Your take based on what evidence, exactly? To date, none of the evidence you’ve cited (very little) supports this. You are clearly afraid to test your hypothesis regarding VDJ functional information.
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That’s @gpuccio’s hypothesis: that conservation is a measure of FI, Gil. I’m glad that we now agree that it is false.
Now, how about YOUR hypothesis that you deliberately misrepresent as fact?
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That would still be quite unrealistic of course, since function comes in degrees for proteins, while combinations either fully open the lock, or don’t, and there’s no feedback from partial combinations that tell you they have “higher degrees” of lock opening.
Yet with something like enzymes, and protein binding sites, the function really does come in degrees from very weak to many order of magnitude improvements. Yet another way in which this combination lock analogy is completely unlike real biology.
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You are correct.
It was, however, better than the analogy that Gil was misrepresenting as an example. It could be improved further by not knowing the number of possible combinations one could try, in addition to not knowing the number of combinations that could open the safe.
You are also correct in noting that after sequences, virtually everything in biology is analog.
For example, for CFTR there is no way to quantitate the relative contributions of the ability to be moved to the plasma membrane and the channel activity.
This is an objectively and empirically false statement. You don’t have much, Gil, if you need to misrepresent the evidence itself.
Since gene editing technologies have off-target activities, such an approach risks causing cancer, in this case lung cancer or leukemia/lymphoma.
Since your claim that the mutation “completely abolishes” function is objectively false, the more conservative approach is to find drugs that promote trafficking of the mutant CFTR to the plasma membrane and its glycosylation, because the mutation does not abolish its function as a channel.
How you can choose a case without bothering to learn the basics about it amazes me.
Gil,
You don’t get to change the scientifically established meaning of FI unless you produce published research to that effect. Like it or not, intelligent design researchers have described the formal definition. That’s the criteria.
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Right back at you.
We can estimate how many possibilities however that ratio between function and total possibilities certainly exceeds the safe example in many cases.
Huh? I’m not cherry-picking anything. I’m showing that your cherry-picking is failing, as it fails for the sarcomere too. Let’s start another thread on that.
You’re not estimating anything. Both of you are just making things up at this point.
Would YOU like to discuss how to test Gil’s hypothesis about VDJ recombination?
That’s pretty minor next to @Giltil’s repeated, deliberate misrepresentations of his hypothesis as fact, particularly given his refusal to think about testing it after it has been pointed out to him.
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I don’t think that the adaptive immune system is very representative of the problems evolutionary theory is facing.
The best test so far is the gpuccio test for complex sequences. Proteins like ubiquitin represent evolutionary transitions. The preservation we are observing is problematic for current evolutionary paradigms.
I think that it, particularly when coupled with catalytic antibodies, provides a clear picture of the ratio of functional to total sequence space and how quickly function can be found by variation and selection.
Isn’t that the very problem you claim that evolutionary theory is facing, Bill?
Then let’s apply it together to cardiac sarcomeric proteins in the other thread.
BTW, it’s not a test for anything. It’s just a hypothesis that all three of you are extremely reluctant to test before proclaiming it to be true.
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I.D. is a giant waste of time for discussions that are supposed to be relevant to the GAE scenarios or Peaceful Science.
This site is about Christians who accept science… not about whether or not Intelligent Design IS a science or not. It’s irrelevant to the issue of God’s miracles and providence in the Universe.
Can you tell why you think I’ve changed the meaning of FI?
You won’t have to wait so long😀
In my safe lock example, the new information (nI) is the amount of information that must be added to the system for it to perform the function. In scenario 2, nI is equal to 3,322 bits.
As for a genomic example of new information I accept, I’ve already provided several. Here is one:
Thank you for stating your mere opinion on this matter but unfortunately it isn’t a relevant factor in this discussion. It does however, manifestly show that evolving proteins with novel functions(binding many different antigens, evolving catalytic activities), is a problem that mere mutation+selection can overcome, among other reasons by showing that multiple functions overlap in sequence space, and that there are selectable paths from low to high levels of function.
No, ubiquitin does not “represent evolutionary transitions”. That statement doesn’t make any sense.
No it just implies a local optimum in a more rugged fitness landscape, where selection has climbed some local peak and got stuck there. This is a rather typical result in problems of optimization on rugged fitness landscapes.
Heck, you can even reproduce that outcome in the Boxcar2D simulation(I have to note that you shouldn’t confuse the track the car drives on with the fitness landscape metaphor of course). At some point you’re going to get long periods of stasis for the “best” car in the population, and eventually the car doesn’t seem to ever improve anymore even after hundreds of generations, that’s when it has got “stuck” on some local optimum.
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I disagree with you on this Bill for I can see a myriad of Irreducibly Complex systems in the immune system, not the least of them being VDJ recombination.
Not at all. You are talking about partial mutation of a sequence followed by binding to a single antigen. This is in no way representative of cellular complexity even at the prokaryotic level.
Sure it is. It directly tests for preservation. You can argue what preservation means and this is where we disagree but it is a test.
I agree with your point but then this discussion should be about the origin of VDJ recombination and not about its function and how it demonstrates RMNS. When we try to test RMNS we are falling back to testing micro evolution. Is that what this discussion is about because we all agree that micro evolution is valid as far as I can tell.
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Ahh this is your latest irrelevant goalpost shift. We’re discussing the origin of functional information, and complex adaptations, new proteins, de novo sequences, irreducible complexity, and what have you, but now suddenly all of it doesn’t count if it doesn’t also constitute macroevolutionary change. Which doesn’t make any goddamn sense. Either a novel protein, with new FI can evolve, or it can not, regardless of whether that occurs concomitant with a micro or macroevolutionary transition.
Macroevolution is simply evolution above the species level. If you want to see evidence for macroevolution, look at evidence for speciation and for common descent. That’s right, it’s the nesting hierarchical structure, and the consilience of independent phylogenies all over again. That other thing you’ve had explained to you a ridiculous number of times and seem to forget again after 5 minutes have passed.
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Does microevolution produce new information Bill? Yes or no, and why?
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I have been explained this untested hypothesis many times. What I have never seen is the hypothesis supported scientifically. What you seem to forget that you are spouting unsupported claims. Do you honestly think this helps your credibility?
Proving a flying object can go 100 feet in the air does not show it can fly to the moon. Major animal transitions are a mystery more now that we understand cellular complexity than in Darwins day were he made this intuitive huge leap from his observations.