Do all deer share a common ancestor?

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Because there are no data supporting it. To make an inference, you need to start with some kind of premise, and that premise must be supported by something. You have none of that.

Finally. Was that so hard? So yes, different species have different genes. And yet the distribution of these genes follows a nested hierarchy. Why should that be?

How many papers have you seen that make no assumption about that of any sort? Is that assumption necessary to the content of the papers? Is it necessary to the evidence of common descent presented in those papers?

No. What morphological data are you referring to? All you have so far is the word “deer”. We would need to see an actual phylogenetic analysis of a real morpohological data set. Have you even looked?

I’m not appealing to any such theory. That’s just what the data show. The causes of gene loss are neither mentioned nor relevant, but the fact of gene loss is clear. And, not much due respect, you have no idea what I claim, because you understand so little of what people say.

If it’s an incorrect assertion, show how separate creation explains the pattern of synteny. Otherwise you must accept it.

No, it does not. Again, the causes of gain and loss are not relevant to the pattern. Why can’t you understand this simple point?

No, that’s not what you reject. Your assumption is much stronger than that: you assume that common descent is just wrong. You refuse to examine your assumption. I ask again: why do you reject common descent as a possibility? Note that I refer not to common descent with purely natural causes of variation, but common descent, period.

Why? Are you saying that multiple losses are not possible? Note how few of those genes there are in comparison to the number that fit the tree exactly. What’s your explanation for the relative numbers?

What data are you referring to here? I see only one muntjac species in the figure we’ve been discussing.

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OK, let’s say all animals have the same genes. No animals have unique genes.

There is not one unique gene in the entire animal kingdom.

No creature is missing a single gene, and none possesses an extra.

Please explain how there would be differences in phenotype without differences in genotype.

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Nowhere do I state that they can’t be considered separately. I see no reason why they both can’t be considered. Is no writer allowed to discuss both the patterns caused by more than one evolutionary mechaism?

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No problem there. Differences in presence and absence of genes are not the only differences in genotype. Even if every species had the same complement of genes they could differ in the sequences of those genes and in the sequences of regulatory elements. And, in fact, differences in phenotype both within and between species are most commonly due to the latter, not the former. But of course Bill doesn’t know that and couldn’t explain any of it, so there’s no point in asking him.

Of course. I merely ask that they not be conflated, as Bill does, and as your statement seems to.

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We have answered this question many, many, many times.

The inference of separate origins does not explain:

  1. A nested hierarchy of chromosomal fusion events.
  2. Degenerate centromeres in the arms of chromosomes.
  3. Preserved synteny as shown in the unfused chromosomes.

You have only ever addressed the nested hierarchy, and have done so with an ad hoc handwave. You simply state that God just decided to fit species into a nested hierarchy for no apparent reason. That’s not an inference. None of what you have presented is an inference. None of your claims follows from the evidence, but is instead forced onto the evidence with no explanation of why the evidence is the way it is.

Why would anyone see preserved synteny and degenerate centromeres and conclude that no chromosomal fusion occurred and that they were just created this way? Why would these smoking gun pieces of evidence lead to any inference other than a naturally occurring chromosomal fusion?

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Correct, but:

That’s not clear without the regular term “allele,” which appears to be far beyond Bill’s understanding. That doesn’t mean we shouldn’t use the term.

The latter being correctly described as allelic differences. The question for Bill to ponder is, “What proportion of genetic differences between species are merely allelic?”

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That’s certainly one way to describe at least the differences in gene sequence. It’s not generally used for non-genic sequences, though, and they’re probably more important.

I find that more confusing than my formulation, though to Bill everything is just a cloud of dimly seen words.

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That all depends on how one defines “gene” vs. “non-gene.”

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True enough. Do you consider all cis-regulatory sequences to be part of the genes they regulate? What about trans-regulatory sequences? I think either would be non-standard.

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I disagree; yes and no, respectively, acknowledging that the definition of “cis” gets fuzzy.

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I’m just going to own that I put that question sloppily.

Bill has steadfastly begged the question, in that distinct proteins are of course represented in the variety of life, and both genes and regulation are generally involved in differentiating species. So of course we would not have nature as is without distinct genes. Not everything, in fact, tastes like chicken.

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From a Mendelian point of view that tries to relate genotype to phenotype I would consider a promoter/regulatory element and its related transcript to be a single unit of some kind. Operon? Gene? Forcing the mess of biology into neatly defined terms is always going to be a losing battle. The only universally true rule in biology is that there is no universally true rule in biology.

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Let me appeal to Larry Moran, who defines a gene as a DNA sequence that’s transcribed to produce a functional product. Promoter regions are not transcribed, so aren’t part of the genes they regulate.

That’s true to a certain degree. For example, we wouldn’t have trichromatic vision without that duplication of opsins. But the majority of visible differences are not due to new genes, and this becomes more so the more closely related the species are.

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Still, it’s a commonplace that most morphological differences are due to differences in gene regulation, not genes. If the gene regulation is considered part of the gene, the dictum makes no sense.

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The premise is separate origin of deer species the data supporting it is different gene arrangements and different chromosome arrangements.

Simply a by product of design where groups of animals have more similar features and gene arrangements that support those features.

I have not seen any papers discussing evolution that do not use reproduction and natural variation as a working assumption.

I am not sure what you are arguing for here.

The data shows different gene arrangements.

You impose gene gain and loss as an explanation based on your prior that common descent must be the cause of the tree pattern.

The explanation is that design will make groups with similarities and differences. The designs with more similar parts (genes) will group together.

Why do you think common descent explains these patterns?

It is relevant to the Venn pattern.

It’s exactly what I reject.

Data is being reviewed though the filter of a hypothesis that cannot identify the mechanism of change. If the hypotheses turns out to be false so will thousands of papers that rely on this filter (common descent) to interpret data.

The explanation for the relative numbers is that design is responsible for the Venn pattern. The tree you see is a natural output of design where gene arrangements are species specific.

If common descent was true we would not likely see these anomalies that require multiple deletions.

There are two different muntjac species compared. M reevesi and M muntjac.

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I am not sure the point you are making here.

We have gene variation therefore the cause is common descent from a single pair deer origin?

Why could the gene variation not be the result of the original animal design?

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I completely agree. Gene regulation is just as important as the sequence of the transcript. The sequence itself can also function as a regulator such as post-transcriptional regulation by micro-RNA’s. I am firmly on the side of combining the transcribed region with its regulatory sequence. If we want to call that a gene, then I’m find with it. Some people describe it as a “gene and its promoter”. That’s fine too. In the end, it’s just semantics (which is still fertile ground for arguments between scientists). Just as long as there is some indication of what they are pointing to it works.

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That’s supporting data only if you assume that different gene and chromosome arrangements can’t arise within a framework of common descent, even with divine help. Why are you making that assumption? Note that separate origin does not even explain the differences other than by saying “it happened that way”. Nothing.

Nope, not an implication of separate creation. You confuse similarity with nested similarity, and they’re quite different things. Nor have you established that different “gene arrangements” are necessary to produce different features. Evolutionary developmental genetics says it’s not true.

What about papers discussing phylogeny? I don’t recall suggesting any such thing in any paper I’ve written, and I don’t recall seeing it in most papers I’ve read. This is you being unable to comprehend what you read again.

When are you ever? I’m saying that you can’t argue on the basis of morphological data when you have never looked at the morphological data. You made a claim, and I was asking for the basis of that claim, which I am doubting you actually have.

Nope. Based on the existence of the tree pattern. Why is there a tree pattern? Why do gene gain and loss explain the data so easily, while you have no explanation at all?

That’s a vacuous explanation. Any random collection of objects will have similarities and differences. You don’t need design for that. It doesn’t take into account the particular nature of those similarities and differences, i.e. exactly the sort of synteny groups we would expect from chromosomal fusions (and the odd fission).

This seems irrelevant to the topic of synteny and seems focused on phylogenetic data instead. You have no idea what synteny means, apparently, or what the current topic is. And even then, you confuse similarity with nested similarity.

