He put the central thesis of the book on a slide and said he agreed with it. The central thesis is something Behe published years ago in QRB, so it shouldn’t be a surprise to anyone.
"The First Rule of Adaptive Evolution
Break or blunt any functional gene whose loss would increase the number of a species’s offspring."
That’s an exact quote from the book, and it occurs on the very first, otherwise blank page all by itself, so it’s obviously the thesis of the book.
I said that it was apparent that HIS Christianity helps HIS scientific work. I see that @swamidass is not confined in his work by any misinterpreted bible passages or the admonishments of any pastor that his work is somehow anti-Christian and would lead him to atheism. He is free to let the data lead where it may and his Christianity seems to be helping him move forward like a tail wind as opposed to a head wind (his YEC upbringing).
And what did I disagree with?
I was asking you to review your objections here in this thread so we can discuss them, if that’s not too much trouble. The video isn’t up yet.
The video is up.
Don’t be too hard on @swamidass. He has enough to do keeping this forum running smoothly. I think I was the one who brought the additional mouse work up to @swamidass, so it makes sense that I should respond. (He would have gotten around to it, I am sure.)
I guess we have different ideas of what an error, a mistake is.
Behe’s reasoning is clear - the mouse model, which is expected to have 50% as much APOB as the wild-type, has lipid and cholesterol metabolism “defects” that would seem to be adaptive for polar bears, hence the putative damaging mutations in polar bear APOB can be adaptive as well. The additional work I cite shows that the same mouse model Behe leans on to support his contention also tells us that, if Behe’s reasoning was correct, male polar bears should have low fertility.
Since polar bears do not exhibit such characteristics, then Behe’s reasoning is wrong. Clearly erroneous, mistaken. This is pretty cut-and-dried.
Note that I am not saying that Behe is being disingenuous or dishonest. That would mean I believe Behe knew about the additional studies and conveniently neglected to mention them. I have no reason to think this.
We all make mistakes. The polar bear APOB affair is one of Behe’s. It would be ever so helpful if he would just get ahead of all this (rather than digging deeper and deeper), adopted a more tentative tone with respect to APOB and his central thesis, and moved on.
One of the many reasons mainstream science rolls its collective eyes at Behe is Behe’s “Rule” has been known to science for almost 70 years. Evolution proceeds by modifying existing features and existing genes. It doesn’t matter if the original genes are “broken” or “blunted” if in the new environment they no longer provide a reproductive advantage to justify their energy cost.
Behe writes this nonsense as "Golly ain’t I smart, look what I discovered!!’ for ignorant lay audiences to push his religious claims. The scientific community is not impressed.
That is exactly right. If he would just come clean on this it would help immensely. Digging in is just prolonging the agony.
Not accurate.
We say that his reasoning is wrong, and it is wrong, even if his hypothesis ends up being right. He justified this with a direct misquote of the authors, and with a misunderstanding of Polyphen 2. Not good.
It’s based on a very selective reading of the literature. In both the Liu paper and the mouse model paper, he sifts through lots of phenotypes and genetic difference to cherry pick one datum about cholesterol levels (among lots of other problems that these mice have!) and tie it to some mutations that he insists are “damaging.” This is not how “weight of the evidence” arguments should work. If a single result is all you have, it’s fair to try to extrapolate meaning from it while you wait for more data. In this case, there is a lot more data and argues against his position.
As we’ve all said exhaustively,
the predictive algorithm does not really predict “damage” in the sense that Behe means it.
He also tried to conceal how many differences there are in APOB that even the PolyPhen program didn’t call “damaging.” (well more than half).
Because there is nothing in the Liu paper to support his claim, he pulls one thing from one of the mouse papers, again ignore everything else in those papers that argues against the idea that diminishing APOB function could be adaptive (beneficial) in polar bears.
The clustering of alterations in polar bear APOB in the domain related to cholesterol/LDL clearance is highly suggestive, not of damaged function, but of modified function. As Behe always tells us, there are thousands of easy ways that mutations can reduce the function of a gene, but it is more difficult and more rare for mutations to enhance protein function. The clustering of mutations in a critical domain suggests the latter, not the former.
Yes, fertility is complex. So is cholesterol metabolism, as the mice show us.
Which could also have other explanations too, such as reduced appetite for being so sickly. 
Maybe you can explain in what sense “damaging” is meant then.
And you claim this is because he didn’t put it in the table on his online article? He put it in the book, quotes it in the article and was quite clear about it. The graphic doesn’t even appear in the book. This is absurd.
Here is the quote from the book that also appears in his article:
“In fact, of all the mutations in the 17 genes that were most highly selected, about half were predicted to damage the function of the respective coded proteins. Furthermore, since most altered genes bore several mutations, only 3 to 6 (depending on the method of estimation) out of 17 genes were free of degrading changes. Put differently, 65%-83% of helpful , positively-selected genes are estimated to have suffered at least one damaging mutation.”
And just before he shows the table: “Below is the relevant information from Liu et al.’s Table S7.” [emphasis added]
You are whining that he didn’t put information in a table in the same article where he puts the information in the body of the article. Absurd. In addition to this, you don’t put all the information in your table either, claiming that “your point is made” all the while claiming Behe misrepresented information by doing the EXACT SAME THING YOU DID, that is leaving out information because his point was made from the information he actually presented.
I don’t understand this. He is making an argument based on the literature that makes sense. What is your hypothesis about why the APOB mutations are adaptive in polar bears?
Why? Behe explained his reasoning and it makes sense to me. Explain yours. Why do you think this is a modified function rather than degraded? What function is being modified and how?
Ben, the central issue is that a complete and accurate accounting of Table S7 from Liu et al. does not lead to the same conclusions that Behe draws. If you take everything into account (which is what Behe is obliged to do), then the relevant table of genes would be:
Benign:
EHD3
OR5D14
SH3PXD2B
Possibly damaging:
ABCC6
POLR1A
Probably damaging:
APOB
COL5A3
CUL7
LAMC3
LYST
OR8B8
VCL
Conflicting prediction:
AIM1
ARID5B
IPO4
TTN
XIRP1.
At the very least, the range of genes that are helpful and positively-selected but have (according to Behe) at least one damaging mutation is 41%-83%. It is not only inappropriate, it is unethical to omit parts of the table so Behe can raise this estimate (so that, I suspect, he can claim “a majority, regardless”).
And that is before we realize that APOB may well not be damaged. This changes things even more.
Make no mistake about it. If you were a student in a class of mine and pulled this stunt (changing a table from a paper so that results that do not agree with your argument are conveniently omitted) on a project or paper, you get a zero. Full stop, period. My institution gives me no choice, and I agree with this rule.
If you submit a grant to a panel I am on and you mis-represent a citation so blatantly, not only is your proposal not reviewed, I would recommend that the powers that be ask you to never submit another grant to the program. Ever.
If this sort of stunt is ever caught on a submitted manuscript, then not only is it rejected, the editor will request that you take your business elsewhere. And I would expect the editor to communicate this sort of unethical behavior to their colleagues.
Needless to say, this is not a small issue.
Best to read the PolyPhen note pages?
Or perhaps you can read what we have written about this, and or what Lenski has written about this already. Behe quote mines them. He misrepresents the data and the conclusion of the authors. What he wrote in the book is just wrong on several points. This is clear as day to everyone outside ID. Maybe Behe ultimate point is right, or wrong, but he is making his case by saying “the authors over their think 1+1=3, just like me”, when in fact they wrote “1+1=2”.
Try asking your question respectfully and maybe I will. You need to recognize that just about everyone on this thread trying to teach you knows way more about all of this than you do. I am not saying that means you have to agree with, but it does mean that we expect respect when discussing topics in which we are experts and you are not. If you can agree to that, I will respond to you. if you don’t, I won’t.
I suspect Behe would do the same in his classes. Remember that he selectively omitted both columns AND rows from the chart. He actually did quite a bit of work to do to make it look the way he wants it to. It is really hard to justify this (and I’ve heard rumors that even some DI colleagues are pissed about that post).
To bring up a painful point once again, this example, above, reminds me so much of cherry-picking a few words from a critical review and then listing them instead as endorsements on the back of your newly-published book. Just sayin’…
Why do you think Mike concludes gene damaging adaptions will be more prevalent than gene enhancing adaptions?