This needs to be understood.
Itâs easily understood. No antibody means no functional antibody.
Gilâs hypothesis is about the relative contribution of germline sequences to antibody function.
You appear to be evading answering my question:
Why is the antibody not being built in the first place? You need to show you can set up the experiment as you are claiming would test the hypothesis.
Why couldnât the array be replaced by a preassembled cassette in the germ line?
Describe the method as you would in an abstract and @Art maybe could weigh in here.
Is there some reason you think that this cannot be done?
Regardless, what does Gilâs hypothesis predict if it can be done?
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I guess that the experiments you have in mind regard the quasi monoclonal (QM) mouse, right? (Thanks to @Jordan for letting me know about this work on the QM mouse). If it is the case, I am afraid that these data donât support your case.
Have you read the paper? The criticisms are corrected. No matter how close a sequence is to another sequence that works, if it has no function then it has no FI.
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Itâs not my case, itâs your hypothesis. How do they support your hypothesis, Gil?
And no thanks to Jordan for helping Gil to evade testing the predictions of his hypothesis. After two weeks, Gil persists in deliberately misrepresenting a testable hypothesis as a fact, when the experiment that falsified his hypothesis was published 20 years ago.
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That seems like an evasion to me.
Why, on a matter of the feasibility of a mouse knockin, would you demand detail from the scientist who has done and published them, while asking another scientist who studies plant RNA processing to âweigh inâ?
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The only problem here is that the QM mouse model completely fails to falsify my claim.
Of course you would say that, Gil; itâs your ego talking.
A person who actually believed that would explain why. Also, please note that I didnât simply say that the âQM mouse modelâ falsifies your hypothesis, I said that the experiment that falsified your hypothesis was published 20 years ago. Youâre engaging in the straw man fallacy again.
So, can we go through the predictions of your hypothesis now, after two full weeks of your evasive bobbing and weaving?
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It was a QUESTION for YOU Bill.
Why canât you ever answer a simple question?
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You are not asking a real question. You are asking a leading question to further your own agenda.
The answer I already gave is I donât know. Then I asked you how you would test this hypothesis and you did not answer. It remains an untested hypothesis.
You acknowledge microevolution is real. You say you donât know if microevolution adds information. Macroevolution is merely accumulated microevolution (as the 29+ Evidences you keep running from shows) yet you say you know for a fact macroevolution canât add information.
Congratulations on shooting yourself in the foot yet again Bill. Not that we need any more evidence you have no idea what youâre blithering about.
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This paper does not help you Tim for the reasons I stated. Itâs outdated and it does not contain a mechanistic explanation. It is an excuse for the ID guys along with the neutral theory guys showing Darwins mechanism was not powerful enough to explain the data. Apparently you are not paying attention to the discussion.
The ID guys solved the problems with finding a complex de novo sequences
The neutral theory guys solved the problem of the molecular clock being able to fix the observed mutational differences between species in the population matching the fossil record.
Evidence please.
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Have you read the paper?
In this essay, universal common descent alone is specifically considered and weighed against the scientific evidence. In general, separate âmicroevolutionaryâ theories are left unaddressed. Microevolutionary theories are gradualistic explanatory mechanisms that biologists use to account for the origin and evolution of macroevolutionary adaptations and variation. These
mechanisms include such concepts as natural selection, genetic drift, sexual selection, neutral evolution, and theories of speciation. The fundamentals of genetics, developmental biology, molecular biology, biochemistry, and geology are assumed to be fundamentally correctâespecially those that do not directly purport to explain adaptation. However, whether microevolutionary theories are sufficient to account for macroevolutionary adaptations is a question that is left open.
Cytochrome C is now known to have multiple applications which account for sequence differences among species.
Humans and chimpanzees have the exact same cytochrome c protein sequence. The ânull hypothesisâ given above is false. In the absence of common descent, the chance of this occurrence is conservatively less than 10-93 (1 out of 1093). Thus, the high degree of similarity in these proteins is a spectacular corroboration of the theory of common descent. Furthermore, human and chimpanzee cytochrome c proteins differ by ~10 amino acids from all other mammals. The chance of this occurring in the absence of a hereditary mechanism is less than 10-29. The yeast Candida krusei is one of the most distantly related eukaryotic organisms from humans. Candida has 51 amino acid differences from the human sequence. A conservative estimate of this probability is less than 10-25.
Itâs still not a paper Bill. Itâs collected evidence from several hundred papers. Thanks for showing youâre so afraid you wonât even click on the link. You make willful ignorance into an art form.
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