Gil's testable ID hypothesis

Because both processes produce FI.

To test your hypothesis, both must be considered. You seem very reluctant to address both at the same time.

All of it? Definitely. And that’s particularly true for FUNCTIONAL information. Some genetic information has much more function than others.

One can design experiments that can address which processes are adding functional information. Why do you seem uninterested in thinking about them, Gil?

@Michael_Callen, do you see the lack of interest in evidence here?


Yes, because the conversation is being had and both sides are present. But this is a blog. For every present participant, there are hundreds of silent readers. Always write for the latter, not the former.


My fellow UCSD alumnus Tonegawa’s point is that the segments get rearranged. You, OTOH, are making a similar statement in the context of denying that this rearrangement produces new FUNCTIONAL information.

No, one is quote mined out of context.

And you predictably failed to read further in that very same abstract:
“In addition, mutations are somatically introduced at a high rate into the amino-terminal region. Both somatic recombination and mutation contribute greatly to an increase in the diversity of antibody synthesized by a single organism.”

You haven’t written anything of the sort.

Those mutations, plus recombination, plus selection, massively increase functional information, which you don’t seem to be interested in assessing experimentally. Why is that?


Actually, not all of them do, because sloppy recombination and somatic hypermutation change the existing sequences. It’s not just combinatorial, and that can be addressed experimentally.


Rather than hammering away baselessly that I’m not interested in evidence, why don’t you present them instead. This will be far more productive.

Rather than talking about claims instead of hypotheses, why don’t you join in thinking about rigorously testing a hypothesis instead of defending your position by quote mining and alternately ignoring the fact that both recombination and mutation create new functional information?

So, which is better–the descriptive approach you’ve outlined, in which “largely” is conveniently left undefined, or a direct, experimental approach employing genetic engineering of hematopoietic stem cells or embryonic stem cells?

Which provides a better understanding of which parts of which sequences contain more functional information–BLASTing or direct tests of immune function?

I’m hammering at the hypothesis. That’s what science is about. Please join me in collaboration instead of looking for ways to make the hypothesis more ambiguous.


We have presented the evidence. A section of DNA is randomly shuffled around to produce a DNA sequence that didn’t exist before. This also includes substitution mutations. This new DNA sequence performs a function that didn’t exist before. If this is not new “functional information” by your definition, then your definition is not relevant to biology.


It is also worth mentioning that the spacers between the different regions are not always cut cleanly resulting in different reading frames. The same V region can be in all three frames in different B-cell clones.


Which is literally an increase in FI, one that would even show up in @Giltil’s descriptive proposal using @gpuccio’s own definition.

This is a turbocharged version of what happens with recombination (required to hold homologous chromosomes in place) during meiosis, as resolution of the breaks involved creates new mutations in addition to the combinatorial increases in information it produces.


We’re still waiting for your definition of “new information” and for you to provide an example in a genome which would count as “new information” for you.


It’s as if all the posts that were written in response to your last one did not even exist at all, as far as you are concerned. Shameful.


@Faizal_Ali, @Timothy_Horton, @T_aquaticus, @Rumraket, @Mercer

It would be so helpful if the discussion could focus on the science and on @Mercer’s excellent suggestion of testing the hypothesis.

I think I understand @Giltil’s suggestion (a stepwise summary would be good) but I’m still trying to work through @Mercer’s. It makes sense to test function by looking at immune (response?/function?). However, I’m still trying to understand the basic biology of it so I’m not sure yet how “genetic engineering of hematopoietic stem cells or embryonic stem cell” would show us what we want.

My plea is this, for the benefit of myself but also people just watching who may want to learn and not fight, please stick to explaining and elucidating the science and avoid jumping to the slam dunk. I think this thread has a lot of potential, but if it just goes to the same old debates we’ll have squandered @Mercer’s excellent setup.

Of course I’d ask the same of @Giltil and other ID folks that want to contribute. I think we need a good-faith attempt to work with the science from both sides.


I disagree. The ID supporters have not presented an idea that can be tested.

Suppose I claimed that I could prove scientifically that God does not exist with the following experiment: If God exists, we should find Gargleflargle. Gargleflargle has been looked for, and its absence confirmed. Therefore, there is no God.

You might reasonably respond I have not yet made my argument, because I have not defined “Gargleflargle” and have not described the process by which its absence can be confirmed.

If I respond in turn by just tap-dancing around these questions and refusing to answer them, would you consider it your responsibility to test my hypothesis for me? Or would it make more sense to either press me to define my terms, or just ignore me altogether because I seem unwilling or unable to actually provide a serious argument?


I’m a little confused. Are you disagreeing with @Mercer that @Giltil’s statement :

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.

is a hypothesis?

[Edited: I had a “not” in there that didn’t belong]

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Yes. “High FI” is as well defined as “Gargleflargle” is in my analogy. Until we get the ID supporters to stop using the equivalent of Gargleflargle as their outcome measure, we have no hypothesis to test. That has already been made clear. @Mercer made a very reasonable and well-intentioned attempt to help the ID’ers out by defining Gargleflargle in a rigorous and testable way, but @Giltil has responded with “No, that’s not Gargleflargle at all.” So that’s where we are at the moment, waiting for @Giltil to tell us what he actually means by Gargleflargle.


For those interested to know more about « the genetic principle for generation of antibody diversity, below is a nice link (I specifically recommend to consider figure 3, for it nicely illustrates what I am claiming here, ie., that the genetic information coding for the V regions of the immunoglobulin receptors within B cells largely preexists in the genome of the stem cells that develop into B cells):

Now, It’s time to celebrate Christmas here in France, so I am going to leave you for some time, not without whishing you all a merry Christmas.


@Faizal_Ali, I see. I think you’re probably right that we need to have at least a rough agreement on how to know what FI would look like experimentally in order to have our test mean anything.

@Giltil, I don’t want to intrude on your holiday celebration (I need to do the same) but I think it is important when you get back to address @Mercer’s proposal for measuring function (assessing immune function). It certainly seemed reasonable to me. If not, please propose a modified experimental measurement that you believe would measure function in this case.


If you think this demonstrates that no Gargleflargle - Sorry! I meant to say “functional information” is created when new antibodies are generated, then you are in effect saying that evolution can occur without the generation of new functional information, which would basically mean the entire Intelligent Design project is now refuted. Which would be fine, but is that really what you intend to accomplish here?


That figure says absolutely nothing about where the FUNCTIONAL information “largely” exists or if it preexists, Gil. That was a very blatant goalpost move. It’s also basically the same as the figure I linked to in the opening post to provide a very big hint as to how one can test your hypothesis, so I’m not sure why you posted a reprise of it.

It’s also about work done 40 years ago. We’ve learned a lot about the importance of somatic hypermutation since then. Why are you so uninterested in testing your hypothesis regarding functional information?

“In addition, mutations are somatically introduced at a high rate into the amino-terminal region. Both somatic recombination and mutation contribute greatly to an increase in the diversity of antibody synthesized by a single organism.” --Susumu Tonegawa

Joyeux Noël.


Mutations and recombination cannot produce Functional Information. Functional Information is that which evolutionary processes like mutations and recombination cannot produce.

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