If a theory claims to be able to explain some phenomenon but does not generate even an attempt at an explanation, then it should be banished. Michael J. Behe, DBB p.186

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This website is made up of posts made on Behe Fails Weblog. Even though it is made up of separate posts, the posts were written to relate to each other sensibly.

18. Evolution of the eukaryote flagellum
19. Eukaryotic flagella are derived from intracellular transport systems (9.23)
20. Common descent is demonstrable only when causes are known (9.24)
21. The cilium evolved into part of the "irreducibly complex" chordate eye (9.27)
22. Behe denies all avenues to understanding the evolution of pathways (9.29)
23. Behe and language origination (9.30)
24. If evolution is true, why can't gazelles run 433 mph? (10.2)
25. Evolution of adaptive immunity I--Phylogeny

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Electric Consciousness
Consciousness as Electric Field Dyanamics

18. Evolution of the eukaryote flagellum

There is not much truly known about how the eukaryotic flagellum evolved, other than that it did and from what cellular components most of it evolved. That is considerable, of course, and is infinitely more than the facts that ID explains (zero). Yet the one good thing about ID and Behe is that they point out how much is not known, which is often not well discussed in scientific circles--although occasionally journals will have articles discussing what is so little known in many areas, including evolution. So there is some point to agreeing that much remains in question, so long as it noted that it is not as little as Behe claims, nor does the evidence indicate anything that differs from the expectations of unguided processes.

There is an online paper that makes some educated guesses about how the eukaryote's flagella/cilia evolved, which is worth a look. It is: Speculations on the evolution of 9+2 organelles and the role of central pair microtubules, by David R. Mitchell. It elaborates on the obvious point that cilia are made from part of the framework of the eukaryotic cell and some of the machines that provide intracellular transport.

Soon it gets to the most interesting, and probably the most questionable, speculation, which is that eukaryotes used microtubules radiating from a centrosome in order to partition duplicated chromosomes. Apparently this idea is patterned on the microtubule-based spindle used to separate chromosomes in present-day animal cells. And from the early proto-cilium that was used to separate the chromosomes evolved the cilium, by asymmetrically growing into a bundle (actually, only two at first) of microtubules that extended the cell outward to create gliding motors that acted both to move the cell and to provide sensory activities.

After that the beating cila/flagella would evolve for swimming, and the numbers of microtubules bundled together would increase dramatically, at least in some lines. From that the 9+2 arrangement would evolve because it is fairly good for the sake of controlling the beat of flagella and cilia. A fair bit of the paper is taken up discussing the evolution of the ancestral 9+2 configuration of the cilium and flagellum. Anyhow, I do not intend to try to re-write what is written in that short paper, particularly not the 9+2 configuration, which seems least relevant to the evolvability of the eukarote flagellum.

What is important is that there does exist at least a somewhat reasonable path toward evolution of the flagellum in the literature, and there seems to be nothing to preclude our cilia and spermatic flagella from evolving in that manner. Surely it could happen.

I have to wonder about the step in which the cilium evolves from microtubules involved in mitosis, however, which is credited to earlier authors by Mitchell. One problem is that in present-day mitosis the spindle only operates during mitosis, and is dissassembled rather quickly afterward. Why would an early eukaryote keep its spindle-equivalent around, when it would just get in the way? Furthermore, the operation and set-up of microtubules during mitosis have relatively little to do with the operation of a cilium. Combining mitotic processes with even the processes occurring in a gliding cilium (gliding cilia, by the way, are found in a few modern eukaryotes) does not appear to be a successful evolutionary "strategy".

Evidently part of the reason various authors want to understand the cilium as coming from microtubules involved in mitosis is that it provides an explanation for how eukaryotic cells become polar. Yet that, too, seems to be insufficient to combine mitotic and ciliary microtubules, because the cells only need to use the polarity provided by mitosis to place a flagellum at one pole. It seems far more likely to me that intracellular transport mechanisms might evolve into gliding motors (for movement, chemosensation, or both), which evolved to be more efficient by protruding from one pole of the cell. This could be somewhat similar to the movements that amoebae have evolved, it's just that in this case the movement became compartmentalized and specialized to a far greater degree.

Like I implied above, this is all just speculation without a great deal of constraint. Take it or leave it, whether it is Mitchell's paper, or my criticisms of the hypothetical mitosis-flagellum link. They are included because, once again, these are examples of how caring about observable causes can lead to thought, as poof "explanations" cannot. What really matters is all of the evidence that the eukaryotic flagellum did evolve, and the hope that this might eventually help us to tease apart the mystery of how our cilia/flagella evolved--though it is not certain that all distant evolutionary processes will be knowable, including this one.

The evidence that it evolved will soon be the subject of another post. The fact is that we have enough reason to believe that the evolution of the eukaryotic flagellum is possible, but more importantly, we have good evidence that it did. Real science proceeds from the evidence that, say, language evolution, or biological evolution, happened to the actual causes behind it. And of course "actual causes" means "observable causes" (at least in principle), if we take epistemology at all seriously.

