The problem is that your calculation is based on the demonstrably false assumption that the sampled variants of sequence space are able to tell us about unsampled areas(they aren’t for reasons I have explained at length), and also the false assumption that functional sequences are uniformly distributed across sequence space, and the false assumption that the sampling process is uniformly sampling sequence space. All those assumptions are false as I have explained before.
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But you didn’t bother to determine how much conservation there was, so your calculation was meaningless.
I only need to point out that you ignored the variation and that your ID hypothesis made you so certain that you made an empirically false claim that there were “a few.”
Now that your personal ID hypothesis has been falsified, how will you modify it?
But in this case, Bill is so wrong that we can grant all of these false assumptions and he is still wrong!
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I calculated around 8500 bits. This was based on 54 differences in amino acid positions out of 1935. If you want to falsify the hypothesis show that including the human variation will change the claim. I predict the human variation data will add nothing appreciable to the calculation.
But the sequence similarity is 97% to chimpanzees, 92% to mice, 86% to zebrafish, 63% fruit flies, 49% to worms, 48% to yeast.
Where did you get the 54 differences from?
https://www.genecards.org/cgi-bin/carddisp.pl?gene=MYH7
I thought the definition of FI included conservation of bases across species?
I don’t have to show anything, Bill. The data show that the @gpuccio’s hypothesis is false.
I think that it would be much more entertaining for everyone to speculate on the magnitude by which you are wrong. How about you all put in $5 and the one who is closest without going over wins!
Bill, define “a few” first!
However, I should preface that challenge with a disclaimer: any number of variants that I estimate will be an underestimate given that new ones are constantly being found.
In summary:
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Your ID hypothesis made a strong prediction that different tissues would have different myosins–so strong that you stated it as fact. Your hypothesis was falsified.
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Your hypothesis also made a strong prediction that there would only be “a few” human MYH7 variants. Not learning from the previous false prediction, you again misrepresented this as fact. Your ID hypothesis was falsified a second time.
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Even within the same system, the cardiac sarcomere, there is not only no correlation, but a negative correlation between protein sequence conservation and functional information. That alone falsifies @gpuccio’s “FI” hypothesis, as does the existence of the major histocompatibility complex.
If @gpuccio’s hypothesis is correct, cardiac myosin, an ~1850-residue, actin-activated ATPase that is not only a motor that forms filaments, but does even more amazing things like binding more tightly to actin as it is stretched, has less functional information than–wait for it–actin, which is an ATPase that forms filaments. Metaphorically, that’s like saying that a train track has more functional information than the locomotive that runs on it. (note: metaphors are explanatory devices, not arguments).
Almost all of the complexities of the actin cytoskeleton, which are many, are mediated by actin-binding proteins. I’m confident that most of them aren’t as well-conserved as actin either, but the myosin heavy chain takes the cake.
What ID hypothesis predicted all of the polymorphism in MYH7, Bill?
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Alpha muscle actin came in at 1650 bits Myosin came in at 8500 bits which confirms your intuition. Myosin has about 200 orders of magnitude FI then Actin.
This may be the best ID supporting evidence yet.
Thanks for posting the DNA sequence information. John is right we are comparing amino acid sequences. The difference is due to the redundancy in the DNA code.
Which nevertheless are evidence for evolution, and for common descent, as the DNA sequences yield a phylogeny congruent with those derived from other loci, and because they’re mostly due to transitions.
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You can’t have it be “ID supporting evidence” if it isn’t predicted by an ID hypothesis. And you have no hypothesis that predicts any particular degree of conservation for anything at all, much less substitution biases or polymorphisms.
As is usual for you, things are diametrically opposite of what you’re insisting.
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It only “came in” that way because you ignored its polymorphism, Bill.
You even made the prediction that there were only “a few” alleles, which falsifies both your and @gpuccio’s hypotheses.
You’re not testing the correlation between conservation and functional information if you’re not bothering to calculate the degree of conservation.
“The past was alterable. The past never had been altered. Oceania was at war with Eastasia. Oceania had always been at war with Eastasia.”
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I disagree. Your assertion is duly noted.
The polymorphisms being very different in a single animal but very similar across animals is very strong evidence the polymorphisms were designed. There is no good evolutionary explanation for this result.
Oh you disagree, then where is the hypothesis that predicts the observed result?
So where is the design hypothesis that predicts this?
Data cannot be evidence for a hypothesis if the hypothesis does not actually predict the data. And you do not have an ID hypothesis that has predicted this result, hence it’s not evidence for ID.
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What you really mean is things Bill doesn’t understand are evidence of design to Bill. To the rest of us it’s just chuckle-bait.
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The hypothesis is the data will supports design (mind) as a mechanism. It does that exactly. Just as starlight curving around the sun supported mass(energy) as a mechanism. How many times do I have to repeat this 
But the data can only “support design (mind) as a mechanism” if you have a hypothesis that predicts the data. And you don’t.
Where? Where is the prediction of the data Bill?
Even if you repeated it an infinite amount of times, that wouldn’t make it true. Where is the predict of the data Bill? Where is the design model that says “due to a mechanism that qualitatively and quantitatively functions in the following way X, we should expect there to be data patterns like this Y” ?
Nowhere, it is nowhere. Such a model does not exist. You do not have a predictive theory of ID, hence the patterns in the data (such as some particular degree of conservation of some gene between different species, or distributions of types of DNA mutations) isn’t evidence for it.
Why don’t you just accept this, what you must at some level know is true, and move on with your life? Do something else with your life, find some other basis for your beliefs.
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As was your false assertion that there were only “a few” MYH7 variants.
How many do you think there are, btw? Feel free to limit yourself to different protein sequences.
That’s not a hypothesis. Science is about preventing yourself from engaging in wishful thinking.
Your ID hypothesis predicted only a few MYH7 variants. That’s not true, so your hypothesis has been disproven.
Always back to the disembodied mind used magic to POOF life into existence. You need a new writer Bill, that joke has gone stale.
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But they aren’t for MYH7. Yet another of your hypothesis’s predictions falsely presented as a fact, and yet another disproof of your ID hypothesis.
Keep those false predictions comin’, Bill!
Bill’s “poof” hypothesis has made three very strong predictions:
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Different tissues will have different myosin heavy chains.
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There will be only “a few” MYH7 variants.
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The polymorphisms being very different in a single animal but very similar across animals.
All three are false. That’s a perfect record, Bill.
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