Build that wall! Build that wall!
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And make Bill pay for it!!
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More word salad. What do you think it actually means?
Note that these are hybrids between individuals with massive chromosomal divergence, not just one difference. Nothing relevant here.
What part of “massive” is unclear?
I am unable to parse the nature of your ignorance here. You seem to be saying that evidence for X does not confirm X, and yet that seems so nonsensical that you must be saying something else.
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The divergence is allowing for hybridization and the male hybrids are sterile. How do you think this helps with fixation beyond the sub species level? These results among hybrids are highly deleterious.
What you call “evidence” does not confirm the hypothesis that all deer share a single ancestor.
Nothing you have said here makes any sense. This divergence is extreme and has no resemblance to the effects of single fusions, which is the actual subject. Further, “beyond the sub species level” is meaningless. If a karyotype that causes hybrid sterility becomes fixed in a subspecies, that subspecies is now a full species, by definition.
Why not? Isn’t it evidence? Why not?
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Then how do you explain the existence of all these mouse populations with different chromosome counts? Are you saying they don’t share common ancestry?
You failed to explain why it doesn’t confirm the hypothesis.
Will chromosomal fusions produce degenerate centromeres and preserve synteny seen in the unfused chromosomes? Yes/No?
Will the chromosomal fusions follow a nested hierarchy if they are passed on from a common ancestor? Yes/No?
Could the non 2n=40 mice instead be considered variants of M musculus with 2n= 40 chromosomes? This appears to make more sense then calling them new species at this point.
What do you predict will happen with these populations given the male hybrid species are sterile and the female hybrid species produce less offspring?
The tree is only one way to look at the data. Another way to look at the data is the gene Venn diagrams which support the multiple origin hypothesis as it explains the different gene patterns among the species.
It’s like a broken record player.
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Common ancestry can easily produce those Venn diagrams. You have yet to explain why the multiple origin hypothesis would necessarily produce:
- Degenerate centromeres and preserved synteny as seen in unfused chromosomes.
- A nested hierarchy of chromosomal fusion events.
Common ancestry explains all of the evidence which is why it is the best explanation.
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Depends on what you mean by a species. If there’s no such thing as speciation, then all descendants of the “wild type” mice would still be Mus musculus. But if there’s speciation, meaning the evolution of reproductive isolation between populations, and hybrids between the two populations are sterile (or dead), as in the paper you cite, then it makes sense to call them different species. Note: we’re not talking about just any variants; we’re talking about the massive differences in that paper.
I predict that they’ll be separate species, and in fact that reinforcement will result eventually in pre-mating isolation
You’re wrong about that. The Venn diagrams support common descent. Remember what I showed with the Howe diagram? Note, by the way, that “the data” we were talking about included a lot more than the tree.
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How do these populations survive with sterile male mice?
I don’t think you have a good argument to back up this assertion.
There is no evidence that I am aware of that reproduction and natural variation can change gene arrangements (different gene families in the Venn diagram) especially if new genes are involved. The gene patterns always being part of the species makes more sense.
They don’t. The sterile males are hybrids between populations. So only mating between populations is selected against. Mating within the population is just fine.
What you think is not closely related to actual reason.
Well of course there’s evidence for that, but this is back to your fundamental misconception. The source/cause of variation is not relevant to common descent. Only the pattern is relevant.
Then why do they follow a nested hierarchy?
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Wow, Bill. That mistake was amazing. How can you have an informed opinion if you can’t even track which mice are sterile?
How then will the populations without 2N=40 compete against the populations with the 2N=40 populations given some of the mating scenarios lead to a dead end. After so many years why is 2N=40 still the dominant population?
Without the source/cause of variation you do not have a good case for a single ancestor unless you can show the reproductive process producing new genes.
If the population of mice with different chromosome counts have different gene patterns this would go a long way to support a single origin for species that are similar like deer.
Common ancestry and evolution can easily produce those gene patterns through gene loss and de novo evolution of genes. You’ve been shown this hundreds of times.
And you are still ignoring the evidence.
You have yet to explain why the multiple origin hypothesis would necessarily produce:
- Degenerate centromeres and preserved synteny as seen in unfused chromosomes.
- A nested hierarchy of chromosomal fusion events.
Common ancestry explains all of the evidence which is why it is the best explanation.
Dominant where? Have you been paying any attention at all? You keep making nonsensical pronouncements that depend on fantasy scenarios that exist inside your head and nowhere else. It’s hard to figure out just what your fantasies entail, and so it’s hard to respond.
That’s your misconception in a nutshell. The evidence doesn’t depend on knowing the source of variation. It depends on the pattern of variation. And of course if we follow your logic, you don’t have a good case for multiple ancestors, because you don’t know the source/cause of variation in created kinds. And it’s worse for you, because you also have no explanation for the pattern of variation.
What does this mean? On the surface it seems exactly opposite from your previous position. But I don’t know what you mean by “gene patterns”.
Do you disagree that the most common chromosome count is 2N=40.
The cause of variation in the multiple ancestor scenario is different designs. A purposeful arrangement of genes to create a unique species.
In the Venn diagrams different species have shared and non shared genes. This is what causes the pattern. If species have all the same genes or no shared genes then there is no Venn diagram type gene pattern.
Have these mice populations with for example 26, 24 or 22 chromosomes generated any new genes?
No, but what does that have to do with anything?
That’s not an explanation, just a handwave. They’re different because they were made to be different. Can you see how that means nothing? And it doesn’t explain why the differences show a nested hierarchy.
No, that’s not the cause of the pattern. That is the pattern. And the pattern is a nested hierarchy. Why?
I don’t know of any data on that question, though it seems likely. Why?
It shows despite the observed variation the n=40 count is conserved. The other variations are likely deleterious.
It’s an explanation that supports why we observe such genetic differences between species. It explains the Venn diagram.
It’s the cause of the pattern. Without shared and unshared genes you will not get the gene Venn diagram.
The pattern being able to form a tree is much less informative then the Venn diagram as you have no explanation (independent of the tree) of the origin of shared and unshared genes when you converted the pattern from the Venn to the tree.
I think given it is likely that these chromosome changes are simply mutations from the reproductive process then this would test reproduction and natural variation as a source of new genes.
I have not found any data yet either.
Then why even bring it up? You’re just blathering again.
As expected of common descent.
As John has been explaining to you now for more than three years, we technically don’t need to known (though we do know, it’s evolution) how genes are gained or lost (magic, mutation, whatever) to know it is their distribution in species that is evidence for common descent. The tree is the expected pattern from common descent. The distribution of genes conforms to a tree. The trees derived from different types of data (sequences, gene contents, comparative morphology etc.) are highly consilient. It’s common descent.
No it doesn’t. To explain the Venn diagram you need to actually explain every single number in it. Why those numbers? Why distributed in that way? Which gens and why? That would be a “design” explanation for the Venn diagram. And then you need some sort of test of the explanation. Like if you’re going to say certain genes in certain numbers are in certain species because they’re necessary, you need to show that in some way.
Just making assertions that “it is so because it’s what the designer wanted” explains nothing. It’s like the kid saying I don’t want to because I don’t want to. Why? Because I don’t want to! Or, “just because.”
Your “theory” of design is literally infantile.
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