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Author Topic:   Rebuttal To Creationists - "Since We Can't Directly Observe Evolution..."
Taq
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Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 262 of 2926 (898676)
09-27-2022 9:11 PM
Reply to: Message 261 by Kleinman
09-27-2022 7:58 PM


Re: Apples and oranges
Kleinman writes:
1/2N is the frequency of the mutant allele.
Yes. That is true for every mutation throughout the genome, not just in genes.
It applies to any mutant allele but only for a single genetic locus.
It applies to all bases in the genome.
You don't understand this equation. You have even confused the number of copies of alleles with population size. There are 2N copies of an allele in a diploid population size N. And if you somehow want to extrapolate this model to the entire genome means that the entire genome is being fixed.
Please learn what chromosomes are, what cross-overs are, and how meiosis works. The entire genome is not passed on as a unit. Recombination happens within a chromosome. The copies of different chromosomes are passed on independently of each other. Just as mutations in genes are evolving independently, so too are the mutations outside of genes.
In a population of 100,000 and a mutation rate of 50 mutations per genome per generation you will get 5 million mutations. The equation for neutral fixation states that 50 of those mutations will reach fixation if all 5 million mutations are neutral.
If you want to do the math for a mutation not in a coding portion of the genome, then the number of bases in that sequence is one and the mutation rate you need to use is 1.1x10-8.
Coding portions of the genome make up just 1-2%. Sorry, but there is more than one base outside of coding regions. In fact, there are billions.
You also never put any units on your 1.1E10-8 figure. Why is that? Is it because it is the per base mutation rate across the entire genome? When they measured the mutation rate in humans do you think they only looked at coding regions?
That's about 9,000,000 generations to fixation.
Mutations don't fix one at a time. They fix in parallel.
ou have a population of about 1 billion population with 2 billion chromosome sets replications and use your mutation rate of 1.1x10-8.
1 billion births with 1.1E-8 mutations per nucleotide per birth in a 6 billion base diploid genome is 1E9*1.1E-8*6E9 = 66 billion mutations. In a 6 billion base genome there are 18 billion possible SNP's. 1 billion births is more than enough to get every possible non-lethal mutation kicking around on the globe somewhere if all mutations are equally probable.
That's about 9,000,000 generations to fixation.
Mutations fix in parallel, not sequentially.
hat's why it takes a billion replications for each adaptive mutation in the Kishony and Lenski experiments for a mutation rate of 1e-9.
Again, where are the units on your mutation rate?
Taq, the math gets orders of magnitude worse if it takes 2 or more mutations to give an improvement in fitness. It introduces another instance of the multiplication rule for each selection condition the population must adapt to.
For such a claim you would first need to calculate all of the possible combinations of 2 mutations that would be beneficial. If there are billions and billions of possible beneficial combinations then they wouldn't be hard to find.

This message is a reply to:
 Message 261 by Kleinman, posted 09-27-2022 7:58 PM Kleinman has replied

Replies to this message:
 Message 263 by Theodoric, posted 09-27-2022 10:12 PM Taq has not replied
 Message 264 by Kleinman, posted 09-27-2022 10:23 PM Taq has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 273 of 2926 (898699)
09-28-2022 10:42 AM
Reply to: Message 264 by Kleinman
09-27-2022 10:23 PM


Re: Apples and oranges
Kleinman writes:
You are having trouble doing undergraduate lower division work so I don't know whether I should give you this paper but why not?
THE AVERAGE NUMBER OF GENERATIONS UNTIL FIXATION OF A MUTANT GENE IN A FINITE POPULATION
Kimura carries out the computation of the fixation of a mutant gene. His calculation doesn't depend on the mutation rate.
The calculation of the number of generations it takes a single mutation to reach fixation wouldn't need the mutation rate. Why do you think it would?
What does require the mutation rate is a calculation of the number of mutations that will move towards fixation.
Now the effective population size can be slightly smaller than the actual population size under certain circumstances that I'm sure you know what they are. Remind me again what the population size you use is. Wasn't it 100,000? That gives the generations to fixation of that mutant gene of 4*100,000=400,000 generations.
Ne is usually drastically smaller than N.
quote:
By comparing the likelihood of various demographic models, we estimate that the effective population size of human ancestors living before 1.2 million years ago was 18,500, and we can reject all models where the ancient effective population size was larger than 26,000.
Just a moment...
That gives the generations to fixation of that mutant gene of 4*100,000=400,000 generations. That really helps. Your lower division equation gave an estimate of 900,000 generations for the fixation of a neutral mutation. How many generations since the divergence of humans and chimps from the common ancestor?
I already explained this a previous post. Let's use an effective population size of 20,000 as described above. That would be 80,000 generations to fix a neutral allele, and at 25 years per generation that would be 2 million years. This means the earliest populations in the human lineage that had just split away from the chimp population would be fixing neutral mutation that occurred 2 million years before that. Every generation after that would be fixing neutral mutations that occurred 2 million years before them. Where is the problem?
You still haven't figured out that different combinations of adaptive mutations give different lineages on different evolutionary trajectories.
You still haven't figured out that lineages combine in a sexually reproducing population. Your genome is the merger of your father's and mother's lineage. Every single birth is a mixture of lineages.

