Another article comes out on Polar Bear ApoB. I honestly lost track of all of them at this point. Once again, unsigned:
From the ENV article:
This is not the phenotype seen in polar bears. Serum cholesterol levels in polar bears is comparable to brown bears. The human phenotype they are pointing to results in drastically reduced cholesterol in humans, but that is simply not seen in polar bears. Therefore, this comparison is not valid.
Again, from the article:
Let’s take a look at the actual paper:
The authors concluded that there was an increase in the clearance function of APOB in polar bears.
What is ENV’s response to this section of the paper:
The authors concluded that there was an increase in clearance of cholesterol in the blood. The real question is if Behe would call this a damaging change. I would assume not.
Some people gotta blast. Me, I download and map.
So, I downloaded the reads from two animals and mapped them back to the polar bear NCBI sequence. The consensuses from these mappings lack the amino acid changes seen in Table S7 of Liu et al. This is very preliminary, but it is looking more and more like Table S7 has variants that are not widely distributed in the population. Which would mean that the polar bear APOB (I am not going to bother with the other genes) actually has none (I repeat - NONE) of the variants Behe claims will break the protein.
i will probably do more animals, at least until I find one of the variants in one of them. I will keep the board posted as I slog through this.
Me too. If there’s anything new, do let me know, but at this point, that seems pretty unlikely.
The key thing is we need to start writing our final post, to bookend the whole thing.
I may suggest we do the polar bears and malaria seperately.
I deliberatly was absent from duscussion for while, because of insults i recived here, However, since this paticular topic is the one that i participated, i will contine to look at it
and why not to say that Science does not care who, where at his home, at his office or at his car downloaded and mapped…Science does not work that way, Your mappings would be valid if you present published results. But this is all that you all could say this means you all failed to respond the last ENV article which is summarised …here Polar Bear Seminar: This Is the End
Also so that we can fully move past this, as they seem ready to do. I’m glad we didn’t fall into the trap of trying to respond to every one of their posts. Even without reading them all, there is a stunning about of repetition and redundancy to all of them. We obviously got them pretty stirred up, but is anyone buying any of it? They’re throwing a lot of pasta at the wall (or, actually, the same noodles over and over), but is any of it sticking? I’m trying to keep an open mind but none of it has given me pause.
The key thing to keep track of is the moving goal posts. This is about Behe’s book. Every argument and peice of evidence they add is an admission his book did not make the case. Every change of claims, also, is a concession that they could not defend Behe’s original point, every unsigned post, moreover, need not be engaged by us.
I’ll save time and apply Betteridge’s law.
Im particularly interested in @swamidass response regarding polyphen unless that was given already ““Polyphen does not attempt to predict ‘biochemical damage’.” That’s wrong”
They misunderstood PolyPhen. I’m a computational biologist, so this is solidly my area. Behe is outside his field. Just saying I’m wrong and quoting back the classification features is not a valid way to overturn our understanding of PolyPhen.
How did this happen?
My best guess is that they quote mined the author. Then, when we pointed this out, Behe painted himself into a corner. It seems he never admits error, so we are stuck.
We are still thinking through our final response. And I hope it will tie up loose ends. There have been so many articles on this that I want to go coallate them too.
Yes, which is his modus operandi. Look at how many changes the definition of “irreducible complexity” has undergone.
I often wonder if their incoherence and inconsistency is part of the point, or if at least coherence and consistency are not important objectives for them. I spend a lot of (too much?) time debating creationists, and they rarely seem to even understand the arguments ID’ers are making. Rather, they will say “Well, sure, scientist X said this, but then Behe responded with this article here, so that takes care of that”, without even bothering to demonstrate that Behe (or whoeve) has addressed the pertinent points. The impression I get is that they are just bamboozled by the amount of “scientific” verbiage and jargon thrown at them and figure they can’t understand it, but Behe is a scientist so he must understand it, and that’s good enough.
If memory serves, that’s what I saw when I looked at the NCBI sequence. None of the variants in Table S7 are in the NCBI sequence, as far as I could tell.
Thanks for slogging through the data. It’s much appreciated.
Do want to add anything to this thread from last month?
- the human phenotype they are pointing to results in drastically reduced cholesterol in humans ONLY WHEN THE TWO APOB ALLELES ARE FUNCTIONALLY DEFICIENT. But heterezygous APOB deficiency in human result only in a mild cholesterol reduction.
- Serum cholesterol levels in polar bears is comparable to brown bears DESPITE THE FACT THAT WHITE BEARS HAVE HIGHER FAT DIET THAN BROWN BEARS. So, metabolic changes are expected in polar bears to accomodate for this higher fat diet, metabolic changes without which too much cholesterol would be present in the blood of polar bears.
- if you combine points 1 and 2, you will see that the comparison made in the ENV article is valid and that Behe’s case regarding APOB in polar bears is strong.
Is this the case in polar bears? Are the individual polar bears homozygous or heterozygous for the specific variants?
Humans who are homozygous for the APOB deletion never attain normal cholesterol levels no matter how much fat they consume, so this argument isn’t relevant.
My understanding of the discussion around APOB in polar bear is that some adaptive mutations were fixed in the polar bears population precisely because they were adaptive. So I would rather say that the current population of polar bears is probably homozygous for the specific variant. This being said, it is easy to imagine how an APOB homzygous variant in polar bear can result in the same phenotype than an heterozygous loss of function variant in human. For example, such an outcome would be obtain if the homozygous variant (allele) in polar bear would result in a 50% activity reduction as compared to the wt allele.