This theater is normally where it ends.
Facing this ink cloud, most scientists just do not have the time or platform to respond. Most scientists find the flurry of articles off-putting, but the public might see evolutionary scientists abandoning a scientific debate.
In this particular case, however, Dr. Lents and I anticipated what was coming. We were prepared. We did not have millions of dollars of funding and a team of staff. But we did have the Peaceful Science forum. That forum made all the difference.
The forum is fairly small, with only 50 or so active participants each day, but it is closely watched by several people in the origins debate. It is also an open forum, where anyone can join the conversation, adding information, expertise, and questions. As an open forum, it is also chaotic and unpredictable, not fully under our control. Still, it proved to be an effective platform, turning the tables on the DI’s typical public theater.
The DI had a turnaround time of days, but the forum had a far quicker turnaround, in minutes at best and hours at worst. Many of our contributors are scientists, and that became important. Quick analysis and rebuttal of DI articles was possible, at the moment when the public was watching, and these rebuttals did not depend on just the three co-authors of the Science review.
Oh that’s very cool. From before I found my way to PS. Had no idea.
I don’t think it’s free online yet, but it eventually will be. I think they keep it exclusive for subscribers for a while first.
@NLENTS , well written article and congrats on getting it published.
With respect to the APOB topic, the mistake Behe made was putting so much emphasis on the PolyPhen predictions, IMO. It isn’t uncommon for authors to run their data through algorithms like PolyPhen to give some context to their data, but these types of data analyses are very often just a jumping off point for further research, not the final word. Recently, I have been learning how to do gene expression data analysis and there are tools like gene ontology analysis that can point to candidates for pathways that may be affected in your model. Is a gene ontology analysis the last word? Absolutely not. At best, PolyPhen can only give us candidates for mutations that affect the function of the protein. You have to follow up with further research to get a reliable answer, be it in vitro or in vivo experimental models.
Thanks for posting that. One quibble, regarding the reference to Darwin’s finches:
I don’t have Grant 1981 handy, but if it says that it’s wrong. The prime example of an avian folivore is the hoatzin, Opisthocomus. Many other bird species eat mature leaves, some almost exclusively in certain seasons, though it’s certainly a small percentage of species. Nothing to do with Behe’s point, whatever that was.
Thanks! I actually really wanted to be done with Behe and DD, but the CFI asked me to give the talk on it last fall and I want to stay on their radar, so I reluctantly agreed (after trying to offer them other talks I could give, to which they said, next time), then SI wanted it written up as an article and, again, I am bad at saying no to orgs that I want to like me. 
Yes, exactly. I use all these tools also and they are always combined with others for a wide array of perspectives. Also, he didn’t even really use PolyPhen correctly, as we showed.
I think in the revision process, this got stated more strongly than I originally meant it. And now I’ve kind of forgotten the details. Maybe it was that none of the finches, nor the ancestors or relatives in the region eat mature leaves?
An old professor of mine just made a REALLY good point in a comment on the Panda’s Thumb post. I am going to repost it here along with my follow-up. I would love to hear what people like @Art , @T_aquaticus , @evograd @swamidass @John_Harshman and others think.
Joel Eissenberg:
Thanks for posting. I went to grad school with Rich Lenski, and Nate Lents was a PhD student at Saint Louis University School of Medicine, where I’ve been on the faculty for nearly 34 years.
There’s a semantic issue in operation here. Behe equates differences between amino acid sequences in polar bears and other bears with “mutations.” This is deeply misleading. What these differences represent are variants. Some variants can be adaptive, some maladaptive (=mutations) and some neutral. We’ve known this for decades. But it is vitally important to make this distinction. There isn’t a Platonic ideal for APOB. There are a variety of APOB sequences found in a variety of organisms. Deviation from an arbitrarily chosen APOB sequence doesn’t make that difference a “mutation.”
Years ago, there was a paper in Nature Genetics on the resurrection of woolly mammoth hemoglobin. The research identified amino acid differences between mammoth beta globin and modern elephant beta globin. When reconstituted with alpha globin and tested, the woolly mammoth globin flattens the temperature dependence for oxygen release. This makes sense for an animal exposed for months to sub-freezing temperature, to allow its extremities to be oxygenated. Thus, the variants in the mammoth beta globin aren’t “mutations,” they are adaptive variants. One might equally well call the modern elephant versions “variants” that allow for more efficient oxygenation of working muscles.
My response
Hi Joel! How are you doing? I don’t believe we’ve spoken since I left SLU nearly 17 years ago now. I hope you’re doing well. I have very fond memories of you and you were one of my favorite professors. One of the smartest guys I know with a razor sharp wit.
Now to your comment and the discussion below: I agree with you 100%. Your position is bolstered by the fact NONE of the “mutations” in APOB listed as polar bear-specifc are fixed in polar bear populations. It’s exactly as you say, they are variants. I made this point toward the end of my Skeptical Inquirer article, but I failed to recognize that referring to these as mutations plays right into their hands. It minimizes the role that genetic diversity - a rich pool of variations in proteins like APOB - plays in evolution by natural selection. There is no “one” polar bear APOB and by implying that there is, Behe is able to better make his argument that unguided evolution could never produce mutations that are needed on-demand. He may be right, but that’s because he’s arguing against a position that we don’t actually hold. We need to be better in explaining this particular misconception. So… thanks for this! I’m actually going to share this on the Peaceful Science forum to spread the word.
And really great to hear from you! Peace!
True, as far as I know no other thraupids are folivores.
If I understand, there are two issues here. First, that the public equates “mutation” with “bad”, which is odd considering that they also appear to give you super powers. Second, a matter of character polarity, that what’s called the “mutant” allele may in fact predate the “wild type” allele, and you can’t tell from current distribution, only phylogenetic analysis. But still, all alleles arise as mutants at some point. Calling the more recently derived allele a “mutation” doesn’t bother me. If the attempt it to paint it as bad, the correction is to point out that mutations aren’t bad just because they’re mutations.
In the current case, it seems true that the polar bear alleles are indeed more recently derived than the brown bear alleles they’re compared to. Aren’t they?
I frankly don’t understand his point. He appears to want to use an…idiosyncratic definition of mutation that I’ve never heard any biologist use before. Apparently in his parlance, only deleterious variants can be called “mutations”. This is not compatible with the definition that is currently used by the vast majority of researchers.
Yes, that was part that I didn’t quite agree with, but also, he’s a fruit fly geneticist, so they think about mutants as LoF most of the time, right?
But the larger point about how we collapse what can be lots of variation down into a single “mutation” is very well taken, especially in the case of the polar bear APOB. Neither the ancestors, nor the modern polar bears had one single ideal APOB. There is a pool of diversity that will gradually skew with selection, as more variation is produced around this sliding bell curve (the bell curve is not the best analogy, but I think you see what I mean).
It’s much harder for Behe to make his point when we think about a pool of variants, rather than as a single form becoming a different single form.
My own thoughts echo @John_Harshman . Using the term variant is more neutral since it is possible that the polar bear sequence was inherited from the polar/brown bear common ancestor, but the phylogenetic analysis strongly indicates that these variants first appeared in the polar bear lineage. I think “mutation” is entirely appropriate given the thesis being put forward and the audience the book was written for. The question we are trying to answer is if new mutations can increase fitness and do so through a gain in function.
I would also agree with Joel Eissenberg that we shouldn’t fall into the trap of using Platonic ideals for protein sequences, but that isn’t happening here. (If I am understanding the phylogenetic methods correct) By using the triad of polar bear, brown bear, and panda they are able to establish an ancestral sequence which they can then use to determine which variants were the product of mutations that happened in the polar bear lineage after the split from the brown bear population. By using ancestral and derived you can stay away from Platonic ideals.
Agreed.
Actually, I think it is, certainly the way that Behe presented it, but also in the way that we discussed it at least some of the time. I think we missed an opportunity here.
I suppose some of them do, though there is obviously a lot more that can be done. But I’ve known a lot of fly people (well, some at least), and none of them use his definition of mutation.
It’s much harder for Behe to make his point when we think about a pool of variants, rather than as a single form becoming a different single form.
Certainly agreed.
That’s one superb article.
It’s a far more important role than that of selection acting on newly-derived variants. Without diversity, extinction of a population is virtually inevitable. The importance of this is lost in most presentations of Darwinian evolution presented to laypeople that I have encountered.
I think you’re missing his point.
A better way to view/frame it is that a mutation is an event. To call an allele a mutation does not make formal sense. For example, a mutation is accurately described as an A->G substitution at a particular nucleotide, with the resulting allele labeled with that mutation’s name (when we are reasonably certain of its recent origin). It’s still formally an allele.
Or put yourself in the shoes of a clinical pediatric geneticist. Would you feel comfortable talking to parents while calling alleles “mutations” and their babies as “mutants”?
I couldn’t agree more. Populations aren’t static, “waiting” for mutations to occur. The title of that Durrett and Schmidt paper, “Waiting for Two Mutations,” was a gift to Behe.
I should add that John Sanford leverages this misrepresentation as well.
Yes, totally agree on all of this. It’s interesting to see the semantic diversity here in this thread. But it’s also an Achilles heel for public understanding, and one that ID folks exploit to sow confusion (or are confused themselves)