In “Darwin”s Black Box” (DBB), ID”s arch-biochemist Behe glibly labeled evolutionary hypotheses for the origin of “irreducibly complex” systems as “hops into the box of Calvin and Hobbes” (for those who don”t know what the heck this refers to, go here to learn about Calvin and Hobbes, and here for info on their box, or even better go spend some time here, and come back tomorrow). This overconfidence has come back to haunt him as more and more evidence accumulated in support of the evolutionary origin of his various IC systems, from the flagellum to the complement and clotting cascades.
The topic where the idea of unevolvability of IC systems has probably taken the most beating is the vertebrate adaptive immune system, where not only evidence for evolution has accumulated at a steady pace, but even more embarrassingly for Behe, it has developed exactly along the lines predicted by those “Calvin and Hobbes jumps” he originally dismissed. A recent paper in the journal PLoS Biology [1] is the latest turn in the death spiral of irreducible complexity of the immune system, and I think provides a good opportunity to take a look at how science works, as opposed to ID navel-gazing.
Let me start with a brief description of the issue. Basically, almost every organism faces the problem of pathogens and parasites, and most of them solve it, in broad terms, using molecular detection systems that can discriminate “self” from “non-self”, allowing the elimination of the latter. Of course, the problem of discriminating you from them is that there is only one you, and an almost infinite variety of them “ so any effective discrimination system has to be flexible enough to recognize very many different forms of non-self, and able to do so in a parsimonious way in term of use of molecular components (no organism can possibly hope to have a genome large enough to encode even one single specific detector molecule for every possible pathogen). In evolutionary terms, any successful immune system has therefore to satisfactorily juggle, among other things, these two contrasting selective pressures: diversity of effective target vs metabolic/genetic parsimony. Jawed vertebrates (which include cartilaginous and bony fish, amphibians, reptiles, birds and mammals) happen to have hit on a solution that is, frankly, way cool. (And I am not saying it just because I work on this.)
In all jawed vertebrates, the adaptive immune system “detectors” (receptors), are encoded not by single, stable genes, but by families of gene segments that change their conformation on DNA (rearrange) during the development of immune cells. By randomly joining one segment from each of the different families (called “V”, “D” or “J”, each containing from a few to a few hundred members) into a single coding sequence, the immune system can generate many thousands of different genetic combinations, each encoding a different receptor capable of recognizing a different molecular target. The proteins that mediate this DNA rearrangement process (“VDJ recombination”) are called RAG1 and RAG2, and they act on specific DNA sequences, recombination signal sequences, or “RSSs”, which flank the rearranging V, D and J segments. (For those who want to know more, Matt Inlay’s excellent summary, especially its “IC system II” section, serves as a very good primer).
Those of you who are used to the ID approach on science, i.e. giving up on it, can probably already see where the problem lies: this is a complex system of functionally inter-related components that, looked at superficially, simply cannot work in isolation. Behe was absolutely certain of this in 1996:
In the absence of the machine [RAG1/RAG2], the parts [V, D and J gene segments] never get cut out and joined. In the absence of the signals [RSSs], it’s like expecting a machine that’s randomly cutting paper to make a paper doll. And, of course, in the absence of the message for the antibody itself, the other components would be pointless.
DBB, p. 130
Now, in evolutionary terms the obvious question to ask is indeed what function could any precursor of this system have had, before the evolution of the adaptive immune system. Some ideas were already around at the time of DBB’s publication, and had been for a while. Already in 1979, Sakano, Tonegawa (who would later win a Nobel Prize for his discovery of VDJ recombination) and colleagues identified the RSSs and noticed that they shared features with the recombination sequences of certain mobile DNA elements called transposons [2].
Transposons are odd fellows in the DNA world, who spend their time physically hopping from genomic site to genomic site, and replicating themselves, pretty much as “molecular parasites”. They do this via a number of mechanisms, but the kind we are interested here are a class of DNA transposons which carry within their own sequences genes encoding the necessary enzymes (“transposases”) for cutting themselves off the genomic DNA (“excision”), and re-inserting somewhere else (“integration”). At the very end of each transposon element is a characteristic sequence, which is recognized by the specific transposase (I am sure you are already seeing the parallel with VDJ recombination).
