Did you forget already?
Catalytic antibodies demonstrates this false. You repeat this claim over and over, and it is demonstrably false. Your response was to move the goal posts. That is not a valid response. Start by fixing your statement and your understanding. Then move on to the next question.
We did not see it in the Lenski experiment from reproduction. This is the above claim.
The catalytic antibody mechanism is a mechanism that exists in multicellular animals. It is not generated from reproduction as far as I know.
Wow, Bill. Even by your standards, this is a shameful display.
What is what the design guys are arguing against?
Random gene deletion would not consistently work and not kill the animal. There is not model for things that donât happen. Gene deletion is a rare event. If the gene is essential to the organism, deletion kills it, possibly at the gamete stage. If itâs not essential but useful, organisms with the deletion will be selected against and the deletion will not spread. If the gene is useless, organisms with the gene will be as good as those without it, and every so often, the deletion will spread through the population. If the gene is actively delterious, the deletion will spread most of the time. See how that works?
That was not your claim above:
Did you forget what you had claimed?
No, it isnât. Itâs a technological exploitation of a natural mechanism that also disproves your claim. Catalytic antibodies just disprove your claim more cleanly. 
I find it hard to believe that you do not know that the immune response involves cell division. Besides, if you donât really know, why not find out before posturing?
Anyone notice that Bill moved the goalpost from âcell divisionâ to âreproductionâ when he realized that catalytic antibodies disprove his very specific claim? Silly, since cell division is a form of reproduction.
Hereâs your claim:
Was your clumsy switch from âcell divisionâ to âreproductionâ an honest mistake on your part, Bill?
No, you did not read for comprehension or you decided to quote mine. Dr Swamidass was smart enough not to double down here. Showing a single protein family that might be able to work within current evolution resources is not a model for evolution.
My quote referenced Rumâs discussion of the LTEE and when I was agreeing on gene duplication that was also observed in the LTEE. What was not observed was the formation of a novel enzyme.
Your claim was generalizing the LTEE to all of sequence space. You canât honestly claim that it was limited to bacteria, because YOU invoked humans:
So, no, you canât pretend that your claim was limited to a single bacterial experiment. You were making a general claim, and catalytic antibodies show it to be false.
Itâs not âshowing a single protein family that might be able to work within current evolution resources,â itâs about how common specific enzymatic activities are in random sequence space (V regions of antibodies), something you rant about routinely without looking at the facts.
Which we observe routinely with catalytic antibodies. Therefore your claim about sequence space is objectively false.
But keep diggingâŚ
The Lenski study is not the only research ever done in evolutionary biology, it might surprise you to know.
Gene duplications are believed to facilitate evolutionary innovation. However, the mechanisms shaping the fate of duplicated genes remain heavily debated because the molecular processes and evolutionary forces involved are difficult to reconstruct. Here, we study a large family of fungal glucosidase genes that underwent several duplication events. We reconstruct all key ancestral enzymes and show that the very first preduplication enzyme was primarily active on maltose-like substrates, with trace activity for isomaltose-like sugars. Structural analysis and activity measurements on resurrected and present-day enzymes suggest that both activities cannot be fully optimized in a single enzyme. However, gene duplications repeatedly spawned daughter genes in which mutations optimized either isomaltase or maltase activity. Interestingly, similar shifts in enzyme activity were reached multiple times via different evolutionary routes. Together, our results provide a detailed picture of the molecular mechanisms that drove divergence of these duplicated enzymes and show that whereas the classic models of dosage, sub-, and neofunctionalization are helpful to conceptualize the implications of gene duplication, the three mechanisms co-occur and intertwine.
Watch @colewd now shift the goal posts and redefine what he means by a ânovel enzyme.â
The work done by Barry Hall on the EBG system in bacteria is another great example of novel enzymes evolving.
Not only did the bacteria evolve a new enzyme, there were also mutations that allowed for changes in gene regulation similar to those seen in the classic lac operon.
I got it John. I knew this already. This is your evidence you have been posting here many times. It is a limited claim not a model.
How is it limited? VDJ recombination produces a library of billions of random sequences, and we can find functions throughout that sequence space. It is a model that is easily generalized.
Then why do you keep making the same claim about sequence space?
No, itâs not my evidence, it comes from dozens or hundreds of labs.
It is an observation that is generalizable. It completely falsifies your general claim about sequence space.
Because you are relying on applications that work because of lots of function in sequence space. This is not true across the board. A model needs to cover evolution and major transitions not simple adaptions.
Because if you open your eyes you will see cases where it is very rare and falsifies the random accident hypothesis.
That is an empty assertion contradicted by evidence. The number of functions found in random sequence in antibody libraries demonstrates this fact.
Do you really consider this to be a scientific claim?
All of the cases I have seen involve the Sharpshooter fallacy. Time and again, you pretend as if what evolved is the only thing that could evolve. That is where you keep getting tripped up.
Yes. Are you going to continue to avoid it?
Then use the evidence and create a model to show the mechanism can do what you claim it can do.
That model is catalytic antibodies.