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

Kleinman:

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How did all these adaptive mutations accumulate in a lineage of humans but didn't occur and accumulate in a lineage of chimps?

AZPaul3:

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Why should a different species with a different genome under different circumstances produce the same genetic anomalies? All those by convergent evolution? That expectation is just stupid.

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If humans and chimps arose from a common ancestor, didn't they start from the same genome? So what adaptive mutations did humans get that chimps didn't that have enabled humans to achieve a population greater than 7 billion yet chimps have a population of only 300,000?

Kleinman:

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If humans and chimps arose from a common ancestor, didn't they start from the same genome?

Taq:

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In the Lenski experiment all of the parallel bacterial populations shared a common ancestor and shared the same genome. However, after growing separately there were different mutations that reached fixation in different cultures. The same for the Kishony experiment.
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You keep talking about these experiments, but you seem to forget about them.

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That's not right, Lenski's bacteria were not all exact clones in his founders' population. For example, his population had drug-resistant variants to a variety of different drugs. His populations were diverse. You seem to forget that every time there is a replication, there is a possibility of a mutation occurring somewhere in the genome. And nowhere in this discussion have I said that there has to be one unique beneficial mutation. If you want to quote me, quote this: Every different beneficial mutation causes that lineage to take a different evolutionary trajectory. What these lineages have in common is that the next adaptive step will take about 1/(mutation rate) replications to have a reasonable probability of the next beneficial mutation occurring. So there is no reason different variants can't take different evolutionary trajectories whether you are talking about the Lenski or the Kishony experiments. The math is the same for all evolutionary trajectories.

Kleinman:

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So what adaptive mutations did humans get that chimps didn't that have enabled humans to achieve a population greater than 7 billion yet chimps have a population of only 300,000?

Taq:

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First off, there are more E. coli in your gut than there have been humans who have ever lived. Are E. coli fitter than humans?

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That is really weird. Are you now claiming that humans and E. Coli share a common ancestor?

Taq:

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Second, humans evolved to live in an open savanna. Chimps did not. It seems rather obvious that different mutations would have been beneficial in each population. Mutations that allowed human ancestors to run on two legs would not have been beneficial to chimps who needed to climb trees. Also, epistasis is a real thing. Different neutral mutations potentiate different beneficial mutations because of the interaction between the two mutations. The random rise and fall of neutral mutations in the genetic background can change the evolutionary trajectory of species after they split off from one another.

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Go for it, explain which mutations allow humans to live in open savanna, desert, arctic,... and chimps don't. If chimps didn't get those mutations, why not?

Kleinman:

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You finally agree that it takes a billion replications for each adaptive mutation in a lineage.

Taq:

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Agreeing to the same mechanisms in no way means I agree that they occur at the same rate. Your dishonesty is noted.

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At what rate does a human lineage accumulate adaptive mutations?

Kleinman:

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So what adaptive mutations did humans get that chimps didn't that have enabled humans to achieve a population greater than 7 billion yet chimps have a population of only 300,000?

AVPaul3:

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Lots and lots of them. All developed after the genomes were separated.

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How many and which mutations gave humans improved reproductive fitness over chimps and why didn't chimps get these mutations?

Kleinman:

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That's not right, Lenski's bacteria were not all exact clones in his founders' population.

Taq:

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From the Lenski paper:

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The long-term evolution experiment, or LTEE, is simple both conceptually and practically. Twelve populations were started the same ancestral strain of Escherichia coli in 1988. The ancestral strain has no plasmids or functional prophages, and E. coli is not naturally transformable, so there is no horizontal gene transfer.
Experimental evolution and the dynamics of adaptation and genome evolution in microbial populations | The ISME Journal

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Do you think that every bacterium in that strain is an exact clone? Do you think they replicate with a zero mutation rate? Every time a replication occurs there is a possibility of a mutation occurring somewhere in the genome. His populations were diverse to start. The starvation selection condition reduced that diversity by natural selection.

Kleinman:

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What these lineages have in common is that the next adaptive step will take about 1/(mutation rate) replications to have a reasonable probability of the next beneficial mutation occurring.