A decade after the discovery of VDJ recombination the responsible enzymes, RAG1 and RAG2, were identified, and lo and behold their genes had a funny look about them: just like transposases, they were almost devoid of introns, and mapped right next to each other in the genome (transposons need to “travel light”, and cannot carry excess DNA as they hop around). This is when David Baltimore, in whose lab the RAG genes were discovered, and others wrote the review in the Proceedings of the National Academy of Sciences USA [3] that was mocked by Behe as proposing a “hop in the box of Calvin and Hobbes” for openly stating the transposon hypothesis: that RAGs/RSSs were the remnants of some sort of transposon system that integrated itself into a non-rearranging immune receptor, and became “enslaved” to it, causing the integrated portion to “pop out” whenever the gene became active, and in so doing generated useful diversity for immune target recognition.
To be fair, at the time the hypothesis was indeed quite a stretch, but still, a stretch that made some specific predictions. No sooner had Behe’s words been put to print, those predictions started coming true. What follows is a short timeline, with the major milestones:
1996:
- DBB published. In it, Behe says:
“ the complexity of the [VDJ recombination] system dooms all Darwinian explanations to frustration. [my emphasis]
DBB, p. 139
- In the same year, the Gellert lab, which had developed a system to study VDJ recombination in a test tube with purified proteins, discovers a striking similarity between the RAG-mediated reaction and that of known transposases and integrases: both proceed through a characteristic intermediate in which the DNA takes an unusual hairpin-like shape [4]. This was really a breakthrough finding, the first solid piece of evidence in favor of the transposon hypothesis. But are RAGs actually a transposase”
1998:
The Gellert and Schatz lab independently discover that RAGs can, under certain in vitro conditions, mediate actual transposition reactions by inserting cleaved DNA ends containing RSSs into double-stranded target DNA. This is the other side of the transposon “life cycle”, the insertion phase. In other words, although the RAGs’ physiological activity requires them only to cut DNA out of the genome, they bear, buried inside their structure, the ability to insert RSSs into DNA, a sort of molecular vestigial structure. This makes sense if RAGs are indeed an evolved transposase, but is harder to justify from a design perspective, because transposition events, by potentially disrupting genes, can actually be quite deleterious, for instance by causing cancer.
2000:
Indirect evidence is identified that suggests that transposition reactions mediated by RAGs can occur not just in vitro, but within mammalian cells [7].
2003:
Direct evidence of RAG-mediated transposition in yeast and mammalian cells is uncovered [8, 9]. In other words, RAGs are a transposase in eukaryotic cells.
2004:
Molecular evidence uncovers a class of transposons called hAT that use a transposition mechanisms essentially identical to that used by RAG proteins, and, in addition, that their enzymes share some basic similarity with RAGs in their active site [10]. (This paper was discussed by Matt here on PT a few months ago)
2005:
RAGs find their long-lost family of transposases [1]. In this paper, Kapitonov and Jurka take a fully evolutionary, biocomputational approach to figure out where RAGs may have come from. Let’s look at what they did, and how.
They started from the observation of a low, borderline significant sequence similarity between a portion of RAG1 and certain transposases of the Transib family. They applied then a different algorithm for protein similarity searches, which uses information from a similarity search to “hone” successive iterations of the same search, by assigning position-specific scores to amino acid residues. In other words, it searches for “deep” homologies that are reflected by the presence of specific sequence motifs within proteins that may otherwise have diverged significantly (and thus yield poor scores at a direct alignment). What they found was that 10 motifs were very highly conserved between RAG1 proteins from various species and Transib transposases. Figure 1 below shows the alignment of these motifs, where every letter corresponds to an amino acid, and color patterns indicate amino acids which have similar physico-chemical properties (and can therefore often replace each other without much disruption of structure and function). The similarities are very statistically significant.
Figure 1 “ Alignment of conserved regions in Transib transposases and RAG1 (Click on the figure to see a larger version from the original paper)
They next compared the sequence of the RSSs to those of known Transib transposon signal sequences (terminal inverted repeats, or TIRs), and they found another striking correlation: all the positions that are strongly conserved in TIRs are also strongly conserved in RSSs. This is shown in Figure 2.
