Hi Tim
Thanks for the suggestion.
That was more word salad, but it won’t take much to make it sensible: just replace the first “between” with “of”. Why are humans in the same row as white-tailed deer? Doesn’t make sense. And I think your count may be wrong.
As it happens, I don’t think it does. But we don’t necessarily expect that anyway. In order for that to be true, there would have to be a strict clock, in which both sequence change and gene loss and gain happen at the same rate in all taxa. Note that phylogenetic trees are not built using “sequence similarity”. Not a good assumption.
Not relevant to the data we see here. And of course the mere existence of copious junk DNA falsifies your expectation.
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A mostly blank page with a few labels and numbers on it-with no connecting reasoning, argument, or explanation-as a metaphor for how Bill thinks?
Yep. Checks out.
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The human and white-tailed deer being in the same row is because they are the second closest to cattle in phylogenetic relationship and gene similarity. I did a recount and the counts are right.
A molecular clock is an important part of the theory. Without it how do you predict change?
It is exactly what we would expect with the divergence of the order between phylogenetic relationships and gene similarities. It also what we would expect from a divergence of chromosome counts creating purposeful reproductive isolation.
Junk DNA (if it is a real concept)has nothing to do with this as we are talking about the part of the genome that contains biologically active function.
But they aren’t. On that tree, if we prune it down to just 4 species, the white-tailed deer is second closest and the human is farthest. If we use the bizarre distance measure you have chosen (number of genes that a cow has but the species being compared doesn’t), the numbers are musk deer 1075, white-tailed deer 405, human 661. So your count for the white-tailed deer was off. Now, this does conflict with the phylogeny if you force a clocklike gain/loss regime, but that’s a poor assumption. And the excess in musk deer is easily explained by a high number of gene losses in that lineage, which if you look is confirmed by the tree: look at the number of contracting gene families in the musk deer lineage, much higher than on any other branch.
Or, better explanation, you counted wrong twice in a row. Don’t know why.
Word salad there. No, a molecular clock is not part of the theory. Don’t know what you mean by “predict change”.
You have no justification for this expectation, which presumably is only your expectation because it’s what we observe. If we observed something else, that would be your expectation. This is not science. Why should different rates of gene loss in different taxa be expected under design? What makes you think the gains and losses are all carefully tailored to some kind of function, other than that you imagine it to be that way? And why should this tailoring to function affect gene sequences and gene existence differently?
The only thing purposeful there is the word “purposeful” dumped into the sentence with no justification. Nor is reproductive isolation a function of chromosome counts. It may be partly a function of karyotype and all manner of other genetic differences on various scales, but that often leaves chromosome count constant. Once again you conveniently expect what you see and your expectation is determined after you see it.
But why would a carefully optimized design contain junk (which is indeed a real concept, one for which there is very good evidence)? Why wouldn’t the active part be the only part? If a genome were designed, it wouldn’t have any junk. I can see why you would want to avoid thinking about that.
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We have agreement in the conflict. I disagree with your assertion which dismisses the conflict.
There is also gene gain. Easily explained “gene loss” is rhetoric. Where is the model that shows this is likely within the evolutionary time frame? How would you create a model without a molecular clock which has a consistent mutation rate.
I counted the wrong 4 genes. I agree with 405.
This has been abandoned? Neutral theory is no longer relevant? Population genetics is no longer relevant? I don’t see how we have a theory without a predictable mutation rate?
With design there is no gene loss. There are different gene arrangements by design. This is then the starting point for population genetics.
Many reasons such as redundancy in the design. Nucleotides used as timing spacers vs relevant sequences. Some degrading from the original design due to mutation.
No, we agree on the values of certain numbers. You don’t know what conflict would look like.
Yes, there is gene gain, but that’s not how you explain the particular features of the data you were talking about. Now, I’m willing to bet that those losses weren’t clean deletions, and that some remnant of most of them would remain in the genome for quite some time. How would your idea account for pseudogenes? But of course this introduction of gene gain is just you changing the subject to distract from your inability to deal with the subject at hand. There are of course models in which the mutation rate is allowed to vary among branches, but more importantly we don’t need a model in order to see the pattern in the data, and the pattern is what your idea can’t explain no matter how hard you squirm.
I’m afraid you know nothing, and your questions are senseless. There is no single molecular clock, not for all areas of a genome and not for all taxa. Mutation and substitution rates vary depending on many factors. You don’t see, period.
All you’re really saying is that whatever we see is what always was. But that’s not a prediction, just a declaration without any attempt to justify it. Why should design predict that different species should differ in just the ways we observe? Where’s your model?
None of that works in explaining 90% of your genome. “Redundancy in the design” is meaningless verbiage. Only a very few sequences could function as spacers. And you would need to explain why the pattern of degradation in different species follows a nested hierarchy, as well as why so much of the genome is degraded without fatal consequences.
Gene gain is in the diagram. You should have mentioned it.
The proposed model is multiple origins of different deer species. This model fits the gene and chromosome arrangements as it looks likely that the fixed gene arrangements do not change much if at all after their origin.
Why is this surprising since we are struggling to explain the variation beyond speculation with no explanation beyond gain and loss?
