I have provided two competing papers on the subject that provide models for gene duplication and variation finding new function. The papers do not support this mechanism accounting for the gene diversity in vertebrates. It shows very limited change is viable in prokaryotic cells.
It does not mean there is no other mechanism.
The problem as I see it is reproductions mechanisms and populations tend to reduce random variation. This contradicts the gene and chromosome data that shows lots of variation. https://doi.org/10.1110%2Fps.04802904
These papers review a current mechanism (gene duplication and divergence) that claims to account for new genes. They build a feasibility model based on this mechanism.
Again are you claiming that these papers support new genes being formed in vertebrates by gene duplication and divergence?
It means that you haven’t shown any observations not explainable by known mechanisms.
No, they don’t. Behe attempts to explain a pattern that IS NOT observed and therefore does not need an explanation. Lynch then points out that even if you accepted Behe’s nonsense, he’d still be wrong.
Because you’ve never presented anything coherent.
Name an observation not explainable by known mechanisms.
Show the mathematics for known mechanisms failing to explain it.
Then, and only then, will you have a point. Until then, there is no problem.
Ah, so your response to my demand that you support your claims is to say that I haven’t supported mine. Why do I need support but you don’t? And of courses there is indeed a model, a very simple one: evolution on a tree, unavoidably producing a nested hierarchy.
You still confuse the pattern of differences among taxa with the mechanism of mutation. Based on experience, there is zero chance you will ever understand this.
This is your job to show they are explainable. The two papers show long times to fix only two mutations. This is a very big obstacle for a natural explanation of the Howe Venn.
When you, as an evolutionary biology student, ask me to prove a negative it shows there is currently no real theory to defend.
The current mathematical models explain how populations change. They do not explain the origin of those populations.
To show what is explainable? You haven’t presented anything in need of an explanation. Why is this complicated for you?
They show long time to fix two specific sequential mutations, which is not an actual observation of how evolution actually works. So the long time is not a problem.
This has been explained to you repeatedly, by myself, by John, by others. There is nothing about it not compatible with normal variation.
Mathematical incompatibility of a model with an observation is not a negative. You don’t even understand what you are talking about.
You and John have not showed a model of how the gene patterns in the Howe formed. The papers by Behe and Lynch show an obstacle to an existing mechanism of gene duplication and divergence. It is your job to come up with a mechanism that explains the pattern. If not then a person with integrity would admit the current single origin event model may be wrong.
As you, John and others have been unable to do this I think separate origins is currently the most coherent model.
Yes, we have. Normal reproduction will produce that pattern.
No, they don’t, because the mechanism Behe discusses is not how evolution actually works. There are no actual observations consistent with the ‘problem’ Behe describes, so there is nothing in need of explanation. If you disagree, you show the math.
If you can’t show a need for anything beyond normal reproduction, there is nothing for me to do but mock you. So show your math or stop lying.
That they are not currently explained is also a claim that requires a burden that you will doubtless also refuse to support…
For you to say that they are not currently explained means that you have made a reasonable examination of the current candidate explanations, and have mathematically excluded them from consideration. Have you done this?
I am doing this now and look forward to you demonstrating a model that works. So far John’s explanation is gene gain and loss. The next step is to show how those changes became fixed in the populations. This is why I referenced the Behe and Lynch papers that attempt to model these changes.