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

Kleinman:

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See Taq, even nwr, the mathematician that doesn't do the mathematics of biological evolution understands that multiple adaptive alleles don't go to fixation simultaneously.

nwr:

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You jumped to a wrong conclusion. This further illustrates your failed understanding of evolution.

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So nwr does believe Taq's claim that multiple adaptive alleles fix simultaneously. Why doesn't that occur in either the Lenski or Desai biological evolutionary experiments?

The Lenski experiments were not aimed at testing that. I have not studied the Desai experiments.

nwr:

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The Lenski experiments were not aimed at testing that. I have not studied the Desai experiments.

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You must be kidding. The Lenski team specifically measured the number of fixations for their experiment. And it is so typical of the posters on this forum to chime in without doing their homework.

You demonstrate confirmation bias. You see what you want to see.The Lenski experiment was designed to follow populations that were kept in relatively constant conditions. If it had been intended to study fixation, the experimental design would have been different.

nwr:

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You demonstrate confirmation bias. You see what you want to see.
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The Lenski experiment was designed to follow populations that were kept in relatively constant conditions. If it had been intended to study fixation, the experimental design would have been different.

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Introduction to the Long-Term Evolution Experiment (LTEE)

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The Goals of the LTEE
The LTEE was designed to explore three sets of broad, conceptual questions. These questions have long interested many scientists, and a lot has been learned from other studies in nature and in the lab. However, the LTEE enables scientists to quantify changes and connect various phenomena with unusual precision.

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The first set of questions concerns the dynamics of evolution.
Is evolution invariably slow and gradual?
Or are there periods of rapid change and stasis, even in a constant environment?
How long can fitness continue to improve, and by how much, before some limit is reached?

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The second set concerns the repeatability of evolution, especially those changes that are adaptive.
How repeatable is evolution?
Will the 12 populations evolve along similar paths?
Or will they find different phenotypic solutions to their identical environments?
How does their similarity or divergence depend on which traits are measured?

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The third set of questions concerns the coupling of phenotypic and genetic changes.
Are the rates of phenotypic and genetic evolution tightly coupled over time?
Or does genetic change continue apace, even after adaptation has slowed or stopped?
What specific mutations are responsible for the bacteria’s adaptation?
What are the molecular and physiological changes that make the later generations better adapted to the LTEE environment?
If and when phenotypes evolve similarly in the replicate populations, does that imply parallel changes at the level of nucleotides, genes, or pathways?

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Fixation (population genetics)

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In population genetics, fixation is the change in a gene pool from a situation where there exists at least two variants of a particular gene (allele) in a given population to a situation where only one of the alleles remains.[1] In the absence of mutation or heterozygote advantage, any allele must eventually be lost completely from the population or fixed (permanently established at 100% frequency in the population).[2] Whether a gene will ultimately be lost or fixed is dependent on selection coefficients and chance fluctuations in allelic proportions.[3] Fixation can refer to a gene in general or particular nucleotide position in the DNA chain (locus).

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In the process of substitution, a previously non-existent allele arises by mutation and undergoes fixation by spreading through the population by random genetic drift or positive selection. Once the frequency of the allele is at 100%, i.e. being the only gene variant present in any member, it is said to be "fixed" in the population.[1]

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nwr, fixation is part of the dynamics of Darwinian evolution. Starvation is the selection condition where Lenski's bacteria must compete for a limited amount of glucose. The most fit variant from this population in this biological competition ultimately takes over the population (fixes) until by the process of descent by modification (mutation and selection), a new more fit variant occurs, and a new competition start for the next cycle in the experiment. Please try and do your homework before you chime in.

Right. Which is why Lenski was measuring it. But this was not the point of his study, as your other quote shows. If his goal had been studying fixation, I would have expected him to introduce genetic changes and then observe fixation of those changes.