9.22.08                                                                                                                       To top

19. Eukaryotic flagella are derived from intracellular transport systems

One of the problems in discovering how cilia/flagella arose in eukaryotic cells is that such a large proportion of the "parts" are used for non-ciliary purposes. As one paper discussing the evolutionary and functional aspects of cila notes, regarding the research that went into it:
Ciliary genes that serve multiple cellular functions were not selected in this screen, mainly because they are still present in organisms that have lost ciliated structures. For example, dyneins are critical components of the ciliary motility apparatus, yet many were filtered out in our screens because they are also involved in intracellular transport in nonciliated organisms. Indeed, we suggest that the reason so few candidate genes were recovered in the "all ciliated organisms" subgroup is because proteins common to all cilia, like those involved in axoneme assembly, are also required in basic cellular processes and therefore conserved in nonciliated organisms (e.g. α-tubulin, β-tubulin, γ-tubulin, centrin, pericentrin, etc.). (Avidor-Reiss, T., et al., 2004. Decoding cilia function: Defining specialized genes required for compartmentalized cilia biogenesis. Cell 117, 527-539)
However many times I have mentioned this, it remains important that even Behe notes that "In Darwinian evolution, only physical precursors count" (DBB, 118). And yes, they exist in great abundance, while the "conceptual precursors" likely in design do not have any credible evidence for existing in life at all (if we exclude our limited meddling). In eukaryotic flagella, we don't just have a great many homologous components, we have a great many components that are simply shared between flagella/cilia and the structures and machines that transport intracellular materials.

What this always comes down to is whether or not someone will accept the evidence, since the evidence for the cilium evolving from existing transport structures and machinery is so very clear. Of course one can always claim that a Designer is responsible for a child having half of his genetic material being identical to a certain man's DNA. It's always just possible, as far as the merely logical goes. But it makes no sense (and is not worth bringing up in a paternity suit)--it is a stupid inference, let alone being unscientific. The shared material between intracellular transport machinery and the cilium exists because they have a common origin (and not a designer, who would be capable of borrowing from archaea, bacteria, and of completely novel constructions), or you're just throwing away all of your bases for doing science.

However, as if to clinch the case against the anti-science faction and their delusions about "designed cilia," researchers were quite capable of finding a set ciliary proteins that are "related to prototypical intracellular transport proteins." The aforementioned research paper mentions some such homologies in the passage below, involving a specific family of ciliary transport proteins, the OSEGs:
OSEGs are characterized by the presence of two major protein-protein interaction domains, WD and TPR repeats, implicated in the assembly of multiprotein complexes. Significantly, the most closely related proteins outside of the family are α- and β'-coatomer, two cargo-carrying proteins intimiately involved in intracellular trafficking (...). Furthermore, clathrin heavy chains display striking domain similarity to the OSEG family: an N terminus consisting of 7 WD repeats and a C terminus consisting of ~35 TPR-like repeats known as CHCR motifs (...). Interestingly, coatomers and clathrin-mediated transport system use small G proteins of the Arf subfamilies as regulators of the transport process. notably , our screen also identified ARL3 and ARL6, two Arf-like proteins, as components of the ciliary compartement group, with ARL6 expression restricted to mechano- and chemosensory neurons. (Avidor-Reiss, T., et al., 2004. Decoding cilia function: Defining specialized genes required for compartmentalized cilia biogenesis. Cell 117, 527-539)
Or in other words, this is an example of the genes and their products involved in eukaryotic flagella which are homologous with cytoplasmic transporters. Page 533 of the same article has a figure (4) showing some of the homologies. No doubt many more homologies could be found in the literature, but anyway it is the proteins that are exclusive to eukaryotic cilia/flagella that are the exception, while proteins shared with cytoplasmic transport are the rule.

This particular paper comes to the only reasonable conclusion:
Surprisingly, the integration of these proteins into a groups of genes related to the main families of intracellular transport proteins had escaped notice. Our results illustrate a common foundation in the organization of intracellular transport systems, whether mediating internalizations of surface proteins, transferring cargo between organelles, or delivering components from the cell body to distal ciliary compartments. (Ibid.)
Anyone who has read Behe's books knows, however, what his response would be to this. He would simply agree that common ancestry is shown by the homologous and shared genes and proteins, while "how" it occurred is an entirely separate question in his mind. Of course it is not separate at all, since one had to show a reasonable mechanism for how life could change before it would be accepted that cyanobacteria and humans share a common ancestor (or actually, that far back it might be a shared set of promiscuously conjugating cells not otherwise closely related), for common ancestry alone would suggest that all organisms are of the same species. After all, no one ever simply looked at micro-organisms and humans and immediately leaped to the conclusion that the two were related, rather this had to be worked out in detail.

"Poof" would be no explanation no matter what, hence ID would fail regardless of the evidence for evolution. Yet because Behe's criticisms of evolution in his books rests upon his specious and appallingly reductive claims that common ancestry, mutations, and natural selection are all separate issues, my next post in the DBB category will be about how they are in fact interconnected.

9.23.08                                                                                                                       To top

20. Common descent is demonstrable only when causes are known

Bear in mind, throughout, that common descent is a distinct concept from the mechanism of natural selection acting on random variation. Edge of Evolution, 64

In the abstract, the quote above is true. It is in reality that Behe's constant resort to the contingencies of "naturalistic" heredity, while denying "naturalistic" contingencies in adapatation, fails utterly and completely, both on the ground of consistency and because he is unable to differentiate between the causes of various effects. If he is unable to constrain "design," as he most certainly is not able to do (indeed, he takes pains to try make his claims of design unfalsifiable), then he cannot constrain anything else in the history of life. If "...anything might have been designed" (DBB, 193)--including mutations which are directed (a favorite claim in EoE)--then we have no reason to believe that the evidence of common descent was not also designed, and produced by miracle.

