Your premise is absolutely, objectively false. Comparing/contrasting myosin and actin, which function in concert, proves it.
Myosin does not require a high level of sequence specificity to perform its multiple, incredibly complex functions. Actin isn’t in the same league in terms of functional complexity, yet it is amazingly conserved.
Bill, why won’t you learn how many variants there are for human MYH7? Wanna take a guess as to the number already known, which is a minimum?
And why did you remove “some” from my earlier statement, then pretend that I had made a universal claim? Was your intent to deceive?
Then why does it require such specific AA sequences such that Rats and Mice have no divergence in AA sequences over millions of generations? I will grant you that it looks more complex but is it?
John, I have looked at it and appreciate you pointing this out. There were more then 100 different recorded mutations. How many of these mutations can a single human tolerate?
A recent report (Gao and Innan 2004) presents evidence that the gene duplication rate is lower by several orders of magnitude than that assumed both by Lynch and by us based on the work of Lynch and Conery (2000). If so, then both his and our calculations for the population sizes needed to fix a mutation in a duplicated gene are substantial underestimates.
Gene duplication rate is very relevant to this discussion and if required favors Behe’s results.
I would think that selection is the dominant factor in conservation, no? Just because a substitution may be lethal or less efficient does not mean it never happens.
It happens all the time as inherited cancer mutations are quite common. The challenge is how mutation become fixed in the population. The more deleterious mutations that occur the longer waiting time for mutations to become fixed in the population. Both Michael’s agree with this in their arguments as the quantity of deleterious mutations estimated is one reason why their results for waiting time are different.
It was a “Why?” question, Bill. Since you claim to understand how things came to be (ID vs evolution) better than I do, I expect your ID hypothesis to explain the data. Why doesn’t it?
If what I am seeing is right regarding mutations relating to disease there is nothing unusual about this data which shows association of disease (heart failure) with many amino acid substitutions. Contrary to your prior claim (mutations in healthy individuals) this gene/protein may contain a high level of functional information as many of the substitutions are deleterious and the protein is well above average in length.
It makes no predictions, at least that I can discern. The methodology seems to be: “evolutionary mechanisms cannot explain X, so X must be the result of design.”
There are variations, of course. “If something requires multiple coordinated mutations, evolution cannot reach it. So such a thing must, like a mousetrap be designed. Now X requires multiple mutations. Therefore it must be the result of ID.”
But it’s all semantics, like information arguments. ID doesn’t make predictions that are testable … therefore it has no methodology that is testable … therefore people who are interested in proceeding in a scientific manner are not interested in it.
Another instance of ID/creationistic dichotomous thinking.
Some - therefore all. Few - therefore none.
Ironically Behe et al appear to be arguing against duplication and divergence in general, and Lynch merely responds by pointing out exceptions to Behe’s overgeneralization. Lynch isn’t saying all proteins can diverge(to the same extent), just that Behe’s scenario is a false generalization, and here’s how some duplicate genes can diverge.
There really might be proteins that can become(as in the strong conservation is another outcome of historical evolution) completely entrenched over time, that still wouldn’t support a generalization that this is true for all proteins. We know conclusively from direct experiment, computer modeling, phylogenetic inference, and real-time observation that it is not true.
The papers are intended to model the likelihood of new functional genes being fixed when a duplication event occurs.
So your statement above is nonsense. It’s like we are arguing over whose cat is heavier and, after we weigh them and find mine is heavier, you respond “Cats are very relevant to this discussion, and if cats are required then this favours my claim.”
Hi Faizal
Do you understand that gene duplication if required points to Behe having the right model for that specific adaption? Lynch’s model counts on gene duplication being less frequent due to a large quantity of neutral mutations so searches can occur prior to gene duplication.
This is a difference in the two models. My position would be that gene duplication is sometimes required depending on the animal and protein type. Since this does occur in nature Lynch’s model is not universal.
If it was, MYH7 wouldn’t stump you. It’s a good method for separating evangelical Christians from their money without doing any real work.
If you disagree, here’s your chance to prove it. You’re failing, and predictably grossly misrepresenting the data themselves, so far.
That’s a completely false dichotomy. You’re assuming dichotomous 100% penetrance because your ID hypothesis is failing you. The vast majority of people carrying these variants do not have any disease. How many of these variants have a penetrance of >5%?
Do you know what “penetrance” means?
You’re not reading carefully. The primary diseases are cardiomyopathies in both directions, corresponding with hypo- and hypercontractility. Heart failure is secondary.
Again, how many of these variants have a penetrance >5%?
Bill, I find your use of blatant falsehoods to falsely accuse me of not knowing my own field of expertise to be profoundly un-Christian, and an attempt to distract from the fact that your ID hypothesis doesn’t work in reality.
Again, the truth, which you are avoiding, is that the vast majority of these MYH7 variants are in healthy people. You are now deliberately misrepresenting the actual data, which is really the only method underlying ID–Behe resorts to it in almost every case.
Thanks for posting thIs and it appears to be supported by the evidence.
This however this is very weak support for your claim that Gpuccio is wrong. Gpuccio is measuring functional information which is different then observed functional complexity. We could go through a complex argument whether MYH7 has less or functional information then alpha actin but at the end of the day it would not be conclusive and given the length of MYH7, despite the variants, would most likely contain more FI given its length.
ID to me is an interesting argument but a limited one. I don’t see it as anti science.
Uhm that’s an extremely misleading citation by Behe. The article is estimating the rate of fixation of gene-duplications, not their rate of de novo occurrence. Those are two very, very different things.
As they say:
(Gao and Innan 2004): Note that by “gene duplication rate” we mean the rate at which a duplicated gene is created by mutation and becomes fixed in the population. The fixation probability of duplicated genes should be largely affected by natural selection (14).
Behe is trying to argue that there is some sort of problem with the timescales at which we can expect proteins coding genes to duplicate and diverge. But to do that he needs the rate of de novo occurence of gene duplications, that is the rate of mutation. Not the rate at which such duplications ended up becoming fixed in the population by natural selection and genetic drift. The measure produced in that paper is actually more accurately described as an average rate at which duplications have been beneficial in yeast.
In any case there is no such thing as the rate of occurrence of gene duplication. It is highly variable depending on locus. In an offshoot experiment of the Long-Term-Evolution-Experiment they propagated the Cit+ mutant in a citrate-only environment (no glucose). In this environment gene duplications of the Cit+ locus and numerous other genes involved in citrate metabolism were extremely beneficial, so much so that within 2500 generations some strains had increased their total genome size by over 20%. In one case a particular gene (maeA) was duplicated over 95 times. Look at table2 in this paper:
Wrong. The frequency of neutral mutations has no effect on the frequency with which gene duplication would occur. That’s just nonsense. Again.
That Lynch’s model allows for neutral mutations, however, makes it feasible for mutations necessary for neofunctionalization to occur prior to the duplication event and therefore increases the amount of time for such mutations to occur. This is one reason that, by acknowledging the existence of neutral mutations. a more realistic estimate of time to fixation can be derived. It also helps explain why Behe’s results are unreasonable.