Kleinman:

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nwr, fixation is part of the dynamics of Darwinian evolution.

nwr:

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Right. Which is why Lenski was measuring it. But this was not the point of his study, as your other quote shows. If his goal had been studying fixation, I would have expected him to introduce genetic changes and then observe fixation of those changes.

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Lenski would "introduce genetic changes"? It appears you don't understand that mutations occur in the process of DNA replication. DNA replication is an error-prone process. And if you would do your homework, you might have encountered this paper edited by Lenski:
Distribution of fixed beneficial mutations and the rate of adaptation in asexual populations

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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. This phenomenon of interference arises from competition between mutations of different strengths as well as competition between mutations that arise on different fitness backgrounds.

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I don't mind going down this line of discussion. I doubt you will learn anything from it but other readers might. We might as well do this while we wait for Taq to try and figure out why the Desai experiment doesn't demonstrate Taq's physically and mathematically irrational claim that multiple adaptive alleles fix simultaneously in a sexually replicating population.

I'll admit to a mistake. My mistake was to ignore the fact that you are a clueless creationist.A researcher could introduce genetic changes by introducing some bacteria which are genetically different. It does not require directly manipulating the DNA.

Kleinman:

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Lenski would "introduce genetic changes"? It appears you don't understand that mutations occur in the process of DNA replication.

nwr:

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I'll admit to a mistake. My mistake was to ignore the fact that you are a clueless creationist.
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A researcher could introduce genetic changes by introducing some bacteria which are genetically different. It does not require directly manipulating the DNA.

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Once again nwr, you demonstrate that you don't do your homework. Lenski tested this and it doesn't make any difference in his experiment.
Experimental Test of the Contributions of Initial Variation and New Mutations to Adaptive Evolution in a Novel Environment

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The primary source of genetic variation has historically depended largely on the study organisms. In the long-term evolution experiment (LTEE) using Escherichia coli, for example, each population started from a single haploid cell, and therefore adaptation depended entirely on new mutations. Most other microbial evolution experiments have followed the same strategy. By contrast, evolution experiments using multicellular, sexually-reproducing organisms typically start with pre-existing variation that fuels the response to selection. New mutations may also come into play in later generations of these experiments, but it is generally difficult to quantify their contribution in these studies. Here, we performed an experiment using E. coli to compare the contributions of initial genetic variation and new mutations to adaptation in a new environment. Our experiment had four treatments that varied in their starting diversity, with 18 populations in each treatment. One treatment depended entirely on new mutations, while the other three began with mixtures of clones, whole-population samples, or mixtures of whole-population samples from the LTEE. By tracking genetic markers associated with particular founders in two of our treatments, we could document the impact of the initial variation during the early generations of our experiment. However, there were no differences in fitness among the treatments after 500 or 2000 generations in the new environment, despite the variation in fitness among the founders.

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I don't mind doing your homework nwr, somebody has to do it. And did you know that drug-resistant variants appeared initially in the LTEE without them ever being exposed to antibiotics? If you understood the mathematics of descent with modification, you would understand why this happened. But you don't.

What relevance does that have with the topic at hand? Look at the graph. Those dark lines are synonymous mutations and they are increasing together. I've already shown that you are wrong. Remember this?It's a lot simpler than that. There are three possible mate pairs:
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aaBB : aaBB
AAbb : AAbb
AAbb : aaBB
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Without even doing the math, we can see that a lot of mate pairings will be between AAbb and aaBB. All of their offspring will have both the A and B mutations. There are going to be hundreds of thousands of recombination events (as you describe it) between the A and B mutations.
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So you have about 1 in the bacterial populations and hundreds of thousands in the human population. That seems like a big difference, doesn't it?