This message is a reply to:
 Message 264 by Kleinman, posted 09-27-2022 10:23 PM Kleinman has not replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


(1)
Message 274 of 2926 (898701)
09-28-2022 11:01 AM
Reply to: Message 266 by Kleinman
09-28-2022 7:18 AM


Re: Keeps going and.going
Kleinman writes:
Taq likes to tell fish stories.
Fish stories? Who is the one claiming that 98% of the human genome outside of coding regions is one monolithic sequence that is all moving towards fixation as a single unit in a way that magically excludes any new mutations that occur?
Do you even think about this? Let's see what consequences this would have. According to you, only coding sequences can differ. This would mean that 98% of the human genome should be 100% conserved across the entire human population. Do you think this is true? If not, how do you explain the differences between non-coding sequences in human genomes? How do you even explain the differences between the two copies of the same chromosome in non-coding DNA?
The other hilarious fish story you tell is that lineages are isolated in human populations. This insane claim shows a near complete ignorance of how human genetics works. It's as if you have never even seen a Punnett square. Mendel knew more about genetics than you do. You can't even understand how two independent mutations can end up in the same genome.
For the peanut gallery, ghost ancestors are an interesting outcome of sexual reproduction and meiosis. There are some human ancestors that are the ancestors of everyone alive today, and yet none of us carry any of their DNA.
quote:
In a randomly-mating biparental population of size N there are, with high probability, individuals who are genealogical ancestors of every extant individual within approximately log2(N) generations into the past. We use this result of J. Chang to prove a curious corollary under standard models of recombination: there exist, with high probability, individuals within a constant multiple of generations into the past who are simultaneously (i) genealogical ancestors of each of the individuals at the present, and (ii) genetic ancestors to none of the individuals at the present. Such ancestral individuals–ancestors of everyone today that left no genetic trace–represent ‘ghost’ ancestors in a strong sense. In this short note, we use simple analytical argument and simulations to estimate how many such individuals exist in finite Wright–Fisher populations.
https://www.sciencedirect.com/...ticle/pii/S0040580915000167

This message is a reply to:
 Message 266 by Kleinman, posted 09-28-2022 7:18 AM Kleinman has replied

Replies to this message:
 Message 277 by Kleinman, posted 09-28-2022 11:35 AM Taq has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 278 of 2926 (898706)
09-28-2022 11:37 AM
Reply to: Message 275 by Kleinman
09-28-2022 11:08 AM


Re: Video not available
Kleinman writes:
OK, here's Haldane's frequency equation again:
You could use any frequency distribution you want. If we divided the world into those who prefer vanilla ice cream and those that prefer chocolate ice cream we could get the same comparisons. That doesn't mean preference for ice cream flavor is a conservation of energy process.

This message is a reply to:
 Message 275 by Kleinman, posted 09-28-2022 11:08 AM Kleinman has not replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 279 of 2926 (898707)
09-28-2022 11:44 AM
Reply to: Message 277 by Kleinman
09-28-2022 11:35 AM


