Gil's testable ID hypothesis

You say that, but you go on to contradict it.

If I were you, I would now spend some time trying to work out just what it is you actually believe because by now it’s clear you have no idea.

Not FI, no. It has zero bits of FI. None of it. Because if the sequence is lacking anything for function, it has zero bits of FI. It doesn’t have “most of” the bits required for the function, it has zero. None.

My feud is pretty simple: You and Gpuccio aren’t using FI correctly as it is defined by Hazen et al 2007. You are assigning FI values above zero to nonfunctional molecules, which is incorrect. Despite your protestation above, you go on to do exactly that here below. As I will show now again.

No, wrong. It means ALL the bits necessary for function are missing. If the system cannot perform the function, then no matter how much of the system is in place, it has NONE of the bits necessary for function. NONE. Yes, despite it missing just a single mutation and yet the entire rest of the sequence is there, if that sequence before mutation cannot perform the function, then is below the minimal threshold for function, is therefore nonfunctional, and therefore has zero bits of FI.

You started by acknowledging exactly that:
“It is exactly what I said for I explicitly recognized that a system (or a sequence) unable to perform the function has zero FI.” - You.

This is from Hazen et al 2007:

In this formulation, functional information increases with degree of function, from zero for no function (or minimum function) to a maximum value corresponding to the number of bits necessary and sufficient to specify completely any configuration of that system.

In other words, how much of the system is present is irrelevant if it fails to perform the function of interest, then it has zero bits of FI.

Functional information is defined only in the context of a specific function x. For example, the functional information of a ribozyme may be greater than zero with respect to its ability to catalyze one specific reaction but will be zero with respect to many other reactions.

So if the system does not perform the function of interest, despite the (in this case enzyme) having a sequence, it has no FI with respect to that function.

Functional information therefore depends on both the system and on the specific function under consideration. Furthermore, if no configuration of a system is able to accomplish a specific function x [i.e., M(Ex) = 0], then the functional information corresponding to that function is undefined, no matter how structurally intricate or information-rich the arrangement of its agents.

So basically a system incapable of performing the function regardless of it’s configuration, is undefined in terms of FI. So FI can go from undefined to however much -log2[M(Ex)/N] is if the system is altered such that it functions.

It may have a lot of information by some other definition of information, but if it doesn’t perform the function of interest, if it fails to meet M(Ex), aka the minimal threshold for function, then it has zero bits of FI.

Not FI, no. Because that one mutation (amino acid) is incapable of performing the function alone, so the FI doesn’t increase by 4.3 bits. It may increase by 4.3 bits of information by some other measure of information, but not according to FI.

Supposing the functional molecule in total scores 300 bits of FI, you are saying it goes from 295.7 bits in it’s nonfunctional state, then 4.3 bits of FI are added by that one mutation, and then it becomes a 300 bit FI molecule. But that’s wrong, because the nonfunctional sequence before the mutation has ZERO BITS of FI.

It goes from zero for the nonfunctional molecule, to however many bits it is given -log2 of the ratio of functional to nonfunctional sequences of that length. That one mutation doesn’t add 4.3 bits of FI, because the molecule before the mutation is incapable of performing the function. Then it by definition has zero bits of FI.

Yes, and if it cannot, then it has none of them. Not 4.3 bits(or however much) less than required, it has none of it.

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No, I’m not building a strawman. I’m genuinely and honestly convinced that I have just demonstrated in my post above how it is you who are getting the concepts mixed up.

Sorry to tell you that, but I am starting to wonder whether you are arguing in good faith on these matters. Hope I’m wrong.

You are. You are wrong about my motivations, and wrong about how you understand FI(and increases in FI) to be calculated.

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Thanks for this. In my case I believed in evolutionary theory and it had little effect on my religious faith. Without an in-depth look I would have supported Bio logos and supported the scientific consensus. In a conversation with my son I learned proteins and DNA were sequence dependent which lead to a 4 year research project including cancer research for a UC professor. Unless function was almost the size of sequence space the current theory based on random mutation and selection for functional advantage would not work. The data started to surface that some proteins had significantly rare functional folds the first evidence came from @Art Hunts critique of Doug Axe. Since then the work of gpuccio and Behe has convinced me that evolutionary theory while solid when talking about adaptions such as change in beak length was not powerful enough the explain major transitions.

At first I was resistant to ID as science as it is limited and can be seen as a science stopper.I then learned about ID and saw others agreed with me. Some I realized were highly motivated for the reasons you stated but others were not as I don’t believe Mike Behe is.

About 2 years into the project I thought I should give it reasonable consideration as a vehicle to think about the world when doing scientific research. Where I see it today is as a valuable alternative hypothesis to keep evolutionary theory honest. Many papers in evolutionary biology use universal common descent as a working hypothesis and I think this leads to faulty conclusions in many cases.

I think ID is good for science and I am happy some in the community are open to dialog about it. If we come to the conclusion that the universe is the product of Devine intelligence all science will run into the design hypothesis it is just a matter of time. Biology has the opportunity to lead here.

Just to clarify matters - I don’t think my critique of Axe lent any support to the idea that proteins may have “significantly rare functional folds”. On the contrary, my critique argued just the opposite.

