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

Lots and lots of them. All developed after the genomes were separated.Can you really not comprehend that different organisms have different genomes? Different genomes convey different phenotypes with different abilities. Why do you insist that each species follow the same convergent paths?Do you know why birds can fly and we can't? According to your logic there has been plenty for opportunity for each species to co-develop flight since those genomes split from each other. Why don't you have wings?You really do not understand evolution.

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?

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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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

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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. Then why does streptomycin resistance occur 1,000 times slower than phage resistance? All life shares a common ancestor. That's what the evidence shows us.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? It's the mutations we have that chimps do not. They probably did get those mutations, but they were either not selected for because chimps were not in the same environment as humans or those same mutations were not beneficial because of epistatic effects. I have explained this multiple times now. There is no such rate because each beneficial mutation is going to have different levels of fitness increase, and the benefice of a mutation is going to depend on what environment humans are in. The fact you think there should be a set rate means you don't understand how evolution works.

I don't know how many mutations it takes to change a light bulb. That information no one has. It has been lost to history. You know that. This is just a stupidity.The reason chimps didn't get the new and improved human genome capabilities is because that are not human. You dispute this?Again, different species with different genomes. Why do you insist they follow the same evolutionary path?

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?

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?Chimps were busy getting their own set of mutations. Why didn't humans get those? You have no way of knowing if either diverging population got some of the same mutations, if they were selected against by the two different environments.Your method of comparing these two modern species as one "over" the other one is flawed.There have been multiple intermediate species in both lineages since their common ancestor and on the human side there has only been on twig that escaped extinction. And there is no way to tell how many or which mutations helped us or hindered the extinct ones.Your problem is that you don't have a clue about how the evolution of complex multicellular organisms happens or how to describe the selective topography of multiple competing species utilizing the same environment. If you are going to refute evolutionary biology as it stands in 2022, you're going to have to up your game significantly more than miscalculating, misrepresenting and misapplying probabilities that you've shown us so far.

That screeching sound you hear is the goal posts you are dragging behind you.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.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? The E. coli in the Lederberg experiment all have the same mutation rate. How do you explain the fact that adaptation to streptomycin occurs 1,000 times slower than phage resistance? So says the person who claims that the Lenski experiment did not start with a single ancestor. I do know. It is the mutations humans have that chimps do not.

He seems to think humanity is the pinnacle of evolution.

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.

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

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.

Yeah, I don't need to, since I'm not a microbiologist. I know he will do better than you.

Are you going to answer my questions in Message 196?

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Can you really not comprehend that different organisms have different genomes?

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Why do you insist that each species follow the same convergent paths?
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Do you know why birds can fly and we can't? According to your logic there has been plenty for opportunity for each species to co-develop flight since those genomes split from each other. Why don't you have wings?

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