You are nit picking. You are technically right they don’t have function until the recombination but the recombination would be inert without the pre existence of the sequence. They are information rich components of the B cell. If they pre exist in stem cells that is very interesting.
The experiment to which I keep alluding is a direct test of your hypothesis, which, as is your habit, have misrepresented as a fact.
What are you and Gil afraid of, Bill?
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So why are you and Gil so obviously afraid of empirically testing the hypothesis that most of the functional information (defined functionally, not by proxy) is present in the stem cell?
Why do both of you falsely present testable hypotheses as known facts?
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This is hilarious, Bill. Keep it up What a great ambassador you are for ID creationism.
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You are avoiding the obvious. The question you are afraid to examine is, “Is the V fragment (not an exon) mission critical?”
We can test this empirically. You and Gil are not demonstrating any interest in testing any hypothesis, only in making assertions, most of them empirically false.
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Yes, a system without function do not have FI. But it may have most of the information necessary for performing the function. In that case, the transition from the system without FI to the system with FI would not at all require the infusion of an amount of information equal to the FI of the working system but only the infusion of the low amount of information that is still missing for performing the function.
To illustrate this point, let’s take the example of cystic fibrosis. Cystic fibrosis is caused by mutations in both copies of the CFTR gene. Imagine that one of the copie of the CFTR gene of a given patient is characterized by a single mutation resulting in say a Phe to Pro transition at position 508 of the protein and that this change in the protein completely abolishes it’s function.
Imagine now that to cure this patient, the physicians decide to correct the mutation, reversing the Pro into a Phe at position 508. Thanks to gene editing technologies, such a thing may not be science fiction anymore.
In the above situation, the FI of the defective protein would be zero, for the protein doesn’t perform its function. But I hope it is clear for everyone here that the defective protein has already almost all the specific bits of information in place for performing the function so that the amount of information that must be infuse by the physicians to cure the patient is only 4,3 bits at most.
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We can test that hypothesis.
And you are ignoring the huge amount of information that comes from sloppy recombination and somatic hypermutation.
I don’t see how any description would be superior to testing that hypothesis directly.
That’s fascinating. How did you determine that F508P has zero function, and therefore zero FI, Gil?
I think you just made that up. But using the identical criterion, since a stem B cell makes no antibody, it therefore has zero FI.
What is clear to me is that the CFTR F508P allele has some function, so your handwaving here is based on an empirically false premise.
And here we are, 108 posts into the topic “Gil’s testable ID hypothesis,” without you showing the slightest interest in even thinking about testing your hypothesis.
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What a spectacle. I wonder how long @colewd and @Giltil can keep twisting and turning, contradicting themselves and each other, as desperately change the definition of FI over and over, in order to keep it untestable.
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Just to be clear, I’m not proposing to test any definition of FI.
I am pointing out that Gil, in the process of desperately avoiding looking at ALL STEPS INVOLVED in evolving functional antibodies in mere weeks, has offered a perfectly (and to me, painfully obvious) testable hypothesis:
Easy to test. No arguing about FI silliness is needed, because we can delete most of that genetic information that Gil hypothesizes is functional, then test immune function directly.
The lack of interest suggests one of two things to me:
- Gil has no faith (neither religious nor intellectual) that his hypothesis is correct.
- Gil already knows that the hypothesis is false, but is deliberately trying to mislead others by misrepresenting his hypothesis as a fact.
As a psychiatrist, what do you think? Of course, they are not mutually exclusive.
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And as for Bill, he has incredibly pointed to an example from human genetics/physiology/evolution that literally, by itself, falsifies the very notion that function is mathematically related to sequence conservation!
And it’s smack in the middle of my area of expertise!
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What you cannot erase is the information that is contained in the invading agent which the adaptive immune system uses to make its target. Your experiment has little value in my opinion. The immune system function does not answer the problem of generating de novo information algorithmically. If the information to solve the problem is contained in the genome already that is interesting. How did it get there?
Wow. Your ability to string together technical sounding science terms with no understanding what they actually mean is truly amazing. It’s probably a marketable skill if you work for the DI. 
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As a Christian, I would be excited if God’s hand in shaping life was experimentally distinguishable from his “ordinary means”. It would be a real faith-booster to have clear and irrefutable scientific evidence that God “reached” into the natural world to shape life. But as a Christian and a scientist, I have to go where the data and evidence leads me. I thoroughly believe God gave us the world he intended for us to have, and that includes its mysteries and providence. If he wishes to use only ordinary means then so be it, I can’t fault him for it.
To the topic at hand, I’ve been convinced by @Mercer that experimental analysis of immune function coupled with editing of hematopoietic stem cells provide a good test of @Giltil’s hypothesis:
V(D)J recombination doesn’t produce high FI for most of the genetic information necessary for implementing the function preexist in the stem cells that develop into B cell.
@Giltil, do you agree that antibody response is an acceptable measure of “function” in the case of B cells?
If we edit the hematopoietic stem cell DNA (information), and see a change in immunoglobulins produced by testing antigen binding diversity and effectiveness (function), that should tell us something about the amount of FI, right?
[Edit: I don’t know if FI is the right term here, the definition is a bit hazy to me in terms of actual biology]
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Are you saying something like “it doesn’t matter how words are spelled, who made the alphabet”?
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Sheesh. I wouldn’t claim anything of the sort.
Bill, in experiments, we use these things called “controls.” Obviously, we have a perfect, undeleted mouse that we test for function in parallel.
Is this really all you can come up with to shore up your obvious lack of confidence?
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I am saying that the invading agent contains information that is used to create the B cell. The sequence is not irrelevant as it must bind to the B cell. This is a slightly modified version of the weasel program. FI copied is different than FI generated. We already know the cell can copy information.
This is more like creating a sentence in English from a Spanish version using a lookup table.
And I am saying that the experiment uses the identical information for the experimental and control mice.
Anything but thinking through the experiment, eh, Bill? Just deceptive rhetoric. I’m pretty certain that everyone here can see how little confidence you have.
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Can you eliminate the invading agent from the experiment? I am saying this is one of the information carriesr that is being used by the adaptive immune system.
You continue to argue against Evolution as if God has no interest in natural laws and processes.
I find this a bizarre position to maintain considering this site is all about God taking an interest in the natural order of things.
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And I am pointing out that the same “invading agent” is used for both experimental and control, wild-type mice, completely eliminating it as a factor.
Do you not understand the most elementary notions of how scientists do experiments, Bill? Because that would explain a lot…
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