That's strange since you have already stated that multiple adaptive alleles do go towards fixation simultaneously."After an AB recombination event occurs, there will be an intersection of the A and B subsets. But then the AB variant will be the most fit variant and in the biological competition, will drive all the A only and B only variants to extinction leaving only AB variants."--Kleinman

Lenski et al. did introduce genetic changes to test the fitness of different mutations:

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To see how genetic context affected citrate metabolism, the relevant module—the citT gene and its newly captured regulatory region—were moved onto a high-copy plasmid, which was then transformed into four clonal backgrounds (Blount et al., 2012). Three of the transformed clones, including the ancestral strain, could grow on citrate in the presence of oxygen, albeit with long delays between the depletion of glucose and the start of growth on citrate and other difficulties (Figure 4a).
Experimental evolution and the dynamics of adaptation and genome evolution in microbial populations | The ISME Journal

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Kleinman:

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Read the quote: "the dynamics of fitness increase are largely repeatable between replicate lines and show a pattern of declining adaptability over time even while the rate of molecular evolution remains relatively constant"

Taq:

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What relevance does that have with the topic at hand?

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I take that line to mean that their experiment largely repeats what Lenski's experiment demonstrates, that of improved fitness over time but each step in improvement becomes smaller as the experiment proceeds. And as you are aware by now from our previous discussions about the Lenski experiment, those improvement in fitness occur one fixation and one mutation at a time.

Kleinman:

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And read the entire paper and see if they found that multiple adaptive alleles fix simultaneously in any of their replicate lines.

Taq:

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Look at the graph. Those dark lines are synonymous mutations and they are increasing together.

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Do you think those lines are showing multiple fixations occurring simultaneously? Did you read how the Desai team defines fixation in order to generate those curves?

Kleinman:

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Descent with modification and adaptation, DNA evolution, works essentially the same for asexual replicators and sexual replicators.

Taq:

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I've already shown that you are wrong. Remember this?
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It's a lot simpler than that. There are three possible mate pairs:
​
aaBB : aaBB
AAbb : AAbb
AAbb : aaBB
​
Without even doing the math, we can see that a lot of mate pairings will be between AAbb and aaBB. All of their offspring will have both the A and B mutations. There are going to be hundreds of thousands of recombination events (as you describe it) between the A and B mutations.
​
So you have about 1 in the bacterial populations and hundreds of thousands in the human population. That seems like a big difference, doesn't it?

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How long will it take for you to understand that descent with modification (DNA evolution) is not recombination? They are different physical, genetic, and mathematical processes. Recombination does not change the mathematics or genetics of descent with modification. You can superimpose recombination on the descent with modification process but you don't understand how to do this mathematics. Biologists aren't well enough trained in mathematics and physics to understand the principle of superposition (actually, for nonlinear systems, the process is called "additive state decomposition"). That's what is required to do the mathematics of the Lenski experiment which has both biological competition and descent with modification acting simultaneously in his populations. You have to do the mathematics of both these processes simultaneously to correctly explain the Lenski experiment. The Desai experiment will require doing the mathematics of biological competition, descent with modification, and recombination to correctly explain its behavior. That's why biologists have been so slow to correctly explain the physics and mathematics of biological evolution. You aren't trained to do this science with your survey of physics and survey of math courses. And you are very slow and resistant at learning how to do this kind of scientific analysis.

Observing what happened in his experiment is not the same as specifically testing. I would expect that. Why do you find it surprising enough to mention?

Kleinman:

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See Taq, even nwr, the mathematician that doesn't do the mathematics of biological evolution understands that multiple adaptive alleles don't go to fixation simultaneously.

Taq:

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"After an AB recombination event occurs, there will be an intersection of the A and B subsets. But then the AB variant will be the most fit variant and in the biological competition, will drive all the A only and B only variants to extinction leaving only AB variants."--Kleinman

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You don't need fixation for a more fit variant to appear. The Kishony experiment demonstrates this quite nicely. Once again Taq, you confuse biological competition, descent with modification (DNA evolution), and recombination. They are each distinct physical processes with different mathematical behaviors. And when you finally learn how to do the mathematics for each of these processes, you will understand why universal common descent is physically and mathematically impossible.