irrelevant to how humans evolved.
You still haven't figured out the difference between DNA evolution, biological evolutionary competition, and recombination.
I'm not the one who hasn't figured it out.

This message is a reply to:
 Message 248 by Kleinman, posted 09-26-2022 7:32 PM Kleinman has replied

Replies to this message:
 Message 251 by Kleinman, posted 09-27-2022 11:38 AM Taq has replied

  
Kleinman
Member
Posts: 1492
From: United States
Joined: 10-06-2016


Message 251 of 2383 (898626)
09-27-2022 11:38 AM
Reply to: Message 250 by Taq
09-27-2022 10:40 AM


Re: Apples and oranges
Taq:
The neutral fixation rate in diploid organisms is essentially the mutation rate, which is 50 mutations per generation. Beneficial mutations would fix at a higher rate than neutral mutations.
Kleinman:
That is hilarious.
Taq:
For a diploid population of size N and neutral mutation rate u , the initial frequency of a novel mutation is simply 1/(2N), and the number of new mutations per generation is 2Nu. Since the fixation rate is the rate of novel neutral mutation multiplied by their probability of fixation, the overall fixation rate is (2Nu)x(1/2N) = u. Thus, the rate of fixation for a mutation not subject to selection is simply the rate of introduction of such mutations.
Fixation - Wikipedia(population_genetics)


It appears that in your microbiology training, none of your instructors taught you what a mutation rate is. If you are able, prepare yourself to be instructed.
Mutation rate - Wikipedia
quote:
In genetics, the mutation rate is the frequency of new mutations in a single gene or organism over time.[2]
And that rate estimated for humans is:
quote:
Using data available from whole genome sequencing, the human genome mutation rate is similarly estimated to be ~1.1×10−8 per site per generation.[15]
The mutation rate is not the ridiculous claim of 50 mutations per generation that you made in your post. You need to put more effort into understanding the equations you use and how you define the variables in these equations. Now put the correct values in your equation and tell us how many generations to fixation for each mutation and then understand why 20,000,000 adaptive mutations are not going to fix in your model.

This message is a reply to:
 Message 250 by Taq, posted 09-27-2022 10:40 AM Taq has replied

Replies to this message:
 Message 252 by Taq, posted 09-27-2022 11:48 AM Kleinman has replied

  
Taq
Member
Posts: 9063
Joined: 03-06-2009
Member Rating: 3.3


Message 252 of 2383 (898628)
09-27-2022 11:48 AM
Reply to: Message 251 by Kleinman
09-27-2022 11:38 AM


Re: Apples and oranges
Kleinman writes:
And that rate estimated for humans is:
quote:
Using data available from whole genome sequencing, the human genome mutation rate is similarly estimated to be ~1.1×10−8 per site per generation.
The mutation rate is not the ridiculous claim of 50 mutations per generation that you made in your post. You need to put more effort into understanding the equations you use and how you define the variables in these equations. Now put the correct values in your equation and tell us how many generations to fixation for each mutation and then understand why 20,000,000 adaptive mutations are not going to fix in your model.
1.1x10-8 per site per generation. Let's see how that works out. That is a mutation every 110 million bases. There are 6 billion bases in the human diploid genome. (6E9)/(1.1E8) = 54.5 mutations per person per generation. On top of that, we have directly sequenced the genomes of parents and offspring to directly measure the number of mutations per person, and that is where the figure you cite comes from. The directly measured human mutation rate is around 50 mutations per person.
Do you also agree that the neutral fixation rate is approximately the mutation rate, meaning that for a mutation rate of around 50 mutations per person per generation that we will see 50 neutral mutations fixed per generation?
Added in edit:
Figure 2 from this paper which directly measured mutations between parents and offspring. The Y axis is the number of mutations per birth, and the x axis is the father's age at conception. As you can see, many of the mutations come from the father due to continual division of germ line cells (i.e. sperm).

