There’s not a speck of evidence to suggest that.
The evidence is that the large number of mutations seen in the human population is not reflected in the consensus sequences of two species that diverged more than 80 million years ago. In the most extreme case all the mutations were eliminated from the consensus sequences.
Does anyone at all have any idea what Bill is trying (failing) to say here? On the surface he seems to be saying that the number of residues different between human and mouse in some protein or other is less than the number of residues known to be polymorphic in the human population. And this is true. But what point is he trying (failing) to make out of that?
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Significantly less despite the long divergence time.
So? Again, please start taking more time to make sure you’re actually communicating. You’re saying here that the number of centimeters in a piece of string is significantly less than the number of gumballs in a jar.
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Under evolutionary theory the at differences are being driven by mutation. In one case there are 3341 residue variants in the human population of a 781 residue protein and the consensus sequence between humans and mice is a 1 residue substitution.
The evolutionary explanation is purifying selection yet if that is true how are there so many variants in the human population.
I think it is reasonable to examine the hypothesis that some of these proteins where there is more than 5% difference in residue type that it is possibly due to a design modification that is animal specific.
What are “at differences”?
What is this “one case”?
Why do you think those observations are incompatible?
Why is it reasonable? Why 5%? What does “a design modification that is animal specific” mean?
Once again, I beg you to pay more attention to what you’re typing.
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How would a designer go about implementing an “animal specific design modification”? Without that it doesn’t seem like you could formulate much of a hypothesis.
I consider my self pretty well versed in both evolutionary biology and creationist arguments and I genuinely have no idea what the point is supposed to be.
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It seems to be that on some level, Bill understands that he has no point.
He doesn’t want to think about how the fact that >4000 differences can accumulate in less than a million years screams that ~200 differences between species separated by 130 million years is no big deal.
Differences between sequences. In the case I showed which is beta catenin there is one residue substitution out of 781 residues.
Purifying selection that is powerful enough to maintain consensus sequences over so many years also allows so many substitutions in humans.
5% is arbitrary place to start looking. Design modification is simply a separate starting point for the sequences explaining the differences.
Alpha actin and Beta catenin are examples showing this extreme preservation of 99% despite a long evolutionary divergence. P53 is showing almost 30% divergence. All 3 show a large amount of residue substitutions in humans
There are biological and biochemical reasons for this conservation. Since you are Gish Galloping away from Notch2, explaining them to you would be futile.
Why do you assume that consensus sequences in databases have some huge amount of biological significance?
Do you now understand why Behe’s assumption of no existing variation is insane?
So the “at” was a superfluous, probably accidental addition. Once again, I suggest that you pay more attention when you type.
Thank you. So it’s a very highly conserved protein.
And in mice too, I imagine. The answer is that selection doesn’t have to be strong as long as it’s constant. Weakly deleterious alleles (especially in a diploid) can drift to a detectable frequency but will eventually be eliminated.
Arbitrary = senseless. I suspect you have a hidden reason, perhaps to rule out any separately created populations within species.
Sigh. Word salad again. Can’t you just try harder? What is the point of “design modification”? What is being modified, some pre-existing object? If so, that’s evolution. “Design modification” and “separate starting point” are mutually contradictory.
So?
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Comparing Notch 2 to different proteins is simply trying to understand if the constraint is consistent among different proteins. It is not and that is indicating that standard evolutionary explanations like purifying selection may not explain the data.
You wanted to look at 100 proteins initially. I have looked at only 5 or 6 at this point.
I know I should just move along, nothing to see here, but… Notch2 is super interesting, and a Notch2 variant is one of many apparently human-specific genes that are involved in brain development. The variant is called Notch2NL and it’s a truncated version of the intact Notch2 gene, derived from a duplication and subsequent deletion (within the duplication). (Described here.) A very recent Science Advances paper shows experimentally how two of these human-specific genes including Notch2NL are likely to influence human cortical development. Link below.
I can’t tell what Bill is trying to claim re Notch2… I don’t think Bill knows either. But polymorphisms in Notch2 and its relatives are likely to be very interesting and important in human evolution.
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You must remember that Bill doesn’t believe in gene duplication. That sucker was designed in from the beginning, and any resemblance to other genes is purely coincidental.