Re: Keeps going and.going
Kleinman writes:
Let's do a little math. 2,000,000 years/25 years/generation = 80,000 generations. Congratulations, you've fixed 1 neutral mutation.
First, there are about 50 mutations that fix in every generation, not 1. Second, every generation has new neutral mutations, and some of those neutral mutations will begin to move towards fixation. The first generation in our lineage would have already had neutral mutations they inherited from their ancestors 2 million years ago.
Since you won't attempt to do the mathematics of recombination,
Why do any mathematics for someone who claims recombination doesn't even exist?
I don't think the non-coding region is one monolithic sequence.
Yes, you do. You claimed that all non-coding sequence is a single allele that moves towards fixation together.
It is like an assembly line. If it takes 24 hours for Ford to make a specific car on a single assembly line, start to finish, does this mean that they only produce one car every day on that assembly line? Obviously not. As the car is finished at one station it is passed to the next, and a new car is placed at the previous station. They are all lined up behind each other moving along the assembly line. Fixation of neutral mutations work the exactly same way.
I don't think the non-coding region is one monolithic sequence.
Yes, you do. You claimed all non-coding sequence was a single allele that moved towards fixation together.

This message is a reply to:
 Message 277 by Kleinman, posted 09-28-2022 11:35 AM Kleinman has replied

Replies to this message:
 Message 281 by Kleinman, posted 09-28-2022 12:26 PM Taq has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 282 of 2926 (898717)
09-28-2022 12:38 PM
Reply to: Message 281 by Kleinman
09-28-2022 12:26 PM


Re: Keeps going and.going
Kleinman writes:
LOL!
That's all you got?
Is Taq now an advocate for intelligent design? Living things are now made on a Ford assembly line.
Given your lack of response, are you tacitly agreeing that we should see fixation of neutral mutations in each generation?
Or are you still so confused that you think only 1 mutation can move towards fixation at a time, and that all other neutral mutations can not begin to move towards fixation until that 1 neutral mutation is fixed?
Now Taq is claiming that all 54.5 of the mutations in a genome don't get fixed.
That's what I have claimed all along.

This message is a reply to:
 Message 281 by Kleinman, posted 09-28-2022 12:26 PM Kleinman has replied

Replies to this message:
 Message 283 by Kleinman, posted 09-28-2022 1:27 PM Taq has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 284 of 2926 (898722)
09-28-2022 1:40 PM
Reply to: Message 283 by Kleinman
09-28-2022 1:27 PM


Re: Keeps going and.going
Kleinman writes:
It makes me really sad that a microbiologist can't explain the evolution of antimicrobial drug resistance.
In the case of beta-lactam resistance, one pathway is mutations produce an enzyme capable of breaking down the antibiotic.
What does this have to do with human evolution?
Watch out, there's a stampede of neutral mutation coming down a Ford assembly line.
Then I will assume you accept the claim that around 50 neutral mutations reach fixation in each generation.
How many neutral mutations are lost?
(N*u)-u
where N is the population size and u is the number of mutations per individual per generation.

This message is a reply to:
 Message 283 by Kleinman, posted 09-28-2022 1:27 PM Kleinman has replied

Replies to this message:
 Message 285 by Kleinman, posted 09-28-2022 2:42 PM Taq has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 286 of 2926 (898724)
09-28-2022 3:04 PM
Reply to: Message 285 by Kleinman
09-28-2022 2:42 PM


Re: Keeps going and.going
Kleinman writes:
Pathway? What pathway? How do mutations take a pathway?
Here you go:
click here
Don't both humans and bacteria have DNA?
That doesn't answer my question.
What does the evolution of antibiotic resistance in bacteria have to do with human evolution?
On what do you base that assumption?
Your inability to address what I wrote.
So for human evolution using your equation you get:
(100,000*54.5)-54.5
Is that new math?
Yes, of the ~5 million neutral mutations that occur in that generation all but ~50 will be lost at some point after that generation. Of course, this depends on the mutation remaining neutral and not being influenced by linkage disequilibrium. At the end of the day, the equation for neutral fixation is an idealized genome and population, something akin to the ideal gas laws.

This message is a reply to:
 Message 285 by Kleinman, posted 09-28-2022 2:42 PM Kleinman has replied

Replies to this message:
 Message 287 by Kleinman, posted 09-28-2022 3:58 PM Taq has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 288 of 2926 (898735)
09-28-2022 6:07 PM
Reply to: Message 287 by Kleinman
09-28-2022 3:58 PM


Re: Keeps going and.going
[qs=Kleinman] Google "evolutionary pathway". Start reading.
Are implying that bacteria and humans both don't have DNA?
What does the evolution of antibiotic resistance in bacteria have to do with human evolution?
Did you write something about how mutations take a pathway?
I wrote this:
I already explained this a previous post. Let's use an effective population size of 20,000 as described above. That would be 80,000 generations to fix a neutral allele, and at 25 years per generation that would be 2 million years. This means the earliest populations in the human lineage that had just split away from the chimp population would be fixing neutral mutation that occurred 2 million years before that. Every generation after that would be fixing neutral mutations that occurred 2 million years before them. Where is the problem?
And this:
Given your lack of response, are you tacitly agreeing that we should see fixation of neutral mutations in each generation?