Figure 2 “ Alignment of TIRs and RSSs. Panel A shows a graph of the nucleotide sequence conservation (with 1.0 = absolutely conserved) at different positions in a large panel of TIR families (sequences shown in panel B). Under the graph are the “consensus” TIR sequence (representing the most common nucleotide at each position), aligned with the consensus RSS, which consists of a 7-nucleotide sequence, followed by a spacer, and another conserved 9-nucleotide sequence. Boxed nucleotides are those that show highest conservation, and are absolutely required for the mechanisms. Panel C shows that not only are the crucial positions in the sequences conserved, but their overall structure also is. Like RSSs, which require “spacer” elements of either 12 or 23 nucleotides to pair for efficient rearrangement, so do the TIRs at the ends of each transposon have different and specified length, which correspond to a 12- or 23 nucleotide distance between the conserved sequences (the reason for these numbers is that each turn of the DNA double helix is about 11-12 bp, so sequences 12 or 23 bp apart will be on the same side of the helix, one or two turns apart, and simultaneously accessible to recognition by any binding factor).
What this means is that a simple system exists, with both a RAG1-like gene and RSSs, as an independent functional unit: what we would expect for a direct, “reduced” predecessor to the supposedly irreducible VDJ recombinase system. But there’s more: while extending their search to the genome databases from various organisms, Kapitonov and Jurka found a number of other RAG1 homologues in various organisms, including some in which the similarity extended beyond the protein “core” they had originally search for, all the way to the so-called N-terminal region of the protein. There is therefore a family of close RAG1-related proteins in various organisms. The distribution of the various homologues in different lineages is shown below.
Figure 3: RAG-like proteins and Transib transposons in various organisms. Red circles represent Transib transposons, orange and blue ellipses RAG1 core and N-terminus homologues, and gray rectangles RAG2 proteins.
Note that these new RAG1-related proteins are not known to be associated with any Transib-like transposons. Some are clearly pseudogenes, and the function of others is unknown. The overall picture that emerges is that of a complex, diffuse and diverse family, which has accompanied metazoan evolution for a while, with multiple instances of horizontal gene transfer (quite common for mobile DNA elements) and of independent “adoption” by the host genomes of family members. Exactly the picture which one would predict would facilitate the occurrence of random integration of a transposable element within a primordial antigen receptor gene, causing junctional diversification (that is, protein variation at the excision site), and therefore an increase in target binding ability: the “transposon hypothesis” for adaptive immune system evolution.
Which brings me to the last item in the story. At the time Behe wrote, no known potential precursor of the immune system receptors existed outside jawed vertebrates. Many proteins belong to the same structural family of antigen receptors, but none carried the same exact sequence hallmarks. That has changed too: at least 3 protein families have been now identified in protochordates and jawless vertebrates which have non-rearranging V-like segments of the same kind of antigen receptors [11-13]. They show presence of multiple, closely related members, suggesting that selective pressure exists for their diversification, and some may even be involved in “innate” immune responses. Although it is almost impossible to say whether any of these proteins is in fact the direct descendant of the ancestral receptor of the adaptive immune system, their existence suggests a rich evolutionary history of non-rearranging immune receptors predating VDJ recombination adaptive immunity.
Let’s summarize: where once Behe saw an “irreducibly complex” system made of
a) a receptor gene,
b) a RAG recombinase, and
c) RSSs,
we now know that
a) whole families of non-rearranging receptors and
b) a whole family of functional RAG1 homologues acting on
c) RSS-like sequences
already existed before the emergence of the vertebrate adaptive immune system.
Exactly what we would expect to see if the adaptive immune system did arise via an evolutionary process, as opposed to poof into existence in its complete form.
So, what next? Well, for one, we still don’t know where RAG2 came from. So far, no RAG2-like genes have not been found, inside or outside transposons. However, the lack of introns and chromosomal location of RAG2, right next to RAG1, are too strong a hint to dismiss, so I think the prediction still remains that a RAG2 ancestor will be found in association with a mobile DNA element, along with a RAG1-like transposase. In the context of VDJ recombination, RAG2 seems to play mostly a regulatory role, so it would not be surprising if its ancestor did something similar. However, it is possible that considerable sequence divergence may have occurred for this protein, since mechanisms for transposon regulation may be significantly different from those required for VDJ regulation. Thankfully, much work remains to be done - that’s what scientists are for.
Is Behe going to concede that evolutionary models for the origin of VDJ recombination are gaining more and more support by the day? Probably not, frankly. No matter how many predictions get verified, how many plausible precursors are identified, Behe and the ID advocates will retreat further and further into impossible demands, such as asking for mutation-by-mutation accounts of specific evolutionary pathways, as if one could meaningfully recreate in the lab the precise evolutionary conditions which some mud-dwelling lamprey-like critter experienced some time in the Cambrian. Too much has been invested by ID advocates in the “irreducibly complexity” concept for them to recognize its significance (assuming it ever had any, given its recurrent reformulations) has essentially collapsed.
For the rest of us, the lesson to be learned is that even wild hypotheses, if rational, consistent with available evidence, predictive and testable, are worth considering and pursuing. Behe said:
We can look high or we can look low, the result is the same. The scientific literature has no answer to the question of the origin of the immune system.
DBB, p. 138
Yet the answer was there all along, in the only place where Behe refused to look: in the box of Calvin and Hobbes.
Acknowledgements
Thanks to Matt Inlay and the rest of the PT crew for info, comments and suggestions.
2 Sakano H, Huppi K, Heinrich G, Tonegawa S. Sequences at the somatic recombination sites of immunoglobulin light-chain genes. Nature. 1979; 280: 288-94.
4. van Gent DC, Mizuuchi K, Gellert M. Similarities between initiation of V(D)J recombination and retroviral integration. Science. 1996; 271: 1592-4.
5 Hiom K, Melek M, Gellert M. DNA transposition by the RAG1 and RAG2 proteins: a possible source of oncogenic translocations. Cell. 1998; 94: 463-70.
6 Agrawal A, Eastman QM, Schatz DG. Transposition mediated by RAG1 and RAG2 and its implications for the evolution of the immune system. Nature. 1998; 394: 744-51.
7. Vaandrager JW, Schuuring E, Philippo K, Kluin PM. V(D)J recombinase-mediated transposition of the BCL2 gene to the IGH locus in follicular lymphoma. Blood. 2000; 96: 1947-52.
8. Clatworthy AE, Valencia MA, Haber JE, Oettinger MA. V(D)J recombination and RAG-mediated transposition in yeast. Mol Cell. 2003; 12: 489-99.
9 Messier TL, O’Neill JP, Hou SM, Nicklas JA, Finette BA. In vivo transposition mediated by V(D)J recombinase in human T lymphocytes. EMBO J. 2003; 22: 1381-8.
10. Zhou L, Mitra R, Atkinson PW, Hickman AB, Dyda F, Craig NL. Transposition of hAT elements links transposable elements and V(D)J recombination. Nature. 2004; 432: 995-1001.
11. Cannon JP, Haire RN, Litman GW. Identification of diversified genes that contain immunoglobulin-like variable regions in a protochordate. Nat Immunol. 2002; 3: 1200-7.
12: Cannon JP, Haire RN, Pancer Z, Mueller MG, Skapura D, Cooper MD, Litman GW. Variable domains and a VpreB-like molecule are present in a jawless vertebrate. Immunogenetics. 2005; 56: 924-9.
13: Suzuki T, Shin-I T, Fujiyama A, Kohara Y, Kasahara M. Hagfish leukocytes express a paired receptor family with a variable domain resembling those of antigen receptors. J Immunol. 2005; 174: 2885-91.
63 Comments
Charlie Wagner · 30 May 2005
Ben · 30 May 2005
For those of you keeping score, it's evolution 12, ID q.
hiero5ant · 30 May 2005
"But... but... it looks designed!"
Why do you people hate Christ so much?
