Yup. Nearly 600 posts of ‘I think deer must have been created because these numbers I haven’t got and wouldn’t know what to do with anyway feel wrong to me’.
I suppose it keeps him off the streets.
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Given that the only data he seems to have to ‘support’ these claims are his (ubiquitous) Venn diagrams, I’d suggest it is “data I haven’t got” in addition to “numbers I haven’t got”.
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Hi John
While you assume evolution (universal common descent) is true I do not think it is. When I see absence of evidence like that unicellular to multicellular “transition” not showing a path for the evolution of WNT/Frizzled/APC etc it is evidence that supports my inference. For you this is simply evidence that is not available for various reasons.
Similar missing evidence is a problem for the prokaryotic to eukaryotic “transition”. Where the spliceosome, nuclear pore complex and chromosome structure have no known transitional path. While absence of evidence may be tentative at this point it supports the multiple origin hypothesis.
From the paper.
Indeed, they appear to be absent from plants (including Arabidopsis thaliana ), fungi (such as Saccharomyces cerevisiae ), and protists (like Dictyostelium discoideum ), although it should be noted that a transducing pathway related to the canonical Wnt pathway has been reported for Dictyostelium (see later). By contrast, in cnidarians, one of the most basal of the animal phyla, 14 Wnt genes have been identified that belong to 12 of the 13 Wnt subfamilies (15, 16); the Wnt-9 subfamily is not represented, while the Wnt-7 and Wnt-8 subfamilies have two paralogous genes (Fig. 1.2). How these Wnt proteins arose is still an outstanding question.
Your opinion has no probative value.
Have you looked? And no, it isn’t. Your “inference” is your foregone conclusion. It needs no support and can’t have any, since anything is compatible with it.
Why wasn’t that included in your bolding? Why is it surprising that particular proteins are not found in organisms that are very distantly related to animals? Do you in fact have a point of any sort? If so, what is it?
If there are good reasons for the evidence to be absent, then it’s absence isn’t evidence for lack of evolution. To anyone. There isn’t a “private” way to deal with evidence, as if things are evidence to you but not to others. Everyone who considers competing hypotheses must deal with the logic of evidence in the same way.
But those assertions are just false. There are known paths by which those could have evolved.
No, the lack of evidence for hypothesis A isn’t automatically evidence for hypothesis B.
Both hypothesis A and B can be weakly supported by different pieces of evidence.
Hypothesis B must predict something about what the data should look like, and the lack of evidence favoring A should be unlikely on the hypothesis that A is true for it’s absence weaken the case for A. But weakening the case for A doesn’t automatically strengthen the case for B.
You don’t understand the logic of hypothesis testing and evidence.
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Because it is different than your opinion? Does Mike Behe’s opinion have probative value? How does one objectively access an opinion for probative value?
The conclusion is based on Behe’s method. It is limited by definition (a purposeful arrangement of parts). The WNT beta catenin pathway has many parts and its purpose is to help regulate the cell cycle and aid in embryo development.
The subject is the origin of the WNT family of ligands. The previous statement and the chart in the paper shows they are not found in these organisms. Also the statement is too vague to have any value.
When I say no known paths I mean beyond speculation. You can make up a speculative story for anything.
In the case of the WNT hypothesis A is that it evolved in a single cell organism and different versions evolved by gene duplication and divergence. Hypothesis B is that it originated as a functioning (designed) family in multicellular organisms. This is what the evidence currently points to.
The evidence fits hypothesis B independent of hypothesis A.
No opinion has probative value. Data and arguments that draw on data have probative value. You present little of the first and none of the second.
No it isn’t. Behe’s method, such as it is, is supposed to test for design, not separate creation. The design is supposedly of some particular features of organisms, not the organisms themselves.
“Purposeful” has yet to be demonstrated, and I can’t see how it could.
That seems to have little relation to my questions. Also, I can’t see the paper, since it’s paywalled. How did you get access to it?
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Let’s see if this works.