Or are you still so confused that you think only 1 mutation can move towards fixation at a time, and that all other neutral mutations can not begin to move towards fixation until that 1 neutral mutation is fixed?
So, every member of your population gets the same 54.5 mutations every generation.
That's what fixation means.
Does every human on earth have the same neutral mutations as every other human?
No, they don't. As already described, neutral mutations occur at different points in the past so they are all at different points in their journey towards either being lost or becoming fixed.

This message is a reply to:
 Message 287 by Kleinman, posted 09-28-2022 3:58 PM Kleinman has replied

Replies to this message:
 Message 289 by Kleinman, posted 09-28-2022 7:53 PM Taq has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 290 of 2926 (898742)
09-29-2022 10:44 AM
Reply to: Message 289 by Kleinman
09-28-2022 7:53 PM


Re: Keeps going and.going
Kleinman writes:
You need to learn that the mathematics of the evolution of adaptive alleles is the same for all replicators, neither ploidy nor recombination changes that fact.
Then you don't know how the mathematics or biology of adaptive alleles works.
In asexual organisms you can't combine mutations that happen in independent lineages. In sexually reproducing species you can combine mutations that are in contemporaneous genomes. That makes a massive difference in how adaptive alleles evolve.
Why don't you try to model a real experiment such as the Kishony or Lenski experiment? Describe how the evolutionary pathway works in either of those experiments and see if any of your models fit these experiments. That's what a scientist would do.
So you aren't going to address what I said?
So every generation every new member of the population gets 54.5 new unique mutations to their genome while 54.5 of the neutral mutations they inherited from their parents are fixed and these same 54.5 neutral mutations are identical to every new member of the population.
The 54.5 neutral mutations that fix in each generation would have entered into the gene pool hundreds of thousands or millions of years before they became fixed. Those mutations would have been found in nearly everyone just prior to reaching fixation. Are we agreed?
How many neutral mutations fixed in the Lenski experiment after 70,000 generations?
An asexual species with a very different mutation rate can not accurately model a sexually reproducing species with a different mutation rate.

This message is a reply to:
 Message 289 by Kleinman, posted 09-28-2022 7:53 PM Kleinman has replied

Replies to this message:
 Message 291 by Kleinman, posted 09-29-2022 11:34 AM Taq has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 292 of 2926 (898747)
09-29-2022 11:55 AM
Reply to: Message 291 by Kleinman
09-29-2022 11:34 AM


Re: Keeps going and.going
Then why has the math that I"ve presented been able to predict that each step in the Kishony experiment would take a billion replications?
The mistake you keep making is in forgetting that sexually reproducing species merge lineages. You keep claiming that beneficial mutations have to happen sequentially in an isolated lineage. This isn't the case in sexually reproducing populations. You also make the mistake of thinking every single adaptation will have the same rate as antibiotic resistance. There is no reason to think this is true as shown by a thousand fold difference for the rate of antibiotic and phage resistance in E. coli.
Taq now thinks that recombination can recombine mutations at the same genetic loci of both parents. How did you get so confused on this subject?
Where did I ever say that?????
You are aware that there is more than one gene in the human genome, right?
You are aware that beneficial mutations can happen in different genes, right?
I'm not interested in some fantasy model that you dredge up in your confused imagination. If you think your ridiculous model fits reality in any way, apply it to a real-world, measured, and repeatable experimental example. You won't because you know you are blowing smoke.
Then all you have is denial.
Do microbiologists know how to computer program? Take your model, and start with a population that has almost identical genomes except for each member in that population has unique random mutations scattered at different sites in the genome. Randomly choose two parents out of that population. Choose a mutation rate. Randomly select portions of each genome and recombine those portions to create a new genome while adding new unique random mutations to that genome based on your chosen mutation rate. Do that to the entire population until you create a new generation of descendants. Repeat that cycle and measure how many neutral mutations are fixed in the population as a function of the number of generations.
I already showed you the model. It's the equations for fixation of neutral mutations.

This message is a reply to:
 Message 291 by Kleinman, posted 09-29-2022 11:34 AM Kleinman has replied

Replies to this message:
 Message 293 by Kleinman, posted 09-29-2022 12:57 PM Taq has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 294 of 2926 (898766)
09-29-2022 4:09 PM
Reply to: Message 293 by Kleinman
09-29-2022 12:57 PM


Re: Keeps going and.going
Kleinman writes:
At least you are admitting that my model of adaptive evolution is correct for asexually replicating organisms.
I've agreed all along that your model for asexual organisms based on the Kishony and Lenski experiments is accurate for asexual organisms. What I keep telling you is that it isn't an accurate model for sexual species like humans.
Of course, adaptive mutations have to occur sequentially.
No, they don't have to. You can have multiple adaptive mutations that are all moving towards fixation at the same time. Even as those beneficial mutations move towards fixation, new beneficial mutations can occur and begin to move towards fixation.
Once you understand that microevolutionary changes are random events, the joint probabilities of these events don't add, you have to use the multiplication rule.
You also have to figure in the number of possible beneficial mutations at any point in the history of a lineage. How many times have I pointed this out?
The mistake you keep making is that you pretend as if only 1 beneficial mutation can move towards fixation at a time. That's wrong. Do you understand why that is wrong?
Aren't you saying that recombination can take half of one allele with one beneficial mutation from one parent to recombine with the other half of that allele with another beneficial mutation from the other parent to give an allele with two beneficial mutations?
Can you just for a moment realize that there is more than one gene in a genome? Please?
Imagine that there is a new beneficial mutation in gene A and a new beneficial mutation in gene B in the same generation. They are on different chromosomes. Both beneficial mutations start moving towards fixation at the same time. Let's say that both mutations reach 5% of the population. This means there is a 0.05*0.05 = 0.025 chance that out of two parents each will have one of the beneficial mutations. Let's say they are both heterozygous for their individual mutations. This means that 25% of their offspring WILL HAVE BOTH MUTATIONS. Do you see how this works?
While these two mutations are moving towards fixation and increasingly found in the same genomes, there will be new beneficial mutations that are appearing, and they too will go through the same process and be combined with the beneficial mutations already in the population.
That and a model of adaptive evolution that fits the experimental data, a published model of random recombination, and an understanding of the physics and mathematics of biological evolution. You should try and learn it, you might understand the subject of microbiology better.
I understand it just fine. The fact you don't understand the difference between asexual and sexual reproduction means you are the one who needs to catch up.
Kimura compared his mathematical model of fixation with a computer simulation. Why don't you? Don't worry Taq, I know you won't do this, you are just blowing smoke. So what do you want to do next, learn the mathematics of random recombination or the mathematics of adaptive evolution to multiple simultaneous selection pressures?
Can you be even more of a douchebag? You can't even understand how chromosomes work, and you want to critique me for not creating a whole program? Give me a break.

This message is a reply to:
 Message 293 by Kleinman, posted 09-29-2022 12:57 PM Kleinman has replied

Replies to this message:
 Message 295 by Kleinman, posted 09-29-2022 6:00 PM Taq has replied
 Message 311 by Kleinman, posted 10-02-2022 2:59 PM Taq has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 296 of 2926 (898772)
09-29-2022 7:02 PM
Reply to: Message 295 by Kleinman
09-29-2022 6:00 PM


Re: Keeps going and.going
Kleinman writes:
Once different resistance alleles at different genetic loci have evolved, then you have the possibility of a resistance allele for one selection condition at a particular genetic locus in one parent recombining with a different resistance allele for a different selection condition at a different particular genetic locus from the other parent appearing in the offspring.
Except that we are not talking about antibiotic resistance in humans. We are talking about adapting to an open savanna. There are going to a lot of different pathways that evolution can take. It isn't anything like antibiotic resistance which is very constrained as to where beneficial mutations can occur. The two selection regimes are very, very different.
You are also ignoring diploidy. You don't even need recombination to get two different beneficial alleles. You just need both mutations from separate parents.
Bottom line, the mathematics of the formation of the resistance alleles in asexual replicators is the same for sexually reproducing replicators. Recombination has no significant effect on this process, that's why combination therapy works for the treatment of HIV, combination herbicides, and combination pesticides work despite they are being used on replicators that do recombination.
Multidrug strategies work because there is very strong selection. If you don't have resistance to all drugs at a moments notice then you don't reproduce. That was not the case for human evolution. Our ancestors could survive just fine without the adaptations we have now. The adaptations they did receive allowed them to slowly move out to an open savanna.
This is another feature you are ignoring.
Different adaptive alleles can increase in frequency in a population if each of the alleles give increased reproductive fitness for each of the variants. But that doesn't happen because the selection pressure for the variant that doesn't have the resistance allele for that pressure is inhibiting its reproduction, and visa versa for the other variant with the other resistance allele.
NO, THAT ISN'T WHAT HAPPENS IN EUKARYOTES. You still don't understand how sexual reproduction works. What you are describing is what happens in asexual species, not sexual ones.
In this paper, I modeled the results Weinreich obtained and published in Darwinian Evolution Can Follow Only Very Few Mutational Paths to Fitter Proteins.
Again, you can't use asexual organisms to model sexual organisms. Please learn how sexual selection works. Also, remember that there is more than one gene in a genome.
Replications of variants in subpopulation 1 do not change the probability of an adaptive mutation occurring in subpopulation 2. Each lineage is on its own particular evolutionary trajectory.
Please learn how sexual reproduction works.
What you are doing is conflating the DNA adaptive evolutionary process and recombination. They are two different physical process with two different mathematical behaviors. Can you just for a moment realize that recombination does not create new alleles? Please?
Can you realize for just a moment that beneficial mutations can happen in more than one gene at a time?
I've had years of training and years of experience doing mathematical modeling of physical systems and have been paid a lot of money for doing this.
Where have you ever done a model for two beneficial mutations on separate chromosomes, each of which is moving towards fixation? What would that look like?

This message is a reply to:
 Message 295 by Kleinman, posted 09-29-2022 6:00 PM Kleinman has replied

Replies to this message:
 Message 298 by Kleinman, posted 09-29-2022 8:46 PM Taq has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 297 of 2926 (898775)
09-29-2022 7:40 PM


Multi-Locus Adaptations
A paper modeled multiple genes that were under selective pressure:
quote:
The allele frequencies at the neutral locus remained relatively stable during the simulation, showing small fluctuations due to genetic drift and gene flow between demes (Figure 5a-d, “LocusD”). The allele frequencies at the adaptive loci showed monotonic increasing or decreasing trends depending on the value of the selective environmental variable in the deme (salinity). For example, in deme 1 (high salinity, x = 38.5; Figure 5b), the frequency of the salinity-tolerant alleles increased and reached unity at all three adaptive loci in about 50 years (Figure 6). In deme 69 (low salinity, x = 32.4), the frequency of the salinity-tolerant alleles decreased to about 0.2 in the same time (Figure 6). These dynamics were driven by strong directional selective pressure at the adaptive loci due to extreme salinity values. Different replicates of the simulations produced the same results (not shown).
Just a moment...
As shown in the paper, all beneficial alleles increased in number with each other. One did not outcompete another, nor do they have to. Why? Sexual reproduction.
And this is just for adaptation to one challenge. The same would apply to adaptations that tackle different challenges. For example, lighter skin color allows humans to produce more vitamin D at higher latitudes. Mutations in the promoter region of the lactase gene allows humans to drink cow's milk in adulthood. These are two different adaptations at two different loci. Did one have to displace the other? No! Both beneficial alleles are driven towards fixation together, and they end up in the same genomes.

Replies to this message:
 Message 299 by Kleinman, posted 09-29-2022 9:09 PM Taq has replied

  
Taq
Member
Posts: 9973
Joined: 03-06-2009
Member Rating: 5.7


Message 300 of 2926 (898798)
09-30-2022 10:39 AM
Reply to: Message 299 by Kleinman
09-29-2022 9:09 PM


Re: Multi-Locus Adaptations
Kleinman writes:
Nope, it is due to the fitness values they use in Table 1. You can get whatever change in frequency you want by manipulating fitness values.
When they are all under any kind of positive selection they all increase in number, contrary to your claims. You are claiming that only the most fit allele will increase in number and outcompete all of the others. That's not what happens.

This message is a reply to:
 Message 299 by Kleinman, posted 09-29-2022 9:09 PM Kleinman has replied

Replies to this message:
 Message 302 by Kleinman, posted 09-30-2022 11:42 AM Taq has replied

  
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