Bill · 30 May 2005
"Those of you who are used to the ID approach on science, i.e. giving up on it. . . " Brilliant!
Bill
steve · 30 May 2005
Bayesian Bouffant, FCD · 30 May 2005
Burt Humburg · 30 May 2005
Great writeup.
My favorite example of Behe citing a failure of science as evidence of design, only to be refuted later, is whales. It's something just about anyone can wrap their brain around: Behe strongly suggested that the absence of whale transitional fossils was evidence of design, but the year after he co-wrote that chapter of the book, three transitional forms were published.
BCH
Descent & Dissent · 30 May 2005
It's good to get Calvin and Hobbes signed up for the cause. It's far funnier than that YEC cartoon B.C.
steve · 30 May 2005
Speaking of that guy, a character in BC last week called a snake "Dust-breath".
Like PZ or someone said, they've fired all the acrobats and jugglers, and it's just clowns, clowns, clowns, all the time.
nidaros · 30 May 2005
When (if?) Behe addresses some of these issues, one could predict it will be just like another Calvin & Hobbes feature, "Calvin Ball".
This was a game that appeared in the strip where the rules of the game were arbitrarily adjusted to favor Calvin should he become disadvantaged.
So not to worry! If the old ideas get straightened out, he can just bend some new ones.
This is one of the great advantages of publishing in books where inconvenient delays from peer reviewers don't happen.
Harq al-Ada · 30 May 2005
Yeah. Ben's "Q to 12" joke came from a C&H Calvinball strip. To be more realistic, we should say something like Evolution 12,312,321; Creationism (including ID) -463 (for the harm to knowledge and critical thought they have induced within the public.)
darwinfinch · 30 May 2005
These mechanisms seem to reflect the several mechanisms science has "evolved" to eventually distinguish "self" from "non-self" (or should that be "sense").
Unfortunately, politics, for "evolutionary" reasons of its own no doubt, seems to lack similar machines. Perhaps because it has evolved in a very different environment: one where sense, facts, and joy have long been selected against whenever possible.
freelunch · 30 May 2005
The one thing ID Creationists have discovered is the rules of Calvinball. They are very good at changing the rules, though even with whatever new rules they promulgate, they still only seem to score own-goals.
Arun Gupta · 30 May 2005
'Rev Dr' Lenny Flank · 30 May 2005
Andrea Bottaro · 30 May 2005
SEF · 30 May 2005
Off-topic:
It looks like someone on PT is infected with a virus that sends empty emails. I'm posting here because it (whoever/whatever it was) used the identity of Andrea Bottaro to do so - which doesn't necessarily mean Andrea is the infected one. As the only Andrea post I recall seeing, it's the obvious place to alert her (or anyone else viewing the site) to the possibility or perhaps find out if it was intentional but bizarre.
Joseph O'Donnell · 30 May 2005
Andrea Bottaro · 30 May 2005
SEF:
Sorry to hear that. However, unless for some reason I know you, and your e-mail address is in one of my accounts' address books, it is unlikely that this is a random virus on any of my computers. It would seem like some sort of purposeful malicious attack. Perhaps you can e-mail me the e-mail address that's spoofing my name?
Joseph:
yes, I read Behe's book in '97 (or perhaps '98, now I can't remember), and already the immune system chapter was a total farce. I had no idea what ID was then. I remember distinctly reading through the first few chapters, especially the flagellum's, and thinking "maybe the guy has a point". Then I reached the immune system description, and I thought "wait a minute - if he can write such b.s. about the immune system, what did he get wrong on the rest?" So I did some more digging, and here I am. The immune system and the complement and clotting cascades were a poor choice on his part, because their origin is relatively recent, and we have a good chance of finding precursors at various stages in living organisms. Notice that ID advocates rarely if ever talk about these systems any more.
Cubist · 30 May 2005
Roadtripper · 31 May 2005
I haven't read "DBB" and apparently it was time better spent on other books anyway. I'm just wondering--is there even a single one of Behe's 'examples of irreducible complexity' introduced in his book which is still standing today, or have they all been de-bunked? So far I've heard about immune responses, clotting mechanisms, bacterial flagellums (er, flagelli?) and for some reason, mousetraps, all of which turned out to be not-quite-IC after all. So what's left, if anything?
