Looking for sources on the information argument

OK, so in a case where the entire space of sequences was one island, natural selection would be able to put functional information into the genome? Somehow I doubt that Giltil will say even that …

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One assumes that starting with a random sequence with an identified function and subjecting it to selection for that function, would result in a sequence improved for that function. Which, unless I am mistaken, would be an increase in the functional information of that sequence according to Hazen regardless of how rough the fitness landscape might be.

@Giltil is still yet to provide a mathematical (or any other sort of) framework by which we could judge if the number of globally optimized traits, relative to the total number of traits and when adjusted for which have multiple islands of functionality in the first place, for known valley crossing methods, and so forth, is problematic.

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How do you think islands of function work for multi gene/protein systems like the ubiquitin system or developmental pathways like WNT or Sonic hedgehog?

They would be larger, because they involve so much protein-protein binding. Binding is simpler. Proteins are incredibly sticky (which you’d know if you ever purified any), and binding is more selective than specific.

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And generally speaking the larger a protein, the more surface area to bind, meaning there’s more real-estate to exhibit some affinity, meaning you’ll need less specificity. Large patches of weaker affinity can have the same effect as a very narrow spot with stronger affinity. The net binding affinity can be equal.

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Don’t be too hard on Gil; SOME potential is a big step from NO potential.

Just like the Hawaiian chain, new islands are arising all the time. This is supported by a mathematical model of the genetics involved:

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AFAICT ubiquitin is a single protein, not a multiprotein system, and Sonic Hedgehog is a protein, not a developmental pathway.

So this is akin to asking how skis work for camels like the Eiffel tower.

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I think he meant the ubiquitin-proteasome complex.

And that thing about valley crossing methods is pretty important, as numerous mechanisms and causes of valley crossing are known from evolutionary biology. Fitness landscapes are also dynamic not static, almost always have more than one contributing cause, and there are other types of mutation than just point substitutions. Heck, you can even cross valleys just by drift through fixation of suboptimal mutants in small populations.

To just note that because fitness landscapes often times have a rugged feature - therefore evolution is impossible - is a complete non-sequitur.

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I think that if a functional island can be found in some ways, then some new abilities can probably in some case be acquired by divergence of gene duplicates through random mutation and natural selection. But one cannot generalize this possibility for it must be experimentally investigated on a case by case basis.

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It seems absurd to demand that any and all cases of diverged duplicate genes be experimentally demonstrated to be feasible, particularly when the fact that one can construct consilient phylogenies from totally independent genes and have these nevertheless strongly corroborate each other. There is simply no other good explanation for this reality than that they really did evolve and diverge through sequence, structure, and function, from common ancestral genes.

The fact that biochemists have been able to use said phylogenies to reconstruct functional ancestors and show which historical changes in sequence were causal for such functional transitions should effectively put any doubts about the general reality of such a phenomenon to rest, even if this has only been done for a small fraction of all known protein coding genes. There just is no basis in physics or chemistry for thinking some specific example that has yet to be experimentally characterized in that way is somehow an exception.

And just to be sure, this is not meant to support a claim that any and all genes can be evolved gradually and incrementally into each other while retaining biologically useful functions, just that where we can detect significant phylogenetic signal in sequence and structure, we already there have very strong evidence that the genes in question share an evolutionary history, and hence whatever functional transition is implied by this phylogeny must de facto be possible, otherwise there is (again) no good explanation for why we should have such evidence in the first place.

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I made this graphic a few years ago for a similar discussion, but the discussion wandered off before I had it ready, and I never used it.

The idea here is the white ring is a moat or valley of no function, surrounded by the blue area moderate function. The green island in the middle is region of high function.
The bubbles from D to C represent step-stones, or a bridge from moderate to high function (if it exist).
The arrows from A and B to C represent a recombination of features in the current population to “jump the moat” into high function. A (x1, y1) and B (x2,y2) recombine to make a new trait C (x2,y1) that did not exist before, crossing the valley.

This is a 2-dimension representation of how recombination can cross a “valley”. Evolution will be operating in higher dimensions (which I cannot illustrate) offering multiple opportunities to jump the valley.

At least I finally got to use this image. :slight_smile:

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I disagree completely and wonder how you can generalize Axe’s extrapolation from a single, poorly investigated case.

But just for fun, for how many of these cases have you personally examined the experimental data?

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Can I use this in my lecture slides? With proper attribution, of course.

Of course, but bear in mind I am no sort of biologist. :slight_smile:

Now I recall my original line of thought. Points A and B represent point on a cartesian coordinates on a plane. Swapping coordinates allows a jump to point C. The analogy to trading alleles or sequences is similar, but it’s not limited to 2D solutions.

I don’t have a good way to describe the higher-dimension situation, and this is probably where I got stuck in my first effort with this graphic. In 3D the valley can also be jumped from above and below, but higher dimensions are a brain bender. The idea is that if sub-sequences of the high function sequence exist in the genome, then recombination can allow the no-function valley to be jumped.

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What I said is true and not that difficult to understand. There is no law of chemistry or physics that explains the DNA sequence, by which I mean the order of the bases. The chemical nature of atoms and molecules does not require or impose any particular order of the bases.

Your response boils down to “heredity” or “evolution”, which does not refute my claim at all. And, of course, you completely skip over the issue of abiogenesis, which is where the ID argument begins. You can’t have heredity without the means of replication, which requires information.

I’m getting the idea that you don’t understand the ID information argument very well.

There is no sequential information in Mt. Everest. You are trying to equate complexity with specified complexity.

Simple complexity: sdflkeoijb lkasd elifdkg iedlji ghckeq iemdboprn dkqzehd

Specified complexity: My username on the Peaceful Science forum is DaveB.

Specified complex information is functional, sequential information. Whether that is telling you my username, or specifying the order of nucleotides or amino acids in a functional rna product or protein.

The ID information argument includes Dembski’s “Explanatory Filter”.

(1) Does a law explain it? (2) Does chance explain it? (3) Does design explain it?

Law and chance can explain Mt. Everest, but not specified complex information.

I think you’ve completely missed my point.

I agree that once the rna or protein is formed, it operates due to chemistry.

I truly don’t understand how you can think that I don’t believe that DNA sequence matters.

What did I say that makes you think that?