Introns are spacers and they are 25% of the genome. Now were at 35% so I think your argument is not very strong. You are a long way from demonstrating much of the remaining 65% is not functionally important especially during embryo development and other non static functions like repair of an open wound.
When you say we struggle to explain the variation beyond speculation with no explanation beyond gain and loss, exactly what do you mean by that? Is variation not the same as gain and loss? Is having an account for how and why gain and loss occurs initially and propagates through the generations insufficient? What would be? What is this “beyond” that you are looking for, exactly? How is understanding of the phenomenon at hand aided in any way at all by the assumption that instead change is either limited, or illusory, or that variance, rather than having come about by mechanisms the workings of which we can experimentally verify, came about by unspecified means and for no particular reason at all?
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How did you determine this?
That’s like telling someone they can’t explain where rain comes from beyond speculation about water condensing in the atmosphere. Gene gain and loss is the explanation, not speculation.
45% of the human genome is defective transposons, the remnants of selfish genes whose function is just to copy themselves and insert randomly all over the genome. Yes, there are a tiny percent that have function as promoters of genes, but those are a tiny, tiny fraction of the whole. I’m counting about 5 million transposons in the human genome according the 2001 human genome paper. If we say there are 30,000 human genes (which is probably higher than the real number), that’s about 150 transposons per gene. I don’t know of a single gene that has 150 transposon promoters. It’s quite obvious that 45% of the human genome is junk in the form of defective transposons.
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Look! There’s Halley’s Comet!
If that’s a model, then common descent is also a model, and yet you demand a different sort of model. Why?
In what way does this “look likely”? Show your work, if any.
But you have no explanation at all, so why do you demand so much more from others? But again, this is not speculation; it’s inference from the data, which fit the prediction of common descent but not of separate creation.
There is no evidence that introns function as spacers. Many genes lack them entirely and work just fine. And many introns vary enormously in size from species to species, with a lot of that variation due to broken transposons. How is that not junk?
We could argue about the evidence that most of your genome is junk, but I’ll just refer you to Larry Moran’s book What’s in Your Genome? for more information. Warning: some of the evidence is phylogenetic so you will refuse to look at it, but there’s other evidence too.
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And we routinely remove all of them, or all but one, when we make transgenes that are expressed just fine in mice.
So, Bill, yet another empirical prediction of your ID hypothesis (which you falsely stated as fact), is falsified. How many falsifications do you need before abandoning it?
How genes are gained and lost in populations is not explained. It is a very complex problem to get all these changes fixed in the populations of white tailed and musk deer we are observing.
The obvious alternative is that the animals gene and chromosome arrangements are almost the same as they were at their origin.
This is the original question. If we base our analysis on common descent of white tailed deer and musk deer being true then it is logical to invoke gene gain and loss.
If you instead want to test common descent of deer vs separate origins then you need to invoke population genetics to explain the differences in gene and chromosome arrangements.
Not true at all. We can see it happening, by looking at polymorphisms, which even you ought to accept, and comparisons among closely related populations and species, which you ought to but won’t.
Ah, but you can’t explain their origin. You have no model. And you can’t explain the distribution and nature of differences among species, which common descent does quite well.
Sorry, but you don’t. The distribution and nature of differences matches what would be predicted from common descent, so that’s a test. That’s enough to tell us that it happened. Population genetics would have something to say about how it happened. Two different things.
You, on the other hand, have nothing to say about either in regard to your “separate starting points”.
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You’re assuming a relationship.
I am not trying to explain their origin because it appears to be out of the reach of science. Like atoms it appears we need to assume white tail and musk deer origin at this point.
I agree the gene and chromosome patterns happened. The process is still foggy.
Only to you, apparently.
I think that at this point your increasing desperation is evident to anyone reading you. You ignore the point about polymorphisms, which require no assumptions of relationship other than that the members of a population are indeed related. Do you deny that assumption? It’s true that cross-species comparisons do require the assumption that a tree exists, but that itself is a conclusion from independent sources of data, not as you seem to think, just an a priori guess.
Actually, we know the origins of atoms too. Surprised you don’t know that. But you are trying to explain the origins of deer species: you claim that they’re independently created. The only reason that’s beyond the reach of science is that the data contradict it. If it were true, there would be ample evidence.
I have to assume that’s an intentional misunderstanding of what I said. Shame on you. And again, your desperation is clear.
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Yeah, I don’t understand what you mean by that, either, but we can get to it after you make some attempt to addressing the message you formed yours to be a reply to.
That’s fine. Would you kindly address any of mine, though? I mean, you don’t have to, but if you are replying to and quoting from my message, I think it is a reasonable expectation for me to have that you would at least try and say something pertaining to the contents of that message.
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DNA insertions, deletions, recombination, and substitution are explained throughout the scientific literature.
This problem was solved a while ago. It’s a basic part of population genetics.
Since when are supernatural explanations a valid explanation when we have mountains of evidence for natural processes?
We can confirm that gene gain and loss happens independently of common ancestry. It happens. It is no different than invoking water condensation to explain rain clouds.
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Saying mutation happens does not mean it is the cause of an observation. There are many mechanisms that are labeled evolutionary mechanisms. How do we know they are the cause of the observed pattern?