Sigh. More word salad that seems to avoid even trying to answer my question. Of course it’s hard to tell what word salad was intended to do.
How did you determine that the Howe diagram shows a purposely arranged set of parts?
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And that concludes our peek into Bill’s psyche.
Meanwhile in actual reality:
Abstract
Beta-catenin functions as a cytoskeletal linker protein in cadherin-mediated adhesion and as a signal mediator in wnt-signal transduction pathways. We use a novel integrative approach, combining evolutionary, genomic, and three-dimensional structural data to analyze and trace the structural and functional evolution of beta-catenin genes. This approach also enabled us to examine the effects of gene duplication on the structure and function of beta-catenin genes in Drosophila, C. elegans, and vertebrates. By sampling a large number of different taxa, we identified both ancestral and derived motifs and residues within the different regions of the beta-catenin proteins. Projecting amino acid substitutions onto the three- dimensional structure established for mouse beta-catenin, we identified specific domains that exhibit loss and gain of selective constraints during beta catenin evolution. Structural changes, changes in the amino acid substitution rate, and the appearance of novel functional domains in beta-catenin can be mapped to specific branches on the metazoan tree. Together, our analyses suggest that a single, beta-catenin gene fulfilled both adhesion and signaling functions in the last common ancestor of metazoans some 700 million years ago. In addition, gene duplications facilitated the evolution of beta-catenins with novel functions and allowed the evolution of multiple, single-function proteins (cell adhesion or wnt-signaling) from the ancestral, dual-function protein. Integrative methods such as those we have applied here, utilizing the ‘natural experiments’ present in animal diversity, can be employed to identify novel and shared functional motifs and residues in virtually any protein among the proteomes of model systems and humans.
Highly informative paper btw, only about 20 years old so we’ve had a very detailed picture of Beta-catenin evolution for over two decades. Just find it on google scholar and there’s a link to the pdf.
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Yep. But it evolved (or was designed) before the existence of our common ancestor with flies, so it doesn’t help Bill much.
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You don’t have one. We do and it has been thoroughly tested.
Why don’t you have one?
Behe doesn’t have a method. Behe refuses to test his own hypotheses, remember?
The signal would need to be in the data as a whole, not in Venn diagrams for which you don’t look at the data.
The word salad does not appear to be a purposely arranged set of parts, unless the purpose is to feign understanding where little or none exists.
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The pattern is a nested hierarchy, and the mechanisms are mutation, selection, neutral drift, and vertical inheritance.
Those are entirely subjective criteria, not scientific ones.
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I have not asserted that design is the default conclusion if a detailed explanation is not available.
This is the way to falsify design as the primary cause of the observation. The discussion was about falsifying design. Design is simply a comparative hypothesis.
By the observation of the pattern and what the pattern results in. Fully formed animals. Genes are critical elements in forming distinct animal types.
Why is it that only Evolutionary Biology is faced with this issue? Where is ID’s “testable mechanism” Bill?
For “Behe’s method” to have any value whatsoever, we need (i) a rigorously objective definition of “his criteria”, and (ii) validation that meeting this criteria is indeed indicative of design.
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It important to remember that Bill actually thinks he has answered the question here. He’s not just trying to entertain and amuse us.
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Of course you have. It’s the entire basis of your supposed test.
Still word salad. And more Texas sharpshooter. You see a mouse with a certain collection of genes and declare that the target. If the mouse had a different collection of genes, or if the organisms were other than a mouse, you would declare that the target. As for “fully formed”, you have no way to distinguish a fully formed animal from a partly formed one, whatever that would even mean. And you see a set of four animals and declare the pattern of their genes to be a target. How do you know any of that was purposely arranged? It’s Texas sharpshooters all the way down.
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How in the world do you determine if an animal is fully formed? That is yet another subjective criteria.
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The only example of a not-fully-formed animal I can think of is “Eric the 'alf-a-bee.” Not a very good pet.
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But properly registered! 
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Unformed animals? What results would you expect given common descent with random variation and selection?
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Of what use is half a mouse?
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Where did I make this claim? My discussion has always been about a comparative hypothesis to test against.
The criteria for judging the patterns design signal is a purposeful arrangement of parts. Can you show that this is a false positive? Purpose is clearly observed and a gene arrangement is also observed.
We know it is purposely arranged (based on Behe’s model) because the output is a differentiated living organism.
Whether this capability is in the cell or these animals were seeded separately we are observing purposeful design according to Behe’s criteria.
How would you create a specification like Behe’s to determine the shooter was actually aiming? How about if you can assign a purposeful arrangement to the bullet holes?
Hi Ron
I would expect less genetic variation then we are observing. The Behe Lynch discussion shows adding even simple function to animal populations takes a long time. Especially when deleterious mutations are prevalent.
A “purposeful arrangement of parts” is not a scientific criteria. It is a subjective opinion.
What specification? All Behe does is claim that whatever he sees was done on purpose. There are no criteria or specifications.
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That is incorrect. Here is what Lynch says in his own words:
Thus, it is clear that conventional population-genetic principles embedded within a Darwinian framework of descent with modification are fully adequate to explain the origin of complex protein functions.
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Please support this claim with a definition of subjective vs objective keeping in mind that purpose here means a function we can assign a reason to.
Please address the question I asked. How would you create a specification like Behe’s to determine the shooter was aiming.
(The shooter should) Call the target before looking at the data.
Ever play pool? (“Eight-ball in the corner pocket”)
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