Evolution of the Wnt Pathways - PMC.pdf (1.3 MB)
Yes, it works. Thank you. Definitely, more data are needed. The phylogenetic distribution and relationships of the various Wnt genes should be dtermined based on much denser sampling, especially in sponges, cnidarians, ctenophores, and choanoflagellates. I would suspect that other elements of the Wnt pathways will be found in various non-animals in addition to Dictyostelium. What we see already looks a lot messier, and a lot more hierarchical, than one might expect if every species were separately created, but of course you have no test for separate creation, since you have no expectations. That there are even homologies among different genes would be unexpected, as far as I can see.
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There are at least 4 issues with that response.
- All you ever do is offer untestable stories to account for something. “It was designed” fails your own criterion for rejection here.
- Evolution makes testable predictions, such as the existence of simpler precursors for many of your favorite eukaryote features in their closest related prokaryote cousins.
- The emergence and diversification of duplicate genes are observed facts.
- It’s ultimately irrelevant to common descent, since even if the genes were designed and put into some ancestral organism, it could still share common ancestry with other organisms.
That isn’t a response to what you quote me saying. It just is logically unassailable that even if evidence favoring hypothesis A is lacking in some instance, that is not in itself, necessarily, evidence favoring hypothesis B.
It is not a meaningful response to just state what you think hypothesis A consists of.
That’s just an assertion. You have stated no fact of the matter with respect to the wnt gene family that is uniquely, or most likely, predicted by the hypothesis that they were designed and put into some organism.
But even if they were, that wouldn’t be evidence against common descent.
You understand nothing about the relationship between hypothesis testing and evidence.
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What we see is no appearance of the WNT pathway prior to multicellular animals. This is evidence for a separate origin of multicellular animals vs single celled eukaryotes.
This fits Behe’s method of a purposeful arrangement of parts allowing design to be inferred. Purpose in this definition is an identified function for which we can assign a reason.
Kinda expected that a topic about the relatedness of “deer” would eventually devolve into a rehash of “irreducible complexity” once the original premise became impossible to defend and the goalposts needed shifting.
6-12 months from now, the venn diagram will reappear with no apparent synthesis of knowledge from the many previous discussions. It’s how the plot for the movie “50 First Dates” would actually play out in real life and not in a romantic comedy. Lather, rinse, repeat.
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We haven’t looked very far. I have suggested some places to look. And of course we have elements of the Wnt pathway in Dictyostelium, apparently the only protist anyone has examined.
No, it’s absence of evidence. This is nothing more than the tired old “God of the gaps”.
You define a term using an undefined term. And it’s a redefinition that varies from the usual. What do you mean by “a reason”?
As usual you duck the main issue, that separate creation, for you, entails no expectations of the data and explains no features of the data.
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Hmm. Let’s try that with other features:
“What we see is no appearance of” feathers “prior to multicellular animals. This is evidence for a separate origin of multicellular animals vs single celled eukaryotes.”
“What we see is no appearance of” eyes “prior to multicellular animals. This is evidence for a separate origin of multicellular animals vs single celled eukaryotes.”
“What we see is no appearance of” blood-clotting cascades “prior to multicellular animals. This is evidence for a separate origin of multicellular animals vs single celled eukaryotes.”
“What we see is no appearance of” cartilage “prior to multicellular animals. This is evidence for a separate origin of multicellular animals vs single celled eukaryotes.”
So it’s not evidence for a separate origin, it’s only evidence that the WNT pathway, along with feathers, eyes, blood-clotting and cartilage, evolved after multicellularity.[1]
It’s also got absolutely nothing to do with common ancestry of deer.
It is evidence that @colewd thinks anything and everything is evidence for separate origins.
“What we see is” a hamburger with bacon and onions but no ketchup. “This is evidence for a separate origin of” tomatoes from ungulates and root vegetables.
If @John_Harshman is right about Dictyostelium, things get more complicated. Because life is messy. ↩︎
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It’s the appearance of evidence in multicellular species. This has nothing to do with “God of the gaps”. The evidence of the WNT pathway in multicellular animals along with the gene Venn diagrams and the chromosome data is evidence of the separate origin of species.
