If you listen to our conversation carefully he does not think common descent fully explains life’s diversity.
The paper has human splicing patterns as a standard and compares vertebrates to that standard. What you will see is the closest to the human pattern is chimps but there is only 50% commonality.
Again, that wasn’t my question, was it?
UCD is a red herring when you are trying to establish common descent between a limited number of species. You don’t have to demonstrate that all species share a common ancestor in order to show that 2 species share a common ancestor. Many times, trying to steer the conversation to UCD is a way of avoiding the evidence for common ancestry between species which is the very definition of a red herring.
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This still comes down to DNA sequence. Differences in alternative splicing are determined by the sequence around the splicing sites, differences in the sequence within genes that control splicing, and so on. There is still large questions as to whether alternative splicing results in functional variants in a minority or majority of cases, and the evidence seems to be on the side of most alternative splicing variants being non-functional and simply the result of sloppy splicing mechanisms.
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How is this a problem?
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It’s good to get a perspective from someone outside of the field. I’d especially appreciate it if you looked at the other thread and offered your opinion on its clarity:
As someone who has done both protein engineering and studied the activities of pathogenic mutants, the latter in inherited cardiomyopathies, I’d say that focusing on nylonase obscures oodles of other relevant data.
For example, in inherited cardiomyopathies, when a new mutant (changing a single amino-acid residue in one of the muscle proteins) is characterized after a teenager dies on the basketball court or the soccer field of hypertrophy and sudden cardiac death, the half of her/his family subsequently found to be carrying the mutant allele is usually normal or subclinically abnormal. So one person’s lethal mutation is her brother’s asymptomatic polymorphism. There’s no bright white line.
The bottom line (mixing line metaphors) is that there’s a lot of wiggle room, even for the complex, highly adaptive, and fast mechanism of cardiac muscle.
Does that make sense?
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I’d agree with @T_aquaticus that it doesn’t seem to be a “problem” for common descent between humans and chimps, as most specific AS events probably represent non-functionally important noise. Most of the differences in the AS patterns between humans and chimp seem to be differences among rare splice events - those most likely to represent noise.
See:
I agree completely. In addition to sloppy splicing, we have sloppy transcription, neither of which suggest intelligent design. Most of this doesn’t get published as it is negative.
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I think you guys need to study AS’s prevalence in embryo development. Cancer often occurs when embryo pathways are activated. Look at pub med and see its prevalence in cancer and other cases. 7000 hits on alternative splicing and cancer.
No one is saying that all splice variants are non-functional, only that a majority are non-functional.
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What issues? I’m curious.
Wow. Where did that come from? Do you want to try again?
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What the…
Attention Moderators.
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Good call on the flags. The trash has been taken out.
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The CNV differences between identical twins is miniscule compared to the differences between two other humans.
Hello, George. Thanks for asking for me.
I still exist, but have been very busy doing a variety of paid work, including teaching a course on some of this stuff. Also, I’ve had less motivation to reply in the past week or so, since the last people I engaged with haven’t given me follow-up replies. I was interested in Daniel Ang’s thoughts on my proposal to relocate (not omit) the evolution unit from ninth-grade biology, as a means of avoiding wasteful culture war, but I guess he got too busy with his grad work and couldn’t continue that conversation, and I was having a good conversation with Glipsnort about what is core and what isn’t core in Christianity, and we were making some headway to a common view, but I didn’t hear further from him, and I asked Allen Witmer Miller for some of the scientific and theological peer-reviewed work he said that he had published, as I was interested in his theoretical approaches to those subjects (myself also having training in Old Testament scholarship, for example) but again, there was no reply, not even a private one. So with no replies outstanding, I used my time to do my day job – which all things considered is a better away of using one’s time than internet debating anyway.
Regarding Behe, he has said any number of times, both in writing and interviews, that he accepts common descent, including the descent of the human bodily form from primate ancestors. So that he accepts common descent is not debatable, and I don’t know why anyone would say that he didn’t – unless they have had very recent private conversations with him where he has indicated that he has changed his mind and now thinks that some species were created miraculously, with no biological ancestors. (Of course, as a Catholic, Behe will accept that the individual soul of each human being is specially created, but that is a different matter, and not in contradiction with the common descent of human beings with other animals on the bodily side.)
On the question of mechanism, of course, Behe dissents from most evolutionary biologists, in believing that the set of proposed mechanisms commonly accepted (mutation, selection, drift, etc.) would not be sufficient, outside of a design framework, to produce the observed results. But for Behe it isn’t an automatic inference that design implies miraculous interventions, and I already linked to a detailed discussion of his on the Discovery website concerning that question.
So I don’t think Behe is “agnostic” on common descent – he thinks the evidence points to it. He doesn’t engage in over-the-top statements about it, e.g., he doesn’t say that “common descent is as certain as the law of gravity” or the like, but he is pretty certain that common descent is real.
The case may be different for Ann Gauger; she may be truly agnostic regarding common descent, i.e., she may be genuinely uncertain whether or not common descent (in the full-blown version, i.e., bacterium to man) actually occurred. As far as I can tell, in her recent statements she has neither affirmed nor denied macroevolutionary change. But she can speak for herself; I don’t want to put words into her mouth.
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That’s not my position.
@T_aquaticus
A mutation occurring in real time under realistic conditions that provides a new, beneficial function–that’s not a new gene, but I’ll grant you that–no, that would be evidence for evolution. But note the qualifying “realistic conditions.” The experiments I know where new genes are claimed are done under conditions that are far from realistic. And a single mutation is always within reach in evolution.
If a new function were to occur that required four mutations, all of which were neutral or deleterious until all occurred, that would strongly suggest intelligent design.
@gbrooks9
You still haven’t got my position straight. I am interested in the possibilities you raise. I just don’t know the relative proportion each played in life’s history.
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