Rt
Russell · 31 May 2005
Forrest M. Mims III · 31 May 2005
Dr. Behe has posted a compelling response to "The Revenge of Calvin and Hobbes" at http://www.idthefuture.com/index.php?p=405&more=1&c=1&tb=1&pb=1
Forrest M. Mims III
www.forrestmims.org
Steve U. · 31 May 2005
Steve F · 31 May 2005
Lets compare and contrast:
Behe wants from Darwinists "a mutation-by-mutation account of critical steps (which will likely be very, very many), at the amino acid level."
What mechanism does Behe provide? I believe its called 'poof.'
Great.
Alan Gourant · 31 May 2005
Since reportedly Behe has repeated in his allegedly "compelling" response the discredited canard about his "successful muzzling" of Russell Doolittle, what credibility can that "compelling" response have? He should have responded to Ian Musgrave's essay where his distortion of his encounter with Doolittle was documented, as well as to many other essays showing the fallacies in his position to which he never responded. I believe Forrest Mims is an ID advocate (or at least a sympathizer) rather than an unbiased observer, hence his characterization of Behe's response as "compelling." The guys seem to be watching PT though. Good for them.
Steve F · 31 May 2005
For everyone's interest, r.e. Doolittle and Behe.
http://www.pandasthumb.org/pt-archives/000884.html
Russell · 31 May 2005
Steve U. · 31 May 2005
Sir_Toejam · 31 May 2005
Russell · 31 May 2005
heck. Forgot to finish my sentence. Meant to say, that asking for such a ridiculous level of detail was equivalent to asking for a molecule-by-molecule account of a system's behavior before accepting the second law of thermodynamics.
steve · 31 May 2005
Sir_Toejam · 31 May 2005
"* Guns, Germs, and Steel"
???
lol.
Russell · 31 May 2005
Sir TJ:
lol? Why?
I found "Guns, germs and steel - the fates of human societies", a fascinating read. You didn't think so?
Steve U. · 31 May 2005
Sir_Toejam · 31 May 2005
I wasn't commenting on the content, just the title as quoted. you gotta admit that is a rather amusing name for a book (at least without the extra bit you added).
sounds like a post-apocalyptic sci fi novel about the rebirth of the old west, six shooters and all, after a widespread plague wipes out most of humanity.
Amiel Rossow · 31 May 2005
Behe has published some peer-reviewed papers on biochemistry (although not recently, apparently being too busy with his creo activities) so perhaps he is not really as dumb as his "compelling" response to Bottaro seems to indicate. Therefore his demand for "mutation by mutation..." etc. proof of evolution sounds more like a deliberate effort to enrage his detractors rather than a real serious challenge. This is a behavior rather typical of people driven into a corner and having no reasonable arguments but desperately trying to save (at least for himself) the remnants of his oppinion. Is he in a mousetrap? (sorry for the pun). If this is not so, the only other interpretation seems to be that he is simply a hopeless fanatic immune to a reasonable discourse. That such people can get a position of a tenured professor at a respectable university says something gloomy about the situation with science and education in the US.
steve · 31 May 2005
386sx · 31 May 2005
Mr. Behe: "after all, Darwin himself was frequently confused!
Well by golly that Darwin must have been some wacky dude! Woo hoo hoo! !!!!!
Mr. Behe: "No matter what it is or who commenced it, I'm against it!
Well Behe didn't really say that. But it's darn close! Many exclamation points!!!!! Whoopeee!
'Rev Dr' Lenny Flank · 31 May 2005
Art · 31 May 2005
Behe's response to Andrea's essay is priceless, and everyone here needs to make a back-up copy. What is especially revealing, and most hurtful to the ID cause, is the attitude of Behe's that new questions and research that arise from the discoveries of late are flaws, weaknesses of evolutionary theory. (This is betrayed by his insistence on hiding behind ever-retreating goalposts, of finding that one experiment that has not yet been done and claiming "aha! no experiment, no evolution!".) This attitude stands Behe, and by association the ID movement in general, quite completely at odds with all true scientists, who know that a scientist looks at "we don't know" or "the experiment hasn't been done" as opportunities and challenges. Most definitely not flaws or weaknesses.
If there's any doubt that "don't ask, don't tell" is THE guiding principle to ID "research", Behe dispels it completely. That he invokes it so clumsily and quickly in response to Andrea's essay tells me that Andrea's arguments were very, very hurtful to whatever scientific argument Behe thinks he has. Nicely done, Andrea.
Henry J · 31 May 2005
Re "a scientific theory of ID,"
They also need a definition of "intelligence" that excludes the abilities of an evolving gene pool from fitting the definition. Without such a definition, standard evolution theory could be called "ID" without actually changing anything it says. ;)
Henry
Sir_Toejam · 31 May 2005
well, i'll say this is a great article by doctor Bottaro... not for the least reason that it seems to have put CW into a coma :)
Gary Hurd · 1 June 2005
Sir_Toejam · 1 June 2005
"I recommend he begin with his personal reenactment of the firebombing of Dresden, the attack on Pearl Harbor..."
He could take a few lessons from the Batley Townswomens' Guild recreation of the battle of Pearl Harbor:
http://orangecow.org/pythonet/sketches/batley.htm
Joseph O'Donnell · 1 June 2005
Congradulations Gary, your post had me in utter hysterics. It's a good idea as well, as I've often wondered why those atheistic materialistic historians have continually validated the debunked theory that there was ever a World War 2.
Gary Hurd · 1 June 2005
Glad you liked it.
I was just shown an essay by Richard Dawkins that is related to Behe's "defense." I am not a big fan of Dawkins, but this was very well written.
Aureola Nominee, FCD · 1 June 2005
Considering that "Bottaro" is most definitely an Italian surname; considering also that, in Italian, "Andrea" is masculine; I'm wondering whether Dr. Bottaro is a he or a she...
Steve U. · 1 June 2005
Gary -- thanks for the link. Dawkins essay is a nice accompaniment to Dr. Botarro's post.
Husserl · 1 June 2005
Russell · 1 June 2005
Dan · 1 June 2005
@Aureola Nominee, FCD:
Dr. Bottaro is male. At least, Behe links to a faculty web page for a male Andrea Bottaro.
JohnK · 1 June 2005
Aureola Nominee, FCD · 1 June 2005
Dan:
Thought so. Thanks.
'Rev Dr' Lenny Flank · 1 June 2005
Unsympathetic reader · 1 June 2005
Interesting response by Behe.
Essentially, he asks for the impossible. The workings of no currently studied biological system of similar size has even been described at the level of detail that Behe *requires* of a Darwinian explanation. That's right: We can't describe how systems that exist *today* actually operate *today* with that level of detail. And yet Behe elsewhere (DBB?) says that biological systems operate according to the basic laws of chemistry and physics. But how would he know this is true given the required level of proof he sets in his recent statements?
Go figure.
Henry J · 1 June 2005
Bayesian Bouffant, FCD · 2 June 2005
SteveF · 2 June 2005
'Rev Dr' Lenny Flank · 2 June 2005
Henry J · 2 June 2005
Re #33161, - does the blog software not handle nested quote tags? That reply didn't display the way I wanted it to.
Henry
Nick (Matzke) · 14 June 2005
Paul N. · 16 June 2005
I'd like to propose a new theory of Intelligent Design, called Intelligent Intelligent Designer Design. The idea is that the Intelligent Designer (whom we will assume to be a perfectly material alien, because we all know ID has nothing to do with religion) would have to be even more complex than the designed creatures in order to pull them out of a puff of smoke. After all, who envisioned all that baroque complexity.
This Intelligent Designer must have had some source for all this incredible complexity. One could posit that this designer evolved on its own, but we can give no mutation-by-mutation account. Therefore, Intelligent Intelligent Designer Design wins by default (see Behe.)
But the Intelligent Intelligent Designer Designer must be complex enough to envision the Intelligent Designer, which is pretty darn complex, so we need an Intelligent Intelligent Intelligent Designer Designer Designer...