I’m not arguing that such obstinate ignorance is not frequently pathological, nor that it is mutable (it would not be obstinate if it were), just that it is a failure to understand, and thus ignorance – be it ignorance of how evolutionary biology actual works (whether Bill accepts the validity of those workings or not), ignorance of the fact that fish don’t live in dried out riverbeds, or ignorance of the fact that salamis don’t talk.
ignorancen. The fact or condition of being ignorant; want of knowledge (general or special).
No we didn’t. The vast majority of that thread was you digressing onto subjects unrelated to deer genetics – probably because you know absolutely nothing about that subject.
What you say is all true based on materialistic thinking. The problem is materialistic thinking does not match the data in this case. This is actually an incredibly interesting case study.
If you look at the fish missing from your fishing bucket and assume there is no fish-evaporating invisible immaterial gremlin in it that despite having no physical form still manages to effectively interact with the fish you think you remember throwing in there, then a dry riverbed is the only possible explanation and we are simply missing the mechanism of how fish disappear from rivers over the course of them drying up.
The problem as we speak is that there is currently no evidence that this mechanism exists. Without a mechanism that explains the fish-devoid riverbed there is no viable model that supports fish emigration and/or asphyxiation being true.
Hi Tim. I never argued that it wasn’t ignorance but whether it was willfull.
The context:
(Boldface my edit)
Willfullness presumes the fisherman is rational. The point is that salami man didn’t possess the agency to conceive a salami couldn’t speak. And we agree that pathology can produce that belief.
Can we conceive that certain participants on this forum may suffer from pathologies (handicaps) that makes them incapable of comprehending contradictory information in a particular area? And if so, how might one respond to an individual that one suspects suffers that handicap?
It does a great job explaining small differences. What we are observing are not small differences. We are observing protein families with radically different sequences. We are observing radically different chromosome counts in closely related species. We are observing radically different gene arrangements.
There is no model that explains genetic changes beyond a few functional mutations. This is the reality of the current condition of the theory. The models by both Behe and Lynch are limited to a few new function producing mutations. Two in Lynch’s case and six in Behe’s.
The limitation is based on the current mechanism of change (mutation- selection) and makes the single origin model for deer speculative if methodological naturalism is not invoked.
I know I’ve said this before, and I know that there is no point in repeating it for you. But…
It really is very simple: We have a good idea when the most recent common ancestor of any two organisms would have existed.
And for many pairs of organisms their genomes have been sequenced such that we can estimate how many mutations would have had to have occurred in order for them to have both descended from that common ancestor.
We also have a good idea of the mutation rate for various organisms. And we know, as both a mathematical and an empirical fact, that the rate of fixation of mutations is equal to the mutation rate.
We also know that the majority of mutations are either neutral, beneficial or not so deleterious that they could not be fixed in the genome. And that those that are highly deleterious are far more likely to be eliminated from the gene pool before they go to fixation.
With this information we can determine how many mutations would have to have been fixed in order for the two organisms to have descended from their MRCA over the time available, and then compare this to how many mutations actually differentiate them.
There are no instances in which these two figures are incompatible. Thus confirming the evolutionary model.
Simple enough. Small differences, over time, can accumulate into big ones.
What do you mean by “closely related”, given that you deny all such relationships?
Of course there is. “A few” + time. What stops differences from accumulating? If you agree that it can happen over the short term, what prevents the long term?
No, the models both assume that particular mutations that produce particular new functions are necessary. The problem disappears if you a) suppose that many mutations are neutral and b) are willing to accept any mutations that produce any function. The latter, of course, is just a rejection of the Texas sharpshooter; don’t ask what accuracy would be necessary to produce exactly the holes you observe in the barn; ask, rather, what accuracy would be necessary to produce any holes in the barn.
I will charitably assume that you have no clear idea what you just said.
This is based on Kimura’s neutral theory it is not a fact. It relies on most mutations being neutral yet we know this is not true in the case of many genes. The Lenski experiment had billions of single mutations occur but only 70 became fixed. Alpha actin has no fixed AA substitutions in all mammals despite hundreds of millions of separation between certain mammals. Many others have much fewer mutations than neutral theory would predict.
To explain the ancestral connection between animals you need to explain the origin of different genes in most cases.
This is what we are hanging on to.
The models (Behe Lynch) show functions that are mission critical to living organisms. The any functional will do argument is not based on how biology works. Coordinated binding is critical for sustaining living cells basic function such as energy production and replication.
No, it has nothing to do with Kimura. It’s a straightforward mathematical derivation
well within the capability of anyone who can do high-school algebra.
In real populations, there is polymorphism. There are multiple variants that only in some cases cause disease and one (R312K) that AFAIK has yet to be associated with any abnormality.
So your claim remains empirically false, because these human beings with variants are mammals.
Stop fabricating. Instead, test predictions of your ID hypothesis. Every one that you’ve come up with so far (and misrepresented as fact) has been falsified.
Polymorphisms are not fixed sequences they are variations inside a population. The only data we have is the consensus sequences for fixation.
You are not seeing the forest through the tree here. The fact the consensus sequences to animals separated by over 100 million generations align perfectly tells us these mutations are far from neutral.
This is compared to consensus sequences to different MYH family of genes that have very little alignment.
That’s just a lie, Bill. We have a massive amount of data for cardiac sarcomeric proteins. I know this, because unlike you, I have published some of it.
Please stop with the arrogance and dishonesty. Please stop claiming that WE don’t know things, just because YOU can’t be bothered to learn the basics.
Straw man. No one is claiming that they are. There is an obvious reason why the actins are subject to severe selection and why the hundreds of proteins that interact with them are subject to much less.
The answer to my question is actually provided within it. I predict that you are so blinded by your own arrogance that you can’t see it.
Yet myosins are orders of magnitude MORE functionally complex than actins. There’s an obvious reason for that, but it escapes you. You are blinded by your arrogance, Bill.
To the best of my knowledge Kimura is the first to introduce this mathematical concept to evolutionary theory. The key was the assumption that most mutations are neutral.