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I agree you argued the opposite but your data along with other data contradicted your conclusion. I thought your paper was excellent as you made on honest assessment of the data. It was a pivotal resource for me. If the world was only made of bacteria with enormous populations and simpler molecular structures your conclusion would be harder to argue with.

When I used your most conservative conclusions for the development of micro machines in the eukaryotic cell real problems surfaced.

Just to get back on track here I’d still like to see John Mercer’s proposed test of Gil’s hypothesis, provided Gil can say something more specific about the information created by VDJ recombination and somatic hypermutation than just that “most” of it pre-exists.

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This seems the very definition of the Texas Sharpshooter Fallacy.

No it is not. Not at all. Either you don’t understand what I said or you don’t understand what is the Texas Sharpshooter Fallacy.

I don’t agree with this either. Seems fairly straightforward to me, that functional information must be defined in terms of function, and if the function is absent then so is functional information. I don’t see any fallacy in this. You may think there’s something wrong with this definition but doesn’t commit a fallacy that I can see.

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I find it quite strange that you blame me for not providing « something more specific about the information created by VDJ recombination and somatic hypermutation than just that “most” of it pre-exists » when I am the only one here who has tried to calculate the amount of information generated by VDJ recombination as well as somatic hypermutation.
For my calculation regarding VDJ recombination, see the link below
Gil's testable ID hypothesis - #62 by Giltil

Perhaps. But to me, painting a circle around sequences based on function can get arbitrary. If a defective copy of a gene leading to CF has a FI of zero, but a functional copy has high FI, what is the FI for genes leading to sickle cell, which has a hobbled or locally advantageous function?

Okay I have to say that your complaint here is fair enough, I had completely forgotten about that post of yours. While I think you’re not doing the FI calculation correctly when you’re assigning FI to individual VDJ segments which (presumably) alone cannot carry out the function of the full immunoglobulin molecule, you are right to say that you have actually attempted a more specific estimation. I stand corrected.

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I’m blaming you for falsely presenting speculation as fact, Gil.

Your evasions lead to the conclusion that you have deliberately fabricated this claim and are compounding it by falsely presenting your uninformed speculation as information.

You have done nothing of the sort; your failure is particularly egregious for somatic hypermutation, as you explicitly specified, three times, naive B cells. The naive comes before somatic hypermutation.

Again, your hypothesis is testable. Why are you so afraid of testing it?

I saw it. There was nothing specific about it. It was ridiculous and evasive, because it was filled with unsupported assumptions.

Why are you afraid to use your clearly stated hypothesis to make specific, quantitative predictions?

  1. We can count V regions.
  2. We can functionally quantitate antibody responses. No FI silliness.

So what are your specific, numerical predictions if we inactivate both alleles of the kappa light-chain gene, Gil?

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Again, Gil’s hypothesis, falsely, but clearly, presented as fact, is:

@Giltil, please note that you clearly specified “genetic information necessary for implementing the function,” so there’s no FI silliness included.

What does your hypothesis quantitatively predict about the relationship between direct measurements of antibody function and the numbers of V, D, and J regions deleted?

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How odd, then, that you have never presented any actual analysis of these data…

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Who needs analysis when you have a disembodied mind using magic to POOF genomes and proteins into existence? Any analysis would only be superfluous. :wink:

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Gil, please be specific. What numbers does your hypothesis predict? Numbers for V, D, and/or J regions deleted and antibody times and/or titer.

You could even produce a graph…

Have you lost confidence in your claim?

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I think @Giltil is learning an important lesson that few creationists appreciate: In science, it’s not enough to come up with a nice-sounding hypothesis. You got to put in the hard grunt work to determine if the data actually support it.

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I think that the more important lesson is that hypotheses should be stated as hypotheses, not as facts. Doing this is perfectly OK as long as @Giltil is humble enough to seek the data that support or demolish his hypothesis. Put another way, hypothesis-driven learning is very effective, even when all of the data are available.

The whole point of doing science is that what intuitively seems to be true often is not the case.

Gil’s 9 days of evasiveness is strong evidence that he is not just making an innocent error in presenting his hypothesis as fact, and that at some level, he has no confidence in his veracity in this matter.

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This shows a lack of understanding of antibody production. V(D)J recombination happens during embryonic development, meaning that humans or mice are born with a set of B-cells that have already produced an initial antibody through somatic recombination. The immune system does not take in an antigen and then recombine a segment of the genome to match that antigen. Instead, antigens will bind to already existing antibodies being displayed on the surface of B-cells.

If a B-cell binds to a an antigen the other immune cells will give it a signal to rapidly divide, pump out tons of the antibody molecule, and initiate hypermutation which affects the antibody sequence. Subsequent to that first binding signal, there will be B-cells with further mutated antibodies that bind the antigen even better, and B-cells displaying those antibodies will be given an extra signal to divide and pump out antibody.

The initial random mutations that produce the antibodies during embryonic development are completely blind to challenges they will see in the future. They are not made to fit a specific target, but are instead random sequences of small chunks of genome. The original genome sequence does not contain the information for producing these antibodies, and that information only emerges after random somatic recombination.

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