The separate origin of species explains genes and chromosomes not following an inheritance pattern. It explains the evidence of sudden emergence of complex functions like the WNT pathway, the spliceosome and the nuclear pore complex.
-It explains why zebra fish can share genes with humans that they don’t share with mice and chickens.
-It explains why we cannot differentiate the relationship between deer, humans and bovine by their gene pattern.
-It explains why deer chromosome variation can range from 70 to 7.
-It explains why we see observed anomalies around fish gene arrangements in Winstons paper .
Dicty is both uni- and multicellular, so you’re getting that most basic fact wrong.
That’s yet another falsification of your ID hypothesis.
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Or it is evidence that WNT evolved concominant with the emergence of animals. Or that they were designed and put into a single-celled organism, that went on to make multicellularity possible.
Since the mere observation that the WNT is absent in some species, but present in others, does not in and of itself allow us to discriminate between these options, this pattern cannot be said to be evidence either for or against common descent. We’re going to need more details about the data and compare them to the expectations of different models. Since you have no model that predicts any particular pattern, the pattern of WNT distribution can never provide evidence for it (you can’t have evidence for a model that doesn’t exist.)
Once again your response reveals you don’t understand the relationship between data, evidence, and comparative hypothesis testing.
That’s not a method, that’s just an assertion. Also, Behe is purporting to infer design, not separate origins. He accepts common descent.
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You have never been able to explain how it’s evidence, and you have never been able to explain why this supposed evidence fits a nested hierarchy so well, and you have never been able to explain, well, anything.
But they do follow an inheritance pattern, so it’s unclear what you could mean by that.
None of those can be shown to be sudden. Regarding Wnt, as I said, nobody has looked in the places we would expect precursors. And note that the Wnt genes themselves follow a nested hierarchy.
No, it explains nothing, because you have no prediction of what should happen. Why should mice and chickens lack random genes? Why those genes? And why so few of them in comparison with the genes that fit the hierarchy?
That’s word salad. But separate creation doesn’t explain whatever you’re trying to say.
No it doesn’t, since you have no expectation of what sort of variation we would see in your model. And of course it doesn’t explain the nested hierarchy of the variation, or the ability of fusions and fissions to explain observed synteny.
That link was just a tree with colors on it, with no explanation of what it represents. No idea what it’s supposed to mean. Did you perhaps link the wrong thing? Or is this just another example of you trying to look all sciencey?
Incidentally, I see that Wnt homologs, as well as homologs of other parts of the Wnt pathway, have been found in a sponge:
https://www.pnas.org/doi/full/10.1073/pnas.0604065103
Is that in accord with your prediction? Do you even have a prediction?
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But all you are observing is that it is absent in some organisms and present in later ones. That isn’t evidence of separate origins. As already explained multiple possible explanations for that is possible.
The separate origin of species explains nothing at all because you have no model of how things should be given separate origin of species.
Incidentally the distribution of genes and chromosome numbers supports a nested hierarchy.
So does two independent losses in the lineages leading to mice and chickens, respectively.
Of course, it is the fact that the overall pattern of gene loss and gain fits a tree better than no tree you don’t seem to understand.
You need to consider the entire pattern of genes lost and gained(not just pick out a small set and then ignore the rest) to see that it yields a nested hierarchy, as the number of genes that can be explained with a singular gain or loss massively outnumber the instances where two or more losses or gains had to happen independently, as we would expect on probabilistic grounds if genes were gained or lost stochastically and the state is subsequently inherited.
So the overall pattern supports common descent. It is actually evidence for common descent.
Once again you reveal you don’t understand the relationship between evidence and hypothesis testing.
But it doesn’t. You have no explanation for any pattern. There is no theory of yours that says that we should not be able to “differentiate the relationship” (whatever the heck that even means?) between deer, humans, and bovine, if they were separately created.
But it doesn’t. You have no explanation for that. You just have an assertion. There is no model that explains why chromosomes should be distributed in any particular way. The situation could be completely reversed, and you’d just say the same. There is no pattern of chromosome numbers that is incompatible with the lack of a model.
Yet again there is no explanation for that anywhere in your not-having-a-model-is-a-model. By design.
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