I don’t need a resource, thanks.
I want you to demonstrate that you know what that estimate is based on. And then that you can figure out on your own how you contradicted your own position,
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But you don’t believe that resource, so how can you make use of it?
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Bill, are you assuming that only one protein can vary at a time, and must lock in place before the next one can begin to vary?
Here I will not comment directly, but my educated guess it the beta catenin has been conserved in mammals from long before the divergence between rats and mice.
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Not only that, he keeps assuming that there’s no intraspecies variation, despite constant reminders. His persistence in promoting this false assumption makes me question his sincerity.
Your guess is correct. Bill keeps eliding the fundamental fact that proteins interact with other molecules, particularly other proteins; these interactions are far more important factors in conservation than any Bill is willing to consider.
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Hi Dan
No I am not as I stated earlier in the discussion.
My educated guess is the Beta Catenin and the system it helps control was designed. It has critical properties and interacts with many other proteins to regulate cell division.
Was it designed by evolution? Is there any other falsifiable hypothesis that can be applied?
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Them being less constrained, depending on their function, expression level, structure and other characteristics. You know, the fact that proteins are not all the same or under equal levels of constraint. This is completely obvious. I already cited you a paper, weeks ago, that explains one of teh strongest constraints on protein sequence is cellular abundance. But different proteins have different levels of cellular abundance, with some being expressed at basically no more than a few copies pr. cell (and in a multicullar organism, some not being expressed by many cells at all, instead appearing only in specific tissues), while still others take up the majority of intracellular space. Did you magically forget that entire exposition in less than what, two weeks?
Neutral mutations are about genomic averages, not specific proteins. Again, because different proteins have different levels of constraint, for ALL the same reasons already explained.
THINK Bill, THINK.
Neutral theory doesn’t predict protein sequence divergence, it just says, basically, that the majority of differences that accumulate in a population, or are different between species, are selectively neutral(or nearly so) It doesn’t say which ones, or where. It’s pretty much just a genome-wide average.
You seem to have completely misunderstood neutral theory to say something absurd, like all mutations are neutral. That’s just completely wrong and really just reveals how you know nothing about these subjects.
Lynch’s model is an in principle calculation, assuming a specific target, spanning a range of rates of selection coefficients and numbers of differences, it can apply to any imaginable protein in any imaginable species. All it says is that, given some number of mutations, with some number of alternatives being possible, and some selection coefficients for these, it would consequently take on average this long for those changes to evolve.
How can you not understand this when it’s been quoted at you by @Faizal_Ali and you’re purporting to have read the paper already multiple times? Please point you what you didn’t understand, because it’s amazing how you can keep forgetting what that paper says.
No, neutral theory says nothing about how much we should expect the beta catenin protein sequence to diverge. Absolutely nothing.
Which just proves that the gene is under purifying selection, and hence most mutations that occur in it are not selectively neutral, but deleterious instead. But that doesn’t tell us anything about how it got to that state to begin with. Wait… suddenly I recall having wrote almost that exact same sentence to you before. Hmm, where did that happen?
Let’s see, it’s here I think:
Wow, an entire post dedicated to explaining this idea. You even responded to it with this on December 21st:
Hi Rum
I think you logic holds together well. Where we differ is in how proteins like alpha actin and MYH7 originated.-Was it designed in the current state we are observing?
-Could it evolve by random change and selection into the state it is in?How would your argument change under the first condition?
As far a Behe and Lynch I think both models are not universal and depend on the protein type.
What the flying @#$&, it’s like you actually read and understood it. But now, about a month later, we see you’ve hit hard reset again. You should try to explore why you seem to forget things you appear to have understood some times mere days ago, again and again.
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Certainly there is no hypothesis that shows how this system evolved by any known mechanism. It fits well with Behe’s method of detecting design. A purposeful arrangement of parts with the purpose of regulating cell division. The WNT “on state” is on during embryo development and other instances requiring rapid cell division. The WNT “Off state” allows the ubiquitin system to target Beta catenin for destruction and this is one of the methods of controlling cell division by reducing the amount of Beta catenin in the cell nucleus.
A complex arrangement of proteins that controls a critical function in vertebrates.
So how would you falsify design?
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As it happens, there is more than just a hypothesis. There is a theory that explains it.
I don’t recall your explanation of how this method has been validated. Could you please repeat it for me? Thanks.
