I did not make this claim. Please read more carefully.
So you were wrong and you falsely accused me of being wrong in my area of professional expertise. Is that what you are trying to say?
It’s very strong support. That’s why you were fudging the data.
No, he claims to be doing that; you’re just playing word games.
Myosin also has far more functional information than does actin. @gpuccio’s central assumption is false.
Length isn’t a proxy for functional information either, Bill. It’s wrong all around.
Weren’t you just claiming that it is a method?
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Functional information is a function of length. Length increases the number of bits of functional information.
No, it is not, because virtually every protein that we’ve studied has regions that have much less functional information than others. Those less-functional parts are more common in larger proteins. That’s why simplistic notions like length and conservation aren’t proxies for information.
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Hi John
From Hazen and Szostak
Complex emergent systems of many interacting components, including complex biological systems, have the potential to perform quantifiable functions. Accordingly, we define “functional information,” I ( Ex ), as a measure of system complexity. For a given system and function, x (e.g., a folded RNA sequence that binds to GTP), and degree of function, Ex (e.g., the RNA–GTP binding energy), I ( Ex ) = −log2[ F ( E x)], where F ( Ex ) is the fraction of all possible configurations of the system that possess a degree of function ≥ Ex . Functional information, which we illustrate with letter sequences, artificial life, and biopolymers, thus represents the probability that an arbitrary configuration of a system will achieve a specific function to a specified degree. In each case we observe evidence for several distinct solutions with different maximum degrees of function, features that lead to steps in plots of information versus degree of function.
Although certain proteins may have more substitutability in certain areas sequence length is a much larger factor as the number of arrangements grows exponentially with the increase in length.
Bill, none of that even suggests, much less demonstrates, that length is a significant factor in functional information.
Do you not realize that myosins also demonstrate this concept beautifully?
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Hi John
The calculation in this case is the number of possible proteins per position to the power of the sequence length: for a 3 AA peptide the number of arrangements is 20^3 or 8000 possible arrangements if you add an addition AA the number of possible arrangements goes up to 20^4 or 160000.
Length is by far the biggest factor in the quantity of functional information. The number of possible arrangements of MYH7 is 20^1935 possible arrangements. This is greater than 1000 orders of magnitude larger then alpha actin.
No, it isn’t, because neither functional complexity nor functional information are functions of peptide length. No one’s decrees are facts.
Why did you leave out the extremely important qualification?
fraction of all possible configurations *of the system that possess a degree of function ≥ Ex
That was quite a strategic omission, wasn’t it? Or do you not understand it?
You’re in full-on Nigel Tufnel mode now, just insisting that your amp goes to 11.
Not according to what you quoted.
So what? If you bothered to read what you quoted, your simplistic calculation of possible arrangements isn’t relevant:
fraction of all possible configurations *of the system that possess a degree of function ≥ Ex
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John I was simply addressing your misunderstanding that length is not important. It is the most important parameter.
There is no way for you to make coherent empirical based claim from the data in uniprot that the functional information of MYH7 is less than alpha actin given the difference in length.
Is it? I would think Kolmogorov complexity would be a better (though imperfect) measure. It is quite possible for a long string to have lower Kolmogorov complexity than a short string.
Best,
Chris
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Well that is certainly a reasonable interpretation of what you wrote here:
Exactly what did you intend to convey there?
And exactly how would Lynch’s model be helped if duplications were less frequent. It seems obvious to me that this would make it less likely for new genes to be generated by gene duplication.
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Oh, good Christ…
The frequency of gene duplications depends on the empirical data based on the animal types in question. By saying “Lynch’s model counts on gene duplication being less frequent” I mean that the adaption can occur without gene duplication. It also could mean that some of the mutational change could occur prior to gene duplication.
Gene duplication makes waiting time longer. If the process requires gene duplication then it favors Behe’s assumptions. If mutations are mostly neutral that minimizes the requirement for gene duplication and favors Lynch’s assumptions.
Laughably wrong.
We’re back to weighing cats without there being any cats.
If there are no cats, we can still weigh things that are not cats. But that is of no help when what we are doing is weighing cats.
Both Lynch’s and Behe’s models assume the existence of cats, because what they are doing is creating models to estimate what a cat is likely to weigh. Metaphorically speaking, of course.
Wrong again. Gene duplication makes it easier for new genes to evolve from already existing genes, because it means the function of the already existing gene is not lost. Pretty basic stuff, Bill.
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I have no words.
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This is all true but it also makes waiting time longer. If you have to wait for a gene duplication prior to any change the process takes longer. The is an important part of the working assumptions.
No one is waiting for anything. Inserting that anthropomorphism is deceptive. It’s part of Behe’s toolkit.
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It’s not a misunderstanding. Cut the laughable condescension, Bill, and quit misrepresenting what I write. There’s a quote function–use it.
Length is simply not a proxy for functional complexity or information.
That’s from your vast experience in computational biology, right?
What happens if we split a conventional myosin II, such as the one from MYH7, in half? Do those halves have equal functional information, or are there orders of magnitude difference between them?
Why would we base it on only the data in Uniprot? Wouldn’t we look for ALL the relevant data?
Are you more interested in learning or fooling yourself into thinking that you are winning?
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Longer than what?
Both Behe and Lynch are assuming, in their models, that gene duplication was necessary for the new gene to evolve.
You really should stop trying to pretend to understand things you plainly don’t understand.
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And falsely claiming that other people don’t understand things you plainly don’t understand.
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