Yet he does believe observable causes are responsible for similarities:
Like the sequence analysts, I believe the evidence strongly supports common descent. DBB, 176
Unsurprisingly, where the actual "naturalistic" causes are unknown, whether in "design models" or in "atheistic models," such certainties have not been obvious or accepted. A philosopher such as Buffon could propose that life arose to fit "internal molds," which shaped organisms into set patterns. Paley states that "This similitude, surely, bespeaks the same creation and the same Creator" (Natural Theology, chap. 25).

One might suppose that Behe has more cause to believe in common descent than Paley did, however. Well, yes, that is true, both in the huge amount of evidence which indicates what is expected of common descent, and at least as importantly, because we understand the mechanisms of both conservation and of non-conservation of genetic information in organisms. The processes of preservation and of change are inextricably tied together within biology, never mind the fact that the concepts are different (the processes themselves are occasionally separable, such as during the early part of abiogenesis). That is, we understand how genetic information is preserved both by reproduction and by natural selection, and we know that because we understand the limits of change imposed by (roughly) the neo-Darwinian model of evolution.

Paley credited God for similarity because he could not conceive of how morphology (which is about the only type of evidence that he had) could be preserved as a "general plan," yet so thoroughly modified. Darwin explained this, which is why he and most modern biologists have understood the evidence of common descent to implicitly support the known causes of organism modification. For, if there is nothing that accounts for the differences between frogs and humans, how are the similarities going to be accounted for via common descent? We have to understand similarities and differences under the same model, and we do so by understanding them all to be due to common descent as modified by mutation plus natural selection (plus other known processes).

Once one believes that an unobservable and unpredictable (in the probabilistic sense of the word) process, or processes, is responsible for the "design" of organisms, how can one possibly determine which aspects of organisms were not poofed into existence? A rat might as easily be descended from, or designed from the template of, an octopus or a petunia, if we are not paying attention to the actual mechanisms of stability and of change. The only apparent reason why Behe accepts the accidents of heredity, and not the evidence of accident in adaptation, is because he wishes his god to be responsible for the latter and not for the former. This goes back to the fact that Behe has absolutely no means of independently observing design in life in an entailed manner, discussed here.

The evidence that life evolved in a process involving natural selection is precisely the evidence of accident and contingency found in life. Two such crucial contingencies are the accidents of heredity and of mutation, and, aside from effects of the filter of natural selection, that is largely what we see in life (I write "largely" because causal regularities exist apart from natural selection and descent). The accidents of heredity are accepted by Behe as causal, even though any accepted meaning of the term "intelligent design" implies that such accidents would not predominate in life as they do--we filter out many undesirable accidents whenever we adapt designs. Then he wants "design" to hide underneath the accidents of mutation, and to be indistinguishable from them, except probabilistically.

Such a position must be called "incoherent," at least if we are being charitable. The filter of intelligence involves rationality, planning, and the correction of defective accidental characteristics, wherever these occur. We accept that a filter quite different (if with some similarity in output) from intelligence produced life precisely because neither accidents of heredity nor of mutation characterize intelligent activity to any great degree, while they are unquestionably predicated of any unguided natural selectionist evolution involving the sorts of organisms we recognize.

I am writing this now because just one day previously I wrote a post about all of the evidence of evolution in the eukaryote flagellum, one of Behe's "examples" of "irreducibly complex" systems. I noted there that Behe would accept the evidence of common descent, but would deny that it indicates that it evolved by the mechanisms by which we say it evolved, rather claiming that it had to be designed. That, however, is an absurd notion on his part, for the terms "intelligence," "design," and "intelligent design" do not even refer to processes adopting the contingencies of heredity and mutation that we observe in life. "Evolution," and "evolution by natural selection," by contrast, do refer to processes including such observed accidents and limitations. We simply match up cause to effect to conclude that eukaryotes' flagella evolved (with no poofs).

So of course it is true that "common descent" and "natural selection" are separate (at least separable) concepts. In science, though, we do what Behe and other IDists do not, which is to combine the two concepts in order to constrain these concepts as they actually (empirically) do pertain to life.

Because Behe does not follow science at all in the area of origins, we are at a loss to understand how his god of the miracle mutations is in any way preferable to, or more scientific than, the belief that some god simply spoke all of life into existence a few thousand years ago, complete with the evidence predicted for organisms that have evolved without any guidance of intelligence.

9.24.08                                                                                                                       To top

21. The cilium evolved into part of the "irreducibly complex" chordate eye

How do we get theories, and what is their purpose? Is a theory something that we have after every phenomenon encompassed by the theory is completely explained? Why would we even need a theory in biology, if we knew everything that happens in the past and present according to physics, and its theories?

Of course Behe and the other IDists' understanding of (or at least rhetoric about) theory is as flawed as their understanding of everything else in science. This is not the post for a long discussion about why theories exist, yet it is worth pointing out, yet again, that theories exist to guide research and to organize knowledge, and are not catalogs of everything that has happened, is happening, and will happen. This is why evolutionary theory is a crucial theory, because it acknowledges the constraints that exist in biology and thus explains the limits of biological change. This would even be true if Behe's mutation-causing God were responsible for some mutations, because in any case this "God" does not transcend the limits of heredity and of mutation, or at best (we have to trust Behe to discuss this claim, since he supplies no evidence for this mutator) only pushes the limits of mutation without doing anything that we understand as design-like (such as giving radio communication to organisms).