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Ultimate design you cannot. If God designed the universe de novo then everything is designed however some aspects like gravity you can assign as primary cause. Design is really just a comparative hypothesis in this case.
Einsteins theory of gravity falsified design for the motion of the planets. If you could show a mechanistic explanation for the origin of the WNT pathway that would falsify design as the direct cause and provide a powerful challenge to Behe’s methods.
Like the force of gravity or the structure of the atom the WNT pathway maybe direct evidence of Devine design.
Nothing so grand is required. I’ll settle for a falsifiable hypothesis for the design of Beta Catenin.
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Yet the name comes almost directly from Drosophila. Bill, before making these ex cathedra pronouncements, could you at least acquire a Wikipedia-level introduction?
The discovery of Wnt signaling was influenced by research on oncogenic (cancer-causing) retroviruses. In 1982, Roel Nusse and Harold Varmus infected mice with mouse mammary tumor virus in order to mutate mouse genes to see which mutated genes could cause breast tumors. They identified a new mouse proto-oncogene that they named int1 (integration 1).[3][9]
Int1 is highly conserved across multiple species, including humans and Drosophila . Its presence in D. melanogaster led researchers to discover in 1987 that the int1 gene in Drosophila was actually the already known and characterized Drosophila gene known as Wingless (Wg).[3] Since previous research by Christiane Nüsslein-Volhard and Eric Wieschaus (which won them the Nobel Prize in Physiology or Medicine in 1995) had already established the function of Wg as a segment polarity gene involved in the formation of the body axis during embryonic development, researchers determined that the mammalian int1 discovered in mice is also involved in embryonic development.[10]
Continued research led to the discovery of further int1-related genes; however, because those genes were not identified in the same manner as int1, the int gene nomenclature was inadequate. Thus, the int/Wingless family became the Wnt family and int1 became Wnt1. The name Wnt is a portmanteau of int and Wg and stands for “Wingless-related integration site”.[3]
We typically call them competing hypotheses, and they are only useful if they both make testable empirical predictions. Evolutionary theory does in spades. If you don’t have any for design, they aren’t comparable.
See above.
Great! Then we’re done.
Behe doesn’t have any methods, because rhetoric isn’t a scientific method.
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You need an alternative mechanistic hypothesis for its origin. Gene duplication and divergence is what has been discussed. Also de novo genes from introns has been proposed. Then you build a model and test it as Behe/Lynch did.
Finally you let everyone argue ad nauseam about who has the right assumptions 
You have just asserted that design is the default conclusion if you can’t produce a detailed explanation. Why should that be?
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I wonder if, when a scientifically informed person tries to explain something to Bill, this is what it sounds like to him. It would help explain why he is perpetually confused.
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It’s the vertebrate homolog of the Drosophila gene armadillo.
Why? By whom? Are you asserting that the common ancestor of flies and humans was designed, but humans were not?
By whom? When? Your use of the passive voice does not inspire confidence.
No, you primarily test hypotheses. Models can be a part of that, but not typically.
Wikipedia is often (not always) your friend:
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Before “you need an alternative mechanistic hypothesis”, you first need a “mechanistic hypothesis” for it to be an alternative to. To the extent that “design” can be considered a hypothesis (which is highly doubtful), it is clearly not a “mechanistic”, as ID advocates never offer a hypothesised mechanism by which the design might be instantiated into reality.
This is why ID’s repeated demands for ever more detailed mechanisms is utterly vacuous.
Indeed. Given that Behe equates “a purposeful arrangement of parts” with design, his bald assertion of the former is equivalent of the bald assertion of the latter. Empty rhetoric.
For this to rise to the level of a legitimate “method”, Behe would have to provide a validated test for objectively identifying “a purposeful arrangement of parts”/design. I have seen no evidence to date that he has done anything close to this.
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Just from looking at the structure I’m quite certain that’s a repeat-protein that evolved by internal duplication and fusion of those alphahelical blocks.
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Hi John
It is about identifying a testable mechanism that explains the pattern. if you cannot then there is a reason.
It maybe the pattern you are observing is part of the fundamental design of the universe.
Could Behe’s method add value in determining this? His criteria (purposely arranged set of parts) is showing a strong design signal in the WNT pathway, the Howe Venn and other Venn diagrams I have recently found.