Taq:

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I already disproved this. In the Lederberg paper the rate of adaptive mutations to streptomycin and phage were different by 3 orders of magnitude:

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The culture is fully sensitive to the phage T-1, as well as to streptomycin, and like most E. coli strains gives rise to resistant mutants at rates of approximately 10^-7 and 10^-10 per division, respectively.
REPLICA PLATING AND INDIRECT SELECTION OF BACTERIAL MUTANTS - PMC

Taq:

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Different adaptations are going to occur at different rates. You can't take the rate of one adaptation and apply it universally to all adaptations.

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I don't, the rate of adaptation depends on the mutation rate. It takes about 1/(mutation rate) replications to give a reasonable probability of an adaptive mutation occurring. E. Coli happens to have a mutation rate of about 1e-9 which means it takes about a billion replications of a variant in a lineage to give a reasonable probability of the next adaptive mutation occurring. Now, if you want to claim that humans have a different mutation rate, give us that mutation rate and tell us what the rate of adaptive evolution is for a human lineage.

Kleinman:

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The math is the same for all evolutionary trajectories.

Taq:

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Then why does streptomycin resistance occur 1,000 times slower than phage resistance?

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Are you now going to claim that the improved reproductive fitness of humans over chimpanzees are due to a phage? And where did that resistance allele the phage is laterally transmitting come from?

Kleinman:

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That is really weird. Are you now claiming that humans and E. Coli share a common ancestor?

Taq:

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All life shares a common ancestor. That's what the evidence shows us.

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There are more E. coli in your gut than there ever have been people. Does this mean E. coli are more fit than humans? Yes or no?

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You can't even give a coherent explanation of the Kishony and Lenski experiments. And we're still waiting for you to tell us the rate of human adaptive evolution and which mutations give us a reproductive fitness advantage over chimps.And it appears that humans haven't evolved sufficiently to live in your gut. It appears that humans have gone downhill on the evolutionary fitness landscape since the days we were fecal bacteria. Taq, you have some really bizarre ideas.

Kleinman:

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Go for it, explain which mutations allow humans to live in open savanna, desert, arctic,... and chimps don't.

Taq:

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It's the mutations we have that chimps do not.

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Why don't you say that you don't know?

Kleinman:

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How many and which mutations gave humans improved reproductive fitness over chimps and why didn't chimps get these mutations?

Tanypteryx:

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Why would you expect anyone here to be able to give you that specific list? Are you daft? What proportion of the 7.5 billion people on this planet do you think has access to that list?

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Finally! Someone on this forum admits that they don't know! So, without knowing which mutations are adaptive or not, how many adaptive mutations could accumulate in a billion replications in a human lineage? And we are not interested in Taq's neutral evolution calculation.

Kleinman:

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Do you think that every bacterium in that strain is an exact clone? Do you think they replicate with a zero mutation rate? Every time a replication occurs there is a possibility of a mutation occurring somewhere in the genome. His populations were diverse to start. The starvation selection condition reduced that diversity by natural selection.

Taq:

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That screeching sound you hear is the goal posts you are dragging behind you.
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The strain came from a single colony. That single colony came from a single bacterium. Every bacterium in that experiment descended from the same exact single ancestor.
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You tried to imply that humans and chimps should have the same adaptations because we started from the same common ancestor. So why don't we see that in the Lenski experiment?

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You really need to get a new playbook. Even when you start with a single bacterium, when the colony size reaches a billion and the mutation rate is 1e-9, you will have on average, a member in that colony with a mutation at every site in the genome. The Markov Process random walk is happening at every site in the genome. What is happening, as the colony size grows, the population is doing an exhaustive search for every possible mutation. When the population has done 1/(mutation rate) replications, the entire sample space will have been sampled and a mutation will have occurred at every site in the genome. When the number of replications reaches about 4/(mutation rate), every base substitution will have been sampled. And don't try to argue that bacteria don't do searches. This is a random process and each replication is a potential search of the sample space, and when the bacteria do enough replications they will have a high probability of sampling an adaptive mutation. At the same time, other members of the population will have sampled all the other possible mutations.And don't be silly, I'm not implying that humans and chimps should have the adaptational mutations. You are assuming that it only takes a small number of replications and beneficial mutations have a high probability of occurring. You don't understand the mathematical process that is going on in the Kishony and Lenski experiments. The reason why each adaptive step takes a billion replications is that the variant is sampling every possible mutation, beneficial, neutral, and detrimental. The environmental selection conditions determine which category the particular mutation falls into. Try doing the math yourself.

Kleinman:

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And we are not interested in Taq's neutral evolution calculation.

Tanypteryx:

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Oh, I'm interested in Taq's calculations, not your mischaracterization of them. Your math is as flawed as your understanding of biological evolution.

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Neither you nor Taq can correctly do the calculations for the Kishony or Lenski experiments. He'll do no better on the mathematics of human DNA evolution.

Tanypteryx:

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Why would you expect anyone here to be able to give you that specific list? Are you daft? What proportion of the 7.5 billion people on this planet do you think has access to that list?

Kleinman:

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Finally! Someone on this forum admits that they don't know!

Tanypteryx:

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So that's an affirmative that you are daft and your reading comprehension sucks too!

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Pardon my error in reading comprehension. And Oh boy! Tanypteryx knows and can list the beneficial mutations that give the reproductive fitness advantage of humans over chimps. List away, it will be a great help to Taq. Of course, if you are in that proportion of the 7.5 billion people on this planet that don't have access to that list, that would mean that you don't know.BTW, you include the quote from Taq in your posts:

Taq:

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

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Does Taq include experimentation in his scientific method and if so, why does it take a billion replications for each adaptive mutation in the Kishony and Lenski experiments? If you duck this question, we will really know who is daffy.

Taq:

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Let's do the math.
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Each human is born with about 50 mutations.

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Mutations generate sequence diversity and provide a substrate for selection. The rate of de novo mutations is therefore of major importance to evolution. Here we conduct a study of genome-wide mutation rates by sequencing the entire genomes of 78 Icelandic parent-offspring trios at high coverage. We show that in our samples, with an average father's age of 29.7, the average de novo mutation rate is 1.20 × 10(-8) per nucleotide per generation.
Rate of de novo mutations and the importance of father's age to disease risk - PubMed

Taq:

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If each base in the human genome has a 1 in 120 million chance of mutation then we would get about 50 mutations in a 6 billion base diploid genome. Agreed?
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With that mutation rate, in population with a steady 100,000 individuals we would see 5 million new mutations in each generation. Agreed?

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The mistake you are making in your analysis Taq is that adaptive evolution occurs along lineages. You are lumping all the mutations that are occurring anywhere in the population. You must get all these beneficial mutations into a single lineage. If you want to claim that this occurs by recombination, you need to present your mathematical and empirical evidence of how this can occur. If you think your analysis is correct, apply it to the Kishony and Lenski experiments and show what your math predicts in these experimental cases.

Kleinman:

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Pardon my error in reading comprehension. And Oh boy! Tanypteryx knows and can list the beneficial mutations that give the reproductive fitness advantage of humans over chimps.

Taq:

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Are the physical differences between chimps and humans due to the sequence differences between their genomes? Yes or no?

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You need to answer this question for yourself.

Tanypteryx:

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And we're still waiting for you giving any reason why microevolutionary events can’t add up to macroevolution.

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Mathematically, microevolutionary events don't add up. They are random events so the joint probability of microevolutionary events occurring is computed using the multiplication rule. That's why each microevolutionary event in the Kishony and Lenski experiments require a billion replication for each adaptive mutation. Each additional selection pressure adds another instance of the multiplication rule for each adaptive step on their particular evolutionary trajectory. That's why combination therapy works for the treatment of HIV despite the fact that the virus can vary rapidly evolve to single drug therapy.

Kleinman:

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If Taq is a scientist then I assume he knows how to use the scientific method.

Taq:

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He is and he does. He is even a microbiologist, and a molecular biologist (hence the username).

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Good! That should help you to understand how to do your mathematical modeling. So far, you are not modeling reality correctly.

Kleinman:

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The mistake you are making in your analysis Taq is that adaptive evolution occurs along lineages.

Taq:

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I'm doing the math, as you requested.
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If each base in the human genome has a 1 in 120 million chance of mutation then we would get about 50 mutations in a 6 billion base diploid genome. Agreed?
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With that mutation rate, in a population with a steady 100,000 individuals we would see 5 million new mutations in each generation. Agreed?

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Your model is crude and inaccurate. Try and think about what actually happens physically. Start with the founders of your new lineage. A population size of two is appropriate. Then you must assume something about the fecundity. You might start with an estimate that the population size doubles every generation but that would be a gross overestimate because, in 30 generations, you would already have a population size of a billion. But for sake of discussion, use a value like that. As the population expands, the number of lineages increases. Then use your 50 mutations per genome/generation and try to estimate the number of different lineages on different evolutionary trajectories. BTW, I can think of many mutations that have been identified in humans because they all cause disease. I don't know of any mutations that have been identified as beneficial. Perhaps genetic studies of large families may identify some unique mutations.Then you have to consider how any one of these lineages can accumulate a set of adaptive mutations. Don't factor in recombination yet until you understand this simpler case. The reason my models accurately simulate the Kishony and Lenski experiments is that they correlate with what is happening physically.

Kleinman:

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You are lumping all the mutations that are occurring anywhere in the population. You must get all these beneficial mutations into a single lineage.

Taq:

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Please learn how sexual reproduction works.

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I know how sexual reproduction works and that is not what you are mathematically modeling.

AZPaul3:

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We have shown you don't comprehend the subject or the math that you are so enamoured with.

Taq:

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People who comprehend the subject would be able to parse this statement from the Lenski paper Kleinman so often cites:
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"When large asexual populations adapt, competition between simultaneously segregating mutations slows the rate of adaptation and restricts the set of mutations that eventually fix."
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Not only did I understand Lenski's statement, but I have also given you the correct physical and mathematical explanation of why this happens. And if you think that sexually reproducing organisms don't require energy to replicate, somebody in your survey of physics course you took to get your degree in microbiology failed in their job in teaching you the laws of thermodynamics.

Kleinman:

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Your model is crude and inaccurate. Try and think about what actually happens physically. Start with the founders of your new lineage. A population size of two is appropriate.

Taq:

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That doesn't happen in nature. Speciation events involve populations, not 2 individuals.

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Populations are made up of individuals. You can't average over populations to determine what is happening with each individual. That's like trying to describe quantum physics with classical physics. Your model is crude and inaccurate. If you think your model is correct, use it to describe what is happening in the Kishony and Lenski experiments. Explain why it takes a billion replications for each adaptive mutational step in these experiments.

Kleinman:

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Populations are made up of individuals. You can't average over populations to determine what is happening with each individual.

Taq:

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I'm not averaging. I'm summing. Do you know the difference?

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Summing what? You start with the assumption that you have a population of 100,000. Is it 100,000 humans, 100,000 chimpanzees, 100,000 common ancestors, or some combination of all 3? If you don't consider each individual and what happens with each replication, you have mush.

Kleinman:

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If you think your model is correct, use it to describe what is happening in the Kishony and Lenski experiments.

Taq:

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You can't use a sexually reproducing population to model an asexually reproducing population. Do you know why?

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So you think that adaptive alleles are formed differently for asexual reproducers and sexual reproducers? Aren't these alleles both formed from DNA (sometimes RNA)? Don't the genetic sequences in asexual reproducers and sexual reproducers both have mutation rates associated? For someone trained in microbiology, you have very little understanding how drug resistance evolves.

Kleinman:

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Explain why it takes a billion replications for each adaptive mutational step in these experiments.

Taq:

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The mutation rate in E. coli is about one mutation per 1,000 replications.

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That would be 5 million bases replicated 1000 times or 1 in 5 billion base replications. I use a mutation rate value of 1e-9 or approximately 1 mutation for every billion replication, a slightly higher mutation rate.Now, think about this in terms of the Kishony experiment. He starts his experiment with a drug-sensitive founder. In the first generation the population doubles to 2, next generation 4, next generation 8,... after 30 generations (doublings), the population size will be over one billion. In other words, every site in the genome will have been replicated a billion times and in those billion replications, some member of the population will have a mutation at some given site. Since there are multiple possible base substitutions, it will actually take 3-4 billion replications or about 32 doublings to get some member of the population with every possible base substitution. It is that lucky member with the base substitution at the particular site that gives some resistance to the drug being used but there is only one member at this time with that first adaptive mutation. This member with the adaptive mutation forms a new colony that again has to do a billion replications so that at least one of its members will get the next adaptive mutation. This process works the same way for asexual or clonal replicators as well as sexual replicators. The 1/(mutation rate) replications are occurring at every site in the genome, the population is doing an exhaustive search of the entire sample space, and all mutations are being sampled, beneficial, neutral, and detrimental. The probability of beneficial mutation B occurring on some member with beneficial mutation A depends on the number of replications the A variant can do. This is how adaptive alleles are formed no matter whether the replicator is asexual or sexual. Replication of a site in a genome is the random trial and the possible outcomes at that site are a mutation occurs or a mutation does not occur.

Kleinman:

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Summing what? You start with the assumption that you have a population of 100,000. Is it 100,000 humans, 100,000 chimpanzees, 100,000 common ancestors, or some combination of all 3? If you don't consider each individual and what happens with each replication, you have mush.

Taq:

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I'm summing the number of mutations that happen in the population in that generation. We can also sum the mutations that happen over generations. I don't understand why this is so hard to understand.

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Is the population of 100,000 exact clones of each other or are there different variants in the population with different sets of mutations?

Taq:

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They would be 100,000 individuals. In the last ~1.5 million years they would be humans. In the last 200,000 years they would be anatomically modern humans, i.e. H. sapiens. Prior to ~1.5 million years they would be human ancestors. They would never be chimps.

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Are all 100,000 individuals on the exact same evolutionary trajectory and do all their descendants over generations remain on that same evolutionary trajectory where each individual gets the same set of mutations as every other individual or do the different individuals get different sets of mutations and the population is genetically diverging?

Kleinman:

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So you think that adaptive alleles are formed differently for asexual reproducers and sexual reproducers?

Taq:

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No, I don't. The difference is how the mutations are passed on to offspring. Do you understand the difference between diploid and haploid genomes? Do you understand how you got half of your genome from your father and half from your mother? Do you understand how this is different from bacteria who only have one parent that they are a clone of?

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Here is one place where you get confused about this mathematical process. Ploidy of the cell only increases the number of replications of the chromosomes. So diploid cells would get two chromosome set replications for each individual replication. If we consider cell lines that replicate by mitosis such as cancers, that would increase the diversification rate because each of the chromosomes will get different sets of mutations with each replication. This is the reason why single drug targeted cancer therapy does not work when the cell population reaches about 1/(mutation rate) replications. There will already be mutant variants at the target site. On the other hand, with meiosis, you have parents each passing half the genome. If I understand your argument correctly, you are claiming that one parent passes beneficial alleles from their set of chromosomes and the other parent passes their beneficial alleles from their set of chromosomes. If I understand your argument correctly, then your population must be diverse and not clones. I have some questions for you about your population. How many beneficial alleles are in your population? What is the frequency of the different beneficial alleles in your population? Which members have the beneficial alleles? Are these beneficial alleles homozygous or heterozygous in each of the members? And how do you compute the probability that a descendant will get these beneficial alleles from any two parents in your population of 100,000?

Kleinman:

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I use a mutation rate value of 1e-9 or approximately 1 mutation for every billion replication, a slightly higher mutation rate.

Taq:

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If you use that number for the human mutation rate then you are way off.

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That's OK, we can use whatever mutation rate you want to use.

Kleinman:

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It is that lucky member with the base substitution at the particular site that gives some resistance to the drug being used but there is only one member at this time with that first adaptive mutation.

Taq:

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How many possible mutations result in antibiotic resistance? That's the first question you need to answer.

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I've already done the math. If you want to try to do it yourself, the way you do it is by doing an "at least one" probability calculation. Let's say you have "m" possible beneficial mutations. What is the probability of at least one of those "m" possible beneficial mutations occurring in "n" replications? It doesn't change the number of replications much from only a single beneficial mutation. You can observe that empirically in the Kishony and Lenski experiments where it still takes about a billion replications for each adaptive step despite the fact there is more than one possible adaptive evolutionary trajectory to the environmental selection condition.

Kleinman:

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This process works the same way for asexual or clonal replicators as well as sexual replicators. The 1/(mutation rate) replications are occurring at every site in the genome, the population is doing an exhaustive search of the entire sample space, and all mutations are being sampled, beneficial, neutral, and detrimental. The probability of beneficial mutation B occurring on some member with beneficial mutation A depends on the number of replications the A variant can do. This is how adaptive alleles are formed no matter whether the replicator is asexual or sexual. Replication of a site in a genome is the random trial and the possible outcomes at that site are a mutation occurs or a mutation does not occur.

Taq:

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The difference is the mutation segregation seen in the Kishony and Lenski experiments. That doesn't happen in sexually reproducing populations except in cases where the mutations are close to one another on the same chromosome.

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What????

Let's get back to Percy's Message 175

Kleinman:

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Note that Haldane's model has been proven to be a conservation of energy process.

Percy:

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I see no such proof in your message.

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I already pointed out previously that Haldane's frequency equation was a conservation of energy process based on the principle that it takes energy to replicate. However, Flake and Grant demonstrate this mathematically in the following paper:
An Analysis of the Cost-of-Selection Concept
Here are two quotes from the paper, the first from the abstract:

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The robust nature of the cost-of-selection concept is examined in the light of a conservation principle.
  —Flake and Grant

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and the second from the paragraph titled "A CONSERVATION PRINCIPLE"

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A quantity that is dependent only on the initial and final state of a system and is invariant to variation in the detailed motion between states is often associated in the physical sciences with a potential energy function. A fixed reference state is normally specified for such a function, and in this case the natural choice for a reference state is the final stage of complete substitution. In this context then, the potential (cost) function evaluated at the initial state (frequency) corresponds to the potential energy associated with the substitution.
  —Flake and Grant

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Kleinman:

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You have to modify his model for the particular case.

Percy:

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If you believe Haldane's model should be modified for each particular case then please describe the various processes of modification and how one selects which to use according to case.

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I could have worded this a bit better. The frequency equation pnA + qna = 1 isn't modified, we use the equation to compute the number of replications of the more fit variant to fixation. In the process of doing this calculation, one also obtains the number of deaths of the less fit variants. This is done because it is the number of replications of the more fit variant that determines the probability of the next adaptive mutation occurring in this subset of the population.

Kleinman:

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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

Percy:

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Please describe how Haldane's model should be modified for the Lenski case.

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There are two issues you have to take into account when evaluating the frequency/fixation equation for the Lenski experiment. One is that you have a varying population starting at 5 million at the beginning of the day and growing to 500 million at the end of the day which is then bottlenecked back down to 5 million, the nutrients are replenished and another day's growth is started. For the initial state of a fixation/adaptation cycle, I assume the number of more fit variants is 1 and the number of less fit variants is 4,999,999. The frequency equation for that state is (1/5,000,000) + (4,999,999/5,000,000) = 1I defined a fitness parameter for the more fit variant and then solved the equation numerically. Allow the population to do 6 generations of doubling and a 7th partial generation to reach a population of 500 million. Each generation the more fit variant increases in number and frequency and the less fit variants decrease in number and frequency. I didn't try to formulate an algebraic solution because of the bottlenecking at the end of a day's growth. That discontinuity introduces a nonlinearity into the math. Interestingly, Haldane's estimate of 300 generations/fixation is the same order of magnitude that my calculation shows and is similar to what Lenski's experiment generated.If this all makes sense to you and you don't have any questions, I'll go on next to show you how to do the adaptation portion of the calculation.