That’s not sufficient to be a nested hierarchy.
The frameshift mutation causing humans and other primates to have a broken GULO pseudogene is something we can positively isolate as a shared mutation.
There are many other examples, such as our broken uricase psuedogene (which causes many of us to have gout), our yolk pseudogenes, etc which all are strong evidence for common descent.
So. It is not an “if we find something that we can positively isolate as a shared mutation”.
We have already found numerous examples, but your cognitive bias does not allow you to accept the abundant evidence.
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But why would a module have slightly different versions? And (this is the important bit) why would those modules each individually show a nested hierarchy, and the same one for different modules?
Since the crocodile data set consists of nothing other than shared mutations I fail to see your problem. I see that you continue with more word salad.
Damn. I wonder if you truly understand what you just said.
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Shhh! I said something similar about Bill but my comment was censored by a moderator. Same might happen to you.
Hi WD
How do you know these are mutational artifacts or purposeful design? The frame shift mutation you show convinced Mike Behe of primate common descent. This was the content of my first discussion with Mike.
Have you thought about the odds of a frameshift mutation getting fixed in a population? Especially one that is deleterious. Do you know what experimental data has shown the differences in alternative splicing patterns are between humans and chimps?
Mike did not have an answer to the problem for the hypothesis this data caused. There are two sides to this argument. My skepticism is due to unresolved contradictory data. These images come from a 2013 paper out of the university of Toronto.
Spliceosome data.pdf (211.7 KB)
“I can write words and post images of graphs. Therefore, I am right.”
Not how it works, Bill.
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So the mutational degradation of the GULO gene in the great apes (including us), which has terminated the lives of millions of people, is purposeful design? What’s the purpose of giving us the GULO pseudogene?
Depends on effective population size. In smaller populations alleles are more likely to get fixed by drift. In larger populations, selection will either fix or eliminate the indel (which cause a reading frame shift). Drift can also do this as well, but is more pronounced in smaller sized populations. This is population genetics 101, something you don’t know about.
Everything I said above applies here too.
We have gone through that data in a previous thread and I exposed your blatant misunderstanding of it. Wanna do it again?
This is hilarious. Even senior undergraduates would easily take you on. The worst part of it all is that you hardly understand any of the things you say.
Nope. You are clueless. Period.
Data you don’t understand.
This isn’t just the great apes. It’s all haplorrhines. And of course when the degradation happened it wasn’t deleterious, since the monkey it happened in got plenty of dietary vitamin C. It’s only when humans started eating diets poor in vitamin C that there was any problem. Bill will never understand any of that, though.
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Wow really?
Bill pulls the Chewbacca Defense!
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What would it take? How do you know if the mechs have not taken over the world and stuffed you into a pod where all your senses are controlled by the matrix? How do you know you are not an avatar in an alien video game where he who dies with the most yields the most points? How do you know you were not created last Thursday with memories intact? How do you know God did not create dinosaur fossils as a test? At some point, you have to go with what is reasonable.
Design proponents claim that we simply do not know the function of all the DNA which may not be directly involved in coding or identified regulation. Here you suggest the GULO deletion segment could fulfill a purposeful design. The problem with that idea is that this is not a stretch of DNA for which we do not know the function. The question posed by the GULO deletion is not just, “this seems to have no function so why would anyone design this?” We do know what the purpose of this DNA is. There is not some mystery or ambivalence. We know what it is supposed to do, we know how it is broken, and that it is useless for anything else. The “maybe it is a purposeful design” counter argument doesn’t make sense, because it does have a purpose and to that purpose it is non-functional.
The odds of getting a particular losing lottery number are the same as the one that wins. How many frameshift mutations have happened, but not been fixed? Perhaps millions? Some mutations must be fixed.
But you raise a good point. John Woodmorappe and Jeffrey P. Tomkins have reasoned that the shared mistake of the vitamin C deactivation is just a case of lightning striking twice, and that the ape and human mutations were independent. As you suggest, the odds are against such mutations being fixed. To have it happen independently, and in exactly the same way, are very much greater than a common instance and is really devastating to their argument.
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I am not sure about whether this noise or not. I am not a big fan of the junk DNA argument as we are in the first inning of really understanding the cell and its functions. Primates may share common ancestry but I think this hypothesis which some claim is a fact has not yet been throughly tested yet at the molecular level.
The data I posted that showed only 50% common alternative exons between chimps and humans is certainly problematic to the hypothesis. Some argue most alternative splicing is noise. It maybe and it may not be. I do know alternative splicing errors are implicated in many cancers. Sorry in advance this paper is paywalled but the abstract and key points are open.
https://www.nature.com/articles/s41571-020-0350-x#citeas
@RonSewell here is a current paper that discusses prevalent alternative splicing during development. Since cancer is accompanied by up regulation of developmental pathways this makes sense.
https://www.nature.com/articles/s41588-021-00851-w#citeas
@RonSewell additional hypothesis on vitamin c.
I know but I just mentioned the great apes.
Sure. However, it was deleterious for those descendant monkeys who couldn’t get adequate dietary vitamin C.
That doesn’t surprise me one bit.
I disagree. How can you be certain?
No, Bill, “some argue” is a gross misrepresentation. The data indicate that most is noise.
Big difference.
But you haven’t looked at the data.
Which is not very relevant, as you haven’t defined “alternative splicing errors.”
I’ve shown that a retroviral insertion causes a mutant phenotype by altering splicing.
Ignorance is not his main problem. Thru this group, he has been exposed to more information than the average layperson could expect to receive in a lifetime.
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By necessity I have not quoted @Michael_Okoko’s complete comment. Any errors in the quote attribution are mine - but I think I fixed it now.
I think he is being wilfully ignorant.
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I don’t believe there is anything inappropriate about telling a person why he has failed to comprehend his own arguments and the objections we raise against them.
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But name-calling is unnecessary.
That is not name-calling. 