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By Andrea Bottaro
Posted June 5, 2005
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
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
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.
recent paper in the journal PLoS Biology  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
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
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:
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 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
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  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:
- 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 . This was really a breakthrough finding,
the first solid piece of evidence in favor of the transposon hypothesis. But are RAGs actually a transposase?
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.
Indirect evidence is identified that suggests that
transposition reactions mediated by RAGs can occur not just in vitro, but
within mammalian cells .
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.
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 .
(This paper was discussed by Matt
here on PT a few
RAGs find their long-lost family of transposases . 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
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, 12, 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
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
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.
Yet the answer was there all along, in
the only place where Behe refused to look: in the box of Calvin and Hobbes.
DBB, p. 138
Thanks to Matt Inlay and the rest of the PT crew for info,
comments and suggestions.
Kapitonov VV, Jurka J. RAG1 Core and V(D)J Recombination Signal Sequences Were
Derived from Transib Transposons. PLoS Biol. 2005;3: e181 [Epub ahead of print]
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.
3. Bartl S,
Baltimore D, Weissman IL. Molecular evolution of the vertebrate immune system.
Proc Natl Acad Sci U S A. 1994; 91: 10769-70.
4. van Gent DC, Mizuuchi K, Gellert M. Similarities between
initiation of V(D)J recombination and retroviral integration. Science. 1996;
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:
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.
Originally posted at The Panda's Thumb.
By Andrea Bottaro
In the Inferno, Dante tells the story of Count
Ugolino della Gherardesca (don't even try to pronounce it, unless you are
Italian). Count Ugolino was locked
up in a tower with his sons, without food or water, by his Pisan political
enemies, whom he had betrayed. To
survive, he ate his own children (he died anyway, and got to spend eternity
stuck in a frozen lake, gnawing at his incarcerator's skull).
Michael Behe also had to face Ugolino's choice: starving for
support for ID, he was forced to eat his own brain-child, "irreducible
complexity" (IC). The meal was
fully consumed in
response to my "The
Revenge of Calvin and Hobbes" post.
Dr. Behe claims that the only evidence that would convince
him of the evolution of an IC system consists not only of a complete
step-by-step list of mutations,
... but also a detailed account of the selective
pressures that would be operating, the difficulties such changes would cause
for the organism, the expected time scale over which the changes would be
expected to occur, the likely population sizes available in the relevant
ancestral species at each step, other potential ways to solve the problem which
might interfere, and much more.
those who are wondering what that "much more" might even be, let me offer
another prognostication: if an IC system was shown to have evolved to the level
of detail demanded by Behe, his next step back would be to demand an account
that each individual mutation was truly random with regard to fitness, as
opposed as "poofed in" by the Designer.
The ID goalposts have well-oiled wheels.)
"Calvin and Hobbes are alive and well in Darwinland"
But does this demand even make sense with respect to
IC? It is worth remembering that
IC, the ID advocates hoped, was supposed to be the silver bullet that takes out
"Darwinism", the one answering Darwin's own challenge:
If it could be
demonstrated that any complex organ existed, which could not possibly have been
formed by numerous, successive, slight modifications, my theory would
absolutely break down.
Origin of Species", Chapter 6, "Modes of Transition"
There is, Behe and the ID advocates argued, something
intrinsically special about IC, that makes it particularly impervious to
irreducibly complex system, if there is such a thing, would be a powerful
challenge to Darwinian evolution.
Michael Behe, Darwin's Black Box, p. 39
Indeed, Dr. Behe has no problem at all with Darwinian
explanations as they apply to other, not irreducibly complex systems. For instance, Behe accepts that
hemoglobin (the protein complex that carries oxygen in red blood cells) evolved
from myoglobin (the protein that stores oxygen within muscle fibers). Here's
what he said about this:
The question is, if we assume that we already
have an oxygen-binding protein like myoglobin, can we infer intelligent design
from the function of hemoglobin?
The case for design is weak. The starting point, myoglobin, can already
bind oxygen. The behavior of hemoglobin can be achieved by a rather simple
modification of the behavior of myoglobin, and the individual proteins of
hemoglobin strongly resemble myoglobin.
So although hemoglobin can be thought of a system with interacting
parts, the interaction does nothing much that is clearly beyond the individual
components of the system.
even goes on to compare hemoglobin to the "man in the moon": suggestive of
design, but almost certainly an illusion.
Michael Behe, Darwin's Black Box, p. 207
But wait a minute: does Behe have in hand the list of
mutations that occurred on the path from myoglobin to hemoglobin? Does he have
"a detailed account of the selective pressures that would be operating, the
difficulties such changes would cause for the organism, the expected time scale
over which the changes would be expected to occur, the likely population sizes
available in the relevant ancestral species at each step, other potential ways
to solve the problem which might interfere, and much more"? You can try asking him, but I doubt
it. The reason why Behe has no
qualms with the evolution of the hemoglobin system is that it makes sense. The
available evidence for precursors, intermediates and their functions, partial
as it is, is sufficient to conclude that known, well-characterized evolutionary
processes were responsible, as opposed to supernatural intervention. It really doesn't matter what every single
amino acid substitution did in the long-extinct critters that evolved
hemoglobins: only someone incompetent of biology, or an unrepentant
Creationist, would require that level of detail. Behe knows that's absurd.
That Dr. Behe asks for such an unnecessary level of detail
for the evolution of the immune system (or any other IC system) carries two
implications. First, it
essentially reduces the concept of "irreducible complexity" to just a special
case of evolution incredulity in general.
Arguments from incredulity never go away (see Behe's "and much
more", discussed above). In
the case of evolution, we cannot have a mutation-by-mutation,
selective-step-by-selective-step of pretty much anything, because the evidence
cannot work that way, just like the evidence for plate tectonics can never be
an inch-by-inch historical account of all the relevant forces involved in the
motion of continents after the break-up of Pangea, or in the rise of the
Even when we can make a very strong inference of selective
effects on a protein's evolution
in this case), we are still stuck with a level of detail that cannot
compare to the absurd detail Behe is demanding.
By insisting on a degree of evidence for IC systems'
evolution that even evolutionary accounts of much simpler systems cannot
provide, Dr. Behe has therefore effectively conceded that the concept of
"irreducible complexity" is utterly meaningless: there is nothing special about
IC systems, they just look fancy. In other words, it is not the "multiple,
necessary, interacting parts" that make IC something that supposedly
resists darwinian interpretations - it is amino acids, selective pressures,
effective population sizes, like every other protein. Sic transit...
To get a sense of how silly the argument actually becomes,
consider the following. Below is
an alignment of the simple, 30-amino acid B peptide of insulin in a few
species. Many positions match, some do not.
With a little luck and hard work, we may be able to
sample enough organisms to have, at least for some branches, a real
mutation-by-mutation account of the evolution of peptide B. But no matter how we try, we will never
have "a detailed account of the selective pressures that would be operating,
the difficulties such changes would cause for the organism, the expected time
scale over which the changes would be expected to occur, the likely population
sizes available in the relevant ancestral species at each step, other potential
ways to solve the problem which might interfere, and much more". Why is insulin peptide B less of
a challenge for Darwinian evolution than the adaptive immune system?
Behe himself had summarized in his book what he saw as the
insurmountable problem of immune system evolution - not amino acids and
selective forces, but:
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
is the "problem" the current data largely address: despite Behe's
disbelief, there was a simple way that machine could be put together, by
integrating a RAG-bearing transposon (which we now know exists) into an
immunoglobulin-like immune receptor already under selection for diversity
(which we now know exists). This
single event, which bypasses all of Behe's objections above, is actually no
more complex than the transition from a monomeric myoglobin to an allosteric
hemoglobin complex ("allosteric" is just a technical word for a
protein that works by changing its shape). In fact, arguably it's simpler.
Michael Behe, Darwin's Black Box, p. 130
But rather than admitting he was wrong, that the evidence
for evolution of the adaptive immune system is solid, and strengthening by the
day, Behe has chosen instead to sacrifice whatever significance IC ever
had. He ate his own child, to
survive another day.
The second issue with Behe's argument goes back to my
original Calvin and
Hobbes post. In it, I was
not trying to make the point that the study of the evolutionary origin of the
immune system is over. Indeed, I said that thankfully there is much more to be
learned. My point was to compare
the lively and steadily progressing field of evolutionary immunology, in Calvin
and Hobbes' box, to the stale air inside the IC cabinet, in which all efforts
are directed at keeping the door tightly shut. This really highlights the difference between the ID view of
science, and what science actually is.
ID is about absolute philosophical claims -- it does not, cannot cope
with the fact that science is a process. As a political movement, ID has no time to let science take
its course -- it must provide an ideologically satisfying answer right
away, for its fund-raisers and activists, and defend it to the end. That is why scientists put their
efforts into collecting data bit by bit, and ID advocates put theirs in
revising definitions and raising the evidence bar to protect their claims from
the new scientific data.
Even Behe now behaves more like a spin doctor than a
scientist. Consider this: in his
post, Behe repeats once again the canard that Russ Doolittle made a mistake
referring to clotting factor-deficient mice a few years back (an accusation
which was nicely debunked by Ian Musgrave
right here on the
Thumb). I am quite sure
people have pointed out to Behe that his claim is false before. In fact, since we know ID advocates
eagerly read the Thumb (it took Behe only 24 hours to respond to my previous
post!), I doubt that Behe was unaware of Ian's argument as he penned his latest
reply. Assuming Behe now will
likely read this post, can we expect him to cease propagating this falsehood? We'll see.
Finally, Behe states that Orr and I "seem to think that
because Darwinists' fantastic claims are very difficult to support in a
convincing fashion, they should be given a pass". That's simply ludicrous: just my own post described a decade
worth of hard-earned experimental results (and that's just the tip of the
iceberg) from dozens of scientists, published in the very best scientific
journals, supporting an evolutionary hypothesis that Behe had embarrassingly
dismissed without a thought.
Compare this level of effort and accomplishment to that of Behe's and
his fellow ID advocates': in the same decade, they have put out not a single
iota of a positive result for ID, while the Discovery Institute was throwing
away Ahmanson's millions at school board challenges and PR campaigns hailing
the upcoming scientific revolution.
I'll leave it to others to judge whether Behe's words are
more arrogant or ignorant. The
real question to consider is: who is asking to be given a pass for "fantastic
claims" here, those who are collecting data to support their hypotheses, or
those who are running away from them?
Originally posted at The Panda's Thumb.