Ah, so you reject my test. Should have done that before getting the results. Now it looks as if you’re trimming the result to fit your desired outcome.
Why?
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Interestingly, GenBank shows mouse and human WNT4 as identical. Why does Bill find them 1% different?
They are 99% identical. You did not set your test to be 100% identical.
With common ancestry and gene duplication we would not expect this level of divergence given the preservation we see between species.
I used uniprot.
And they get more dissimilar the more distantly related the species are. By the time we get to cnidarians, they’re ~45% identical to humans or other mammals.
Well technically we don’t know, but regardless it’s irrelevant because the size of the nonfunctional space isn’t what matters for divergence of proteins that retain function.
So you’re okay with a couple of mutations having fixed in the divergence of mice and humans. So if we had approximately ten times as much time to diverge, we could expect approximately ten times as much divergence?
When were mice created again, Bill?
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How many over what amount of time? Give math.
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By what math?
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So you don’t know what “identical” means? Not surprising.
Not good enough. I asked why, not what. What level of divergence would we expect from common ancestry? What level of divergence would we expect from separate creation?
Are you absolutely sure you used it correctly?
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I get 98.86% human-mouse Wnt4 with uniprot.
https://www.uniprot.org/align/clustalo-R20230729-182009-0327-88718502-p1m/percent-identity-matrix
Even Genbank shows there’s 1 amino acid mutation in Pan compared to human for Wnt4:
https://www.ncbi.nlm.nih.gov/protein/BAC23080.1?report=fasta
https://www.ncbi.nlm.nih.gov/protein/XP_524597.5?report=fasta
https://www.ncbi.nlm.nih.gov/protein/AAA40566.1?report=fasta
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We would expect consistent divergence from common ancestry and gene duplication.
This is based on preservation level and mutation rate.
Instead we see an unexplained inconsistency between cell types. Given the single origin hypothesis starts from a single WNT ligand.
This again is explained by different designs for different cell types.
WNT and Frizzled are also part of a regulation system it makes sense that a WNT specified for one cell was designed not to bind to frizzled specified for a different cell.
I have just skimmed this paper but it shows the regulatory nature of the WNT beta catenin pathway.
What is consistent, as opposed to inconsistent, divergence?
What does that mean? Different cell types are different. And?
What does “start from a single WNT ligand” mean? You’re blathering.
What is [this] that is explained by different designs? What designs, where did you find them?
Guys, look, here’s a collection of irrelevant factoids that takes up space in my post and makes it seem larger and more technical. Cargo cult clownery!
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But GenBank also shows human, mouse, and rat as identical. It’s clearly an unusually highly conserved protein.
https://www.ncbi.nlm.nih.gov/tools/cobalt/cobalt.cgi
Apparently I can’t link the actual alignment, just the page that lets you do alignments. But pick human, mouse, and rat Wnt4 to see.
Hey, I’ve compared the alignments. GenBank shows the differences; it just fails for some reason to mark them on the alignment. What the heck?
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More word salad. Do you never tire of it?
Yeah I was confused by that too. I had to go to Alignments instead of Graphical overview, and pick identity to see the differences:
The most logical explanation for the WNT sequence divergence between cell types is they were designed that way. Gene duplication and a high level of preservation should result in similar sequences between cells.
Were they designed to be cell type-specific? ARE they even cell-type specific?
Why is that the most logical? And note that this is not divergence between cell types. It’s divergence between genes and the corresponding proteins. But why should those genes and proteins be similar at all? It seems that design can account for any degree of similarity or difference.
This is true but there is evidence that different WNT’s are expressed in certain tissues.
If their origin is from gene duplication plus an environment that that is resistant to sequence divergence then you would not expect the divergence we are observing. These genes have not been found in single celled organisms or plants.
Here is a paper that speculates about the origin of the WNT family.
Why are you assuming it is “resistant to sequence divergence”? To what degree?
That is just a question-begging assertion. You are merely asserting what you should be working to substantiate.
Do the math. Oh wait, you can’t do any math, so you’re just typing worthless crap with no way to back it up.
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Wow how nice, a reference out of nowhere that supports nothing you’ve said but, hey, surely that made your post look a bit more sciency.
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That’s why you should pay more attention to what you’re saying. Try to say what you mean, not its third cousin. You will be somewhat more comprehensible and seem somewhat more intelligent.
This doesn’t address my question at all, so I have preserved it in case you want to have another go. And “environment that that is resistant to sequence divergence” is more gibberish, even if you eliminate the duplicated word. I’m not sure why you consider their absence in protists and plants to be significant either, nor what you are getting out of the linked article, but the abstract already falsifies your claim that Wnt genes are not found in protists.
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