Edited by Taq, .


This message is a reply to:
 Message 251 by Kleinman, posted 09-27-2022 11:38 AM Kleinman has replied

Replies to this message:
 Message 253 by Kleinman, posted 09-27-2022 12:46 PM Taq has replied

  
Kleinman
Member
Posts: 1492
From: United States
Joined: 10-06-2016


Message 253 of 2383 (898635)
09-27-2022 12:46 PM
Reply to: Message 252 by Taq
09-27-2022 11:48 AM


Re: Apples and oranges
Taq:
1.1x10-8 per site per generation. Let's see how that works out. That is a mutation every 110 million bases. There are 6 billion bases in the human diploid genome. (6E9)/(1.1E8) = 54.5 mutations per person per generation. On top of that, we have directly sequenced the genomes of parents and offspring to directly measure the number of mutations per person, and that is where the figure you cite comes from. The directly measured human mutation rate is around 50 mutations per person.

Do you also agree that the neutral fixation rate is approximately the mutation rate, meaning that for a mutation rate of around 50 mutations per person per generation that we will see 50 neutral mutations fixed per generation?
The correct value to use in your equation is 1.1x10-8, not 50. Your value is off by about 9 orders of magnitude. There are many reasons why the number you are trying to use is wrong but one of the biggest is that nowhere in your equation is the genome length a variable. That's why I brought up the Mexican Salamander example because its genome is 10x larger than the human genome. That doesn't make the number of fixations 10x larger, 500 in every generation! For neutral evolution, it will take 1/(1.1x10-8) or about 90 million generations for each neutral fixation. Haldane's fixation rate of 1 fixation for every 300 generations under selection is much more generous. How you could imagine that every member of a population ends up with the same 50 neutral (or any) mutations every generation is a mystery.

This message is a reply to:
 Message 252 by Taq, posted 09-27-2022 11:48 AM Taq has replied

Replies to this message:
 Message 254 by Taq, posted 09-27-2022 1:10 PM Kleinman has replied

  
Taq
Member
Posts: 9063
Joined: 03-06-2009
Member Rating: 3.3


Message 254 of 2383 (898645)
09-27-2022 1:10 PM
Reply to: Message 253 by Kleinman
09-27-2022 12:46 PM


Re: Apples and oranges
Kleinman writes:
The correct value to use in your equation is 1.1x10-8, not 50.
1.1x10-8 per nucleotide per generation is the same as 54.5 mutations per person per generation for a 6 billion base diploid genome.
Moreover, we can count the mutations by comparing the genomes of parents and their offspring. That number is about 50, on average. Check out this paper:
Rate of de novo mutations, father’s age, and disease risk - PMC

Edited by Taq, .

Edited by Taq, .

Edited by Taq, .


This message is a reply to:
 Message 253 by Kleinman, posted 09-27-2022 12:46 PM Kleinman has replied

Replies to this message:
 Message 255 by Kleinman, posted 09-27-2022 1:27 PM Taq has replied

  
Kleinman
Member
Posts: 1492
From: United States
Joined: 10-06-2016


Message 255 of 2383 (898647)
09-27-2022 1:27 PM
Reply to: Message 254 by Taq
09-27-2022 1:10 PM


Re: Apples and oranges
Kleinman:
The correct value to use in your equation is 1.1x10-8, not 50.
Taq:
1.1x10-8 per nucleotide per generation is the same as 54.5 mutations per person per generation for a 6 billion base diploid genome.

And 54.5 is not the correct value to use in your equation. Just because the number of mutations that occur in a replication is 54.5 doesn't mean that all 54.5 are fixed. The correct value to use in your equation is 1.1x10-8.

This message is a reply to:
 Message 254 by Taq, posted 09-27-2022 1:10 PM Taq has replied

Replies to this message:
 Message 256 by Taq, posted 09-27-2022 1:36 PM Kleinman has replied

  
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