Which patterns? What was that link supposed to show?

No, it’s not. The pattern is independent of the causes of differences.

You really have no clue. Data are sometimes viewed through the assumption of common descent, in fact of a particular tree structure. But that’s not an a priori hypothesis. It’s the result of the analysis of other data. And you can use the data to test the hypothesis. The mechanism of change is irrelevant, so your next bit is meaningless. If the hypothesis is false that would be surprising, since those thousands of papers that tested it should have failed to find it valid. And no, that’s not what you reject. You don’t reject the assumption of common descent. You reject the possibility of common descent and assume separate creation as a default. Why? You won’t say. You can’t say.

Note again that you ignore most of what I say and most questions I ask you.

That explains nothing. Tell me first what relative numbers you would expect under design. Why would we expect most differences to be explicable by single events with only a tiny number explicable by two events? My expectation would be that genes should almost never be gained twice and much more rarely lost twice than once. But you would appear to have no expectation at all.

Why not? Suppose that loss is random, and it’s probably fairly close to random. If hundreds of genes are being lost in each lineage, shouldn’t we expect the occasional parallel loss?

I’ve lost sight of which of many Venn diagrams you mean. Please cite again.

Nobody says the origin is from a single pair. Where did you get that notion?

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Then the observation of different gene arrangements and different chromosome arrangements in mice would indicate they were separately created. We know this isn’t the case. Those mice were not separately created. Your premise fails.

That’s not an explanation for why those similarities and differences would produce a tree pattern. You can have groups with similarities and differences and not have a tree pattern. There are similarities and differences between groups of vehicles, but vehicles do not fit into a tree pattern. There is absolutely no reason why reusing design would necessarily produce a tree pattern.

There is absolutely no reason why design would produce a nested hierarchy in our muntjac deer example either. For each species there could be an entirely different pattern of chromosome arrangement. There is absolutely no reason why we should see the same synteny as that seen in the unfused chromosomes. There is absolutely no reason why we should see degenerate centromeres in any of the chromosomes since they were never the product of chromosomal fusion in your separate origins explanation.

Instead, we see all of the evidence we would expect to see with common ancestry and naturally occurring chromosomal fusions (and the occasional fission). We see a nested hierarchy of chromosomal fusions that we would expect to see from common ancestry but not from separate origins. We see the degenerate centromeres which we would expect from naturally occurring chromosomal fusions but not from separate origins. We see the preservation of synteny associated with those centromeres and fusions which is exactly what we would expect to see from naturally occurring chromosomal fusions but not from separate origins.

There is absolutely no reason why anyone would infer separate origins based on this evidence. All of the evidence is exactly what we would expect from common ancestry and chromosomal fusions.

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Why are you needing to sneak Devine design into the argument? If Devine design is needed it is a separate origin event. This is a claim that a Devine mind was behind the changes how the Devine mind did it is another discussion.

We know different genes can generate different features.

In your paper on flightless birds why did you conclude multiple losses of flight?

They explain it easily only when you assume common descent or a single point of origin.

Synteny does not exclude design as it would be expected from a design strategy of parts reuse including where genes fit on chromosomes.

Does your hypothesis consider the possibility God is required for for these changes?

You have no idea if chromosomal fusion are sustainable in a population of species to the point of becoming fixed in more then a subpopulation.

Why do you think synteny cannot be a product of design?

The link discusses the design strategy of reusing parts.

The mechanism of change is of most importance. The tree or Venn pattern should be used to help isolate the mechanism of change. In the multiple origin of model no mechanism of change is required.

You have already asserted gene gain and loss as the mechanism to explain the gene arrangement differences in the Venn diagram. The problem is that you are counting on common descent or a single point of deer origin to support this claim.

The multiple origin hypothesis does not have to deal with the hard to explain gene gain loss scenario you are describing.

I would not expect a population of species to sustain go the point of fixation any appreciable amount of random gene loss.

http://dx.doi.org/10.1038/s42003-020-1096-9

Single pair or single isolated population.