The above follows up on my last two posts involving DBB, here, and here, and it introduces the following discussion of how the structures of cilia provided opportunity and constraint in evolution after the cilium first became a fixed eukaryotic structure. No, not everything about the origin of cilia is known, nor is everything about the evolution of cilia into parts of sensory structures understood, but only evolution makes any kind of sense at all of the distributions and modifications of cilia that we find in noses, in eyes, and in the motility of ciliated cells, in addition to its origin.

Sensory reception via cilia appears to be evolutionarily ancient (Mitchell), so the fact that cila comprise parts of the vertebrate eye, olfaction, and of taste buds is not especially surprising. Presumably, cilia have had a sensory role from very early in evolution both because they provide extensions into extracellular media, and because they can set up currents in liquids in order to sense media which would otherwise be beyond the reach of the ancestral free-living cell. Nevertheless, the evolution from what were probably moving cilia to the outer portions of the rods of our eyes is the kind of transformation that we would not suspect, if the evidence of it were not so clear. Here is a photograph (bottom) of a rod cell of the eye, with a cilium clearly visible as part of it.

The transformation of part of the cilium into stacks of lamellae, and the role played by the cilium as a photoreceptor, indicate a rather extensive evolutionary change of this supposedly "irreducibly complex" organelle. Indeed, most (perhaps all) of the "irreducibly complex" visual biochemical pathway that Behe discusses in DBB chapter one (see figue on p. 20) occurs exactly in the region of the rods which are made up substantially of cilia, although these originally evolved for quite different purposes (motility and chemoreception).

My point here is not to go through the complexities of these matters (which can be found on the web quite easily), but rather to show that we have "nested" complexities which reveal successive evolutionary events--not the sudden creation at the Cambrian hinted at by Behe and other IDists--having all of the accidents (hereditary and mutational/selectional) expected in evolution, and highly complex modifications of previously evolved complexities. Importantly, evolution proceeds just as predicted by evolutionary theory, with evolved complexity itself almost certainly providing a major constraint on the evolution of later complexity (of P. falciparum, for instance), so that the complexity of the cilium is utilized by the chordate eye in order to supply the complexity needed for photoreception.

What is perhaps at least as interesting is that the modification of the cilium to function for the eyesight of chordates was not the only solution to the problem of photoreception. We have ciliary photoreceptors, while many animals have rhabdomeric photoreceptors, which apparently evolved from the same cells from which retinal ganglion cells are derived (Evolution of eyes and photoreceptor cell types). Again, the story is of accident, where no design reason can be given for our ciliary photoreceptors, and it is the accidental (initial and subsequent) evolution of cilia that gives us any reason for such an odd switch from rhabdomeric photoreceptors to ciliary photoreceptors in the chordate line. That anyone would try to claim that such obvious accident is the result of "design" strains any notion of design that reasonable people have.

I do not plan to revisit the evolution of the eye after this, since the incorporation of the "irreducibly complex" cilium into the "irreducibly complex" vertebrate eye while all of the hereditary and mutational/selectional constraints of evolution apply, is the only possible, and easily sufficient, evidence that unguided evolution is responsible. Complexity builds upon complexity in the same sorts of evolutionary (cladistic) patterns as exist in microevolutionary processes, and only a fool would fail to match up cause and effect in both microevolution and in macroevolution.

However, since this is probably the only substantial discussion I will have of eye evolution (at least while discussing Behe's books), I'd like to point to a some more evidence of the evolution of the eye from simple to complex that may be found in the last link/reference. Never mind Behe's peculiar and unjustified demands for evidence, here is some of the reasoning (from evidence) and conclusion for evolution from simple to complex:
The prevalence of pigment-cup eyes in Bilateria, and their stereotype, simple design, tells us that eyes started off with merely two cell types, photoreceptor cells that associated with pigment cells to detect the direction of light (...). Additional cell types were added during subsequent eye evolution, such as lens cells, various kinds of support cells, muscle cells etc. that also formed part of the eyes. Cell type diversity reached its maximum in the vertebrate and cephalopod camera eye, as well as in the arthropod compound eye. Evolution of eyes and photoreceptor cell types
Opsin homologies go back at least to before the evolution of bilateral animals ("bilaterians"), such as ourselves:
On the molecular level it is long known that all eye photoreceptor cells so far described use a vitamin-A-based light-sensitive photopigment, comprising a chromophore and an apoprotein, opsin. Phylogenetic analysis approves that all opsins trace back to one opsin precursor molecule that predated bilaterians. Evolution of eyes and photoreceptor cell types
Beyond that, the homologies are extensive throughout vertebrate eyes, and yet however common a gene like pax6 may be in animal eye development, it, too, appears to be so due to accidents of heredity, for it is neither exclusive to eye development, nor needed for the development of all animal eyes:
In the vertebrates, pax6 is required for the formation of virtually all retinal cell types.... In Drosophila, the pax6 orthologs eyeless and eye gone are required for the formation of the entire eye disc (...), which gives rise to all ommatidial cell types including the photoreceptor cells. Eyeless and another pax6 ortholog, twin of eyeless are also expressed in precursor cells of the photoreceptive Bolwig organ and ocelli (...), and in the late Bolwig organ (...). In line with a general affiliation with photoreceptor cell specification, pax6 expression also covers the early eye anlagen in cephalopods (...), planarians (...) (...), nemertines (...), and polychaetes (...). However, and even if pax6 started off as an early photoreceptor specification gene in pre-bilaterians, in none of the species investigated is pax6 photoreceptor cell-specific, or even eye-specific (...). This means that the ancestral function of pax6 in cell type specification or differentiation (whatever it was) is not exclusively required in photoreceptor cells. It is also clear that in few cases photoreceptor cells can form in the complete absence of pax6, such as the Hesse eyecups in Branchiostoma (...). Evolution of eyes and photoreceptor cell types
The animal eye is an exquisite adaptation, an organ that is extremely important to the lives of most animals that have eyes, and so eyes are finely-honed instruments. A very crucial point to the use and intellectual sense of the achievement of understanding, however, is how to account for all of the accidents of heredity and apparently of mutation/selection. Thus, we like to know why the chordate eye is a complex of preceding parts, such as cilia, and in turn, why cilia are composed of parts of cytoplasmic transport systems which preceded the cilia.

None of these questions are asked by IDists, for they know that they have no answers via design. Accident is the antithesis of design, despite the fact that Behe tries by analogy to claim that apparent accidents are within the realm of "design" (DBB 193-194). Of course he tries to do so, since he knows that life is shot through with evident accident, including complex accidents (coupled, of course, with natural selection) like ciliary eyes. He does the only thing he can do, however, which is to try to claim that some complexes of accidental characteristics are too complex to be the result of accident, then to claim design without any actual evidence in favor of design.

Actually, though, complexes of accident ought to be accepted as being the result of accident (plus ordering principles, like natural selection) so long as design characteristics (purpose and rationality being the biggest) cannot be demonstrated. For the fact is that when you have the sequential accidents found in life, like oxygenic photosynthesis producing the necessary oxygen for the Ediacaran and the Cambrian "explosions", or cilia being composed of intracellular transport biochemicals and then cilia hosting crucial photoreceptor biochemical pathways, you really can only honestly conclude that the accidental effects are due to accidents which natural selection filters, not to design.

For, again, design is itself the opposite of accident, if not totally devoid of accident. That is, design filters out most accidents, leaving primarily non-accidental rational organization--at least when it is good design. When it comes right down to it, natural selection only refines accident--it really only filters organic traits out of the accidents of mutation, duplication, deletion, and environmental contingencies--for an incomplete list--and however many accidents are excluded, only accidents remain. Because we see only accident and natural selection behind the integrated complexities of life, we must pick evolution as the cause of life's configurations.

9.27.08                                                                                                                       To top

22. Behe denies all avenues to understanding the evolution of pathways

This is just a short post, following up recent posts that point to evidence that does indeed give very good hints at how metabolic pathways evolved, such as through the adaptation of cilia for photoreception, gene duplications in general, and duplication of the genes for photosystem I, which allowed for the evolution of photosystem II.

You can see the satisfaction that Behe has in the idea that his claims are beyond the reach of the evidence, in the following DBB quote:
Thus biochemistry offers a Lilliputian chalnge to Darwin. Anatomy is, quite simply, irrelevant to the question of whether evolution could take place on the molecular level. So is the fossil record.... Neither do the patterns of biogeography matter, nor those of population biology, nor the traditional explanations of evolutionary theory for rudimentary organs or species abundance. DBB, 22
Unsurprisingly, he ignores rather crucial issues of falsifiability of unguided evolution, such as whether or not cladistics map out to the expected evolutionary predictions, which, so far as anyone can demonstrate, is indeed the case. He also ignores the fact that if evolutionary thinkers were unable to garner positive evidence in favor of "darwinian evolution" from the various lines of evidence, the exact same fact would exist for ID. But then he fails to understand the need for positive evidence for his claims, unlike the far better scientific thinker, Rev. William Paley (See here).

Above all, he wants to pretend that science should not simply use the evidence of origination that fits taxonomy, biogeography, comparative anatomy, and the fossil record, unless actual evidence is found that something else is responsible--or if one found actual evidence that it could not have evolved (he isn't even close).

But another issue crops up in the book, for note that the quote above came from page 22. Only rather later does he even bring up genetic evidence of molecular evolution, and then denies it without justification or a mention of evidence. The denial is bad enough, and reveals an apparent stupidity on his part, though it could be mendacity instead. Yet, worse, it would seem as though he left this issue alone at the beginning because he actually knew that it could provide such evidence (or if he's too deeply into denial, he seems to know that others say so). Otherwise, why would he not bring it up on p. 22? On pp. 180-181 can be found his blank, unevidenced denial of this crucial issue (though the same stupid denial is on p. 90, its first appearance I believe):
...Although sequence data can be used to infer relationships, they cannot be used to determine how a complex biochemical structure originated. DBB 180-181
Never mind that he does exactly this time and again, including mitochondria and even to a degree with his "irreducibly complex" examples, for, although he denies that they evolved by "Darwinian" means, he does not deny that genes were adapted from previously existing genes. This is acknowledged more explicitly in Edge of Evolution.

This is not the only time that he brings up crucial issues only when (it appears) he hopes to have already confused people sufficiently that they won't catch on. I have mentioned this before, but he writes on p. 245 of DBB "...Large questions remain (as they inevitably do in basic science),...." Suppose he had admitted as much at the beginning, rather than well after he had claimed that evolution doesn't work due to the difficulties we have in the basic historical science of biology? It would have completely undermined his whole case.

Oh, I am quite convinced that he crafted his book to avoid many of the honest questions, at least until after he had already dishonestly misconstrued the science of evolution. Of course even at the end he quite continues to deny the obvious, that genetic sequences give us considerable insight into the evolution of metabolic pathways, no matter that he himself makes many claims based expressly upon genetic sequences.

Could he ever admit that we can indeed find out how genes evolved by observing the evidence of gene splits? Of course he could not, because then he'd have to honestly face (or at least would be pressed to do so) the evidences of duplications behind the evolution of the clotting cascade and in the evolution of oxygenic photosynthesis, as well as having to notice that his "irreducible pathways" in the eye are mainly in an highly modified cilium, which in turn is a highly modified set of pre-existing cellular transport system.

Since he never once was interested in supplying any evidence for design, he doesn't mind closing off all avenues which provide the evidence that life evolved. The mere fact that he ends up basing his pathetic analogies and "arguments" on exactly what he has denied is not a problem for someone who isn't concerned about either science or consistency.

9.29.08                                                                                                                       To top

23. Behe and language origination

When Behe was told that both Greek and Latin derive naturally from the ancient Indo-European language, as evidenced by the similarities between the family of languages which includes those two, he said:
Although one may determine relationships of languages by looking at similarities of words and of grammer, how duplications, modifications, and the shuffling of words actually occurred is completely beyond the knowledge of science. One cannot know whether they arose gradually or suddenly, by human selection, or by the intervention of a language designer.

In fact, since no human has ever been able to invent a single language with the complexities of a natural language, as opposed to artificial language, it appears highly unlikely that natural human selection could possibly produce the complexity of Greek and Latin. How could inflections "suddenly appear" in Greek and Latin, if there were no intelligence capable of designing grammar? Furthermore, languages don't fossilize, so the fossil record will provide no evidence of "naturalistic evolution," nor will anything else.

Remember, frater might in some way resemble φρατηρ, and Latin verb inflections might resemble Greek verb inflections, but the similarities say nothing about how a language like Latin is produced. The sheer complexity of both Greek and Latin, which has only been understood by humans recently, could hardly have been produced by humans who did not understand the complexities of language.
Well okay, he didn't really say that, but he wrote something equally unscientific and just plain divorced from reality. What I wrote above is based on the following:
By itself, however, the hypothesis of gene duplication and shuffling says nothing about how any particular protein or protein was first produced--whether slowly or suddenly, or whether by natural selection or some other mechanism. Remember a mousetrap spring might in some way resemble a clock spring, and a crowbar might resemble a mousetrap hammer, but the similarities say nothing about how a mousetrap is produced. In order to claim that a system developed gradually by a Darwinian mechanism a person must show that the function of the system could "have been formed by numerous successive, slight modifications." DBB 90
Of course I had to change it to fit language evolution, and perversely, I had to shift his analogy to one that actually is roughly analogous with biological evolution, hence it becomes absurd to say that the similarities of an evolved language say nothing about how these originated, although of course the (non-accidental) similarities of his designed object really do give no indication (by themselves) of how they were actually made. When I change his dis-analogous comparison into an analogous comparison, it becomes a senseless claim (think of how differently aliens might make these objects).

I briefly discussed his denial that genetic evidence tells us about evolution yesterday, along with his denial of all of the other evidence. But this particular denial cuts so close to the heart of Behe's errors and apparent lack of understanding of science that I thought it would be worth discussing further, especially since it tantamount to denying the evidence used to understand language evolution (although the selectional mechanisms are different, which shows up in the details of both evolutions, including their taxonomies). For, nucleotide sequences, coupled with their organization, have many similarities to languages and their structures, even though they also have many dissimilarities.

By contrast, there is no "phenotype evolution" of language comparable to the evolution of phenotypes in biological evolution, and all "language fossils" (texts) are quite recent, certainly more recent than the Indo-European language, which is inferred solely from the vocabulary and grammar of the languages derived from it. We're stuck comparing evolution of the "languages" of biology and of humans, if we wish for the most honest analogy of the evolutions of both.

And of course one may study languages in context to understand the mechanisms of language evolution. This, by the way, opposes how a science touching upon intelligent cognition actually operates, versus ID which has no mechanism or meaningful causes whatsoever. Indeed, even the rates of language evolution are thought able to be studied, so that one study concluded (as most biologists also conclude regarding organic evolution) that languages typically go through bursts of evolution, as in "punctuated equilibrium."

Among IDists there seems to be quite an aversion to actually considering evidence. Behe does not look at the gene sequences and ask what they tell him, instead he looks at them and denies that the evidence matters. In addition, he brings in a canard in the above quote, using Darwin as the standard for what sorts of changes are possible in evolution, when in fact many consider that at least some of the changes (like gene duplications) can be quite dramatic and not "slight" changes as such.

If one looks at genes one may observe whether or not gene duplications provided the opportunities for "slight modifications" (at least relatively small changes are thought responsible for modifying most duplicated genes) which in time could produce dramatic changes. In a similar manner, one may detect whether or not there was a single ancestral gene, if one is able to do enough comparison of the appropriate genes, and thus whether or not two or more copies evolved from one or more duplication events (important in the evolution of the adaptive immune system, soon to be discussed here). One may observe ancestral functions of genes by genetic comparisons, and therefore what later genetic capacities have evolved. Above all, one may discover what constraints existed in the evolution of a certain capacity, for instance what sorts of genes were needed for a function like adaptive immunity, and to discover precursor genes that already had some of the needed function. Indeed, that is often enough how the precursor gene itself is found, through the function, and only then it is found to have an ancestral sequence.

Indeed, the constraints of biological evolution are rather more strict--hence cause is more easily matched up with effect--than in language evolution. Yet no one really thinks that we can't come to reasonable conclusions about many of the mechanisms of the evolution of a given language. Biological evolution is much more precisely understood than is language evolution, and yet the IDists do not complain about the latter, only the former.

I brought up such obvious evidence of origination in the penultimate paragraph in part because I intend to discuss mainly the evidence that adaptive immunity evolved, and not so much the questions about how it "could evolve"--though clues about such possibilities are also to be found in genes, without being resolvable at this time--as has happened often. Someone like Behe (unlike many traditional creationists) does not deny the massive evidence for language evolution merely because no one has ever truly shown that humans are capable of functioning to effect such complex evolution--indeed, one simply uses the evidence of language evolution to understand presently known mechanisms and possibly some remaining unknown ones (on the other hand, Behe would be likely to simply credit "intelligence" as the cause of language evolution, and thus would probably fail once again). Likewise, when we observe genes in agnathans (jawless fish) and gnathostomes (jawed vertebrates) which gave rise to different families of genes for their divergent adaptive immune systems, we understand evolution to occur by sufficient and observable means, crucially via "natural selection," and seek to understand how these systems evolved by such known means--and possibly by unknown means--if effects of these may be discovered.

The fact is that genomes are coming on-line more and more swiftly--for many reasons--with one of the prominent reasons being in order to discover how genes and pathways evolved. Fortunately for us, several of the "irreducibly complex" pathways not only were reasonably well understood when Darwin's Black Box was written, but are even better understood today. The evolution of adaptive immunity may be one of the best examples of learning from genetic comparisons how it evolved from innate immunity (primarily), and so, far from being a problem (though questions remain), it is in fact one of the best counterexamples to Behe's complaint that he doesn't understand how it evolved, so it must not have done so. And that is what will be discussed soon in the Darwin's Black Box category.

9.30.08                                                                                                                       To top

24. If evolution is true, why can't gazelles run 433 mph?

The thrust and parry of human-malaria evolution did not build anything--it only destroyed things. Jettisoning G6PD wrecks, it does not construct. Throwing away band 3 protein does likewise. Sickle hemoglobin itself is not an advancement of the immune system; it's a regression of the red blood cell. Even the breaking of the normal controls in HPFH doesn't build a new system; it's just plugging another hole in the dike. Edge of Evolution 42

Behe has a creationist view of these matters, so that hemoglobin remodeled to confer partial immunity to malaria for those who are heterozygous for sickle cell anemia is "regression." Scientifically and philosophically, that is nothing other than nonsense. The other mechanisms we have evolved that are mentioned in the above quote have varying degrees of deletion (which science would consider to be a functional regression, if still an improvement to fit current conditions) and/or change. Leaving those aside at the present, let us just note here that the changes that cause sickle cell anemia in homozygotes is definitely an improvement for heterozygotes, and his comparisons to a utopian defense against malaria of the kind a true designer (especially his omniscient "designer") might produce has no place in understanding evolution.

The larger concern involves something quite different, which are the constraints of evolution. Even Behe mentions the constraints, oblivious to the fact that we accept evolutionary theory precisely because it fits the constraints seen in life. He writes:
Darwinian processes are incoherent and highly constrained. EoE 19
Well, Behe is incoherent, because in other places he claims that evolutionary processes mimic intent (also not true), which is typically not incoherent, even if incoherent statements are the norm in intentional ID arguments). Yet he is correct that evolution is highly constrained. Indeed, why else would the basic elements of our adaptive immune system remain the same for nearly half a billion years (though many of the parts have been significantly modified, added, or deleted)?

Beyond that, well, why can't gazelles run 433 miles per hour, and cheetahs run somewhat faster, if evolution is constantly selecting both to optimize speed? Said that way, it sounds absurd, as if there are no limits to animal speed, let alone limits to what can evolve. Nevertheless, Behe's "argument" about malaria and humans not evolving better "strategies" to attack and to defend, respectively, is about as intelligent and apropos as claiming that gazelles ought to run at least 433 mph by now.

What is more, chordates have evolved what is really quite a wonderful immune system, first evolving the innate immune system, and then a supplement to it which uses many of the same components, the adaptive immune system. That he denies that this is the case is hardly of any consequence, for the evolution of the adaptive immune system fits the constraints that he himself brought up, that "Darwinian evolution requires physical precursors.” DBB, 45 If not all such precursors have been found (and it is likely that not all will be, as extinctions of gene lines are not unexpected or uncommon), many have been, and the cladistic patterns map out to evolutionary expectations.

Importantly for our purposes, the complexity of our immune system evolved in stages, and according to the "nested hierarchies" predicted of organisms which are mainly limited to vertical transmission of information. The odds against evolution producing the innate and adaptive immune systems all at once are decisively against, and innate system precursors were needed for the adaptive system to operate and to evolve (not all adaptive system precursors come from the innate system, according to the evidence).

My previous post in this category (Darwin's Black Box), and this one, are leading up to future posts dealing with the evidence of the evolution of immunity, framing the issue. After all, Behe manipulates the argument by framing everything according to his perspective, which truly does amount to dishonest framing. I am indeed framing (in the way more writers on these matters should do), by restoring the context that Behe stripped away from his own discussions of these things, and I do not doubt that this is quite an honest frame. The immune system is very important in both of his books, so I have an additional point to bring in as introduction, which is that the evidence of the evolution of the immune system goes directly against Behe's claims of the inadequacy of evolution, in both of his books--but especially in Edge of Evolution (which is why this post is also in the EoE category, and will be put on the EoE cumulative post).

So I want to make clear how Behe's criticisms of the "inadequacy" of evolution in response to malarial infection in humans fail so badly, since I will be bringing in good evidence that adaptive immunity did evolve. Crucially, we already have evolved an immune system that is both complex and to a considerable degree optimized. This is where the gazelle analogy comes in, for while gazelles run very fast and often leave cheetahs hungry, they can't just simply keep evolving to run ever faster, due to physical limitations and to evolutionary limitations (indeed, evolution gave birds a better breathing system than it gave mammals, a typical non-design, makes-sense-only-in-the-light-of-evolution, limitation).

It is foolish to ask why evolution has the observed limitations, when the meaningful question is why Behe's "design" seems to have so many limitations--and notably the same ones that evolution has. Furthermore, Behe still has absolutely no answer to the question of how he can determine what evolved and what has not. This is all the more true in Edge of Evolution, where he brings up the possibility that mutations "look accidental" but are not.

On the science side, I would like to get into a likely problem for evolving the immune system to better resist malaria, which is that Plasmodium falciparum, like many other parasites, actively subverts both the innate and the adaptive immune systems. This is not as important as the above points, in my opinion, but it is likely to play a role in the difficulty of evolutionarily responding to malarial infection.

One way malaria avoids our defenses is that it has an alternative method for taking up iron, that bypasses the body's sequestration of iron (iron is a crucial element to nearly all life, especially so to growing life which has a high metabolic rate) effected to starve pathogens of iron.

A couple more ways that P. falciparum thwarts the immune system are mentioned in the quotes below:
In vitro studies involving human cells have shown that macrophage functions, including phagocytosis and ROI [reactive oxygen intermediates] generation, are severely impaired after uptake of an insoluble degraded host hemoglobin, called homozoin, generated during blood-stage malarial infection.
From the same source:
One of the more consistent and striking dysfunctions observed in macrophages infected with protozoan parasites [which include P. falciparum] is their inability to produce IL-12, which--as the main physiological inducer of interferon-γ (IFN-γ) and T helper type 1 (TH1 cell differentiation--is an essential cytokine for the development of acquired resistance to most intracellular pathogens. Nature immunology
The same paper details how malarial (and other parasitic protozoa) down-regulate many of the signaling pathways, particularly but not exclusively those involved with IL-12 (interleukin-12), and apparently also prevent maturation of the crucial dendritic cells. Again, I do not think that going into the details is especially instructive, since one can always use the link given, or search engines, to find out about those.

The question pertinent to this subversion of our immune system is: how are the highly evolved protozoan abilities to bypass or suppress our immune response really supposed to be countered by evolution? No doubt evolution has indeed tweaked our immune response to malaria, but our immunity is not an infinite god, it is a limited system whose adaptations are met with even more malarial adaptation. The very complexity of immunity likely inhibits further evolution, and, in any case, no gazelle will be able to evolve to run 433 mph. We have never outrun all parasites in our evolution, and likely we never will.

However, we do manage to fend off pathogens better than most ocean bacteria can, as their death rate is enormous at the hands of viruses. And they can evolve much more quickly than we can. The fact that our adaptive immunity has evolved to allow our line to exist for nearly half a billion years is certainly a testimony to the importance of of that evolution.

The ability of P. falciparum to be able to avoid much of the powerful effects of our immune system is merely one of the many stories of evolution wherein a "stalemate" of sorts has appeared. It is no fault of evolution that gazelles have topped out at around 50 mph, nor that our immune systems are able to handle most infections fairly well, but not the subversive virulence of P. falciparum. That evolution can recruit other changes in parallel with immune system evolution only speaks to the power--and the limitations--predicted of evolution.

Thus it is that the evidence of the evolution of our immune systems is crucial both to demonstrate what evolution can do, and, of course, what it cannot do. While one would like to endlessly ask the IDists how they account for the limitations of organisms, until they either reply to at least one crucial question or learn to keep quiet, the fact is that they will avoid all of the hard questions.

We, on the other hand, can answer a great deal about evolution's abilities and limitations, so I plan for the next post to begin to lay out the evidence that the adaptive immune system evolved from the innate immune system. Evolution of the innate immune system could also be discussed (and may be in a limited way), but we almost certainly know more about how adaptive immunity evolved, and it is the part of immunity that Behe claimed could not evolve, even as he ignored the evidence that it evolved substantially out of the innate system.

25. Evolution of adaptive immunity I--Phylogeny

This is posted specifically in response to Chapter Six of Darwin's Black Box, which claims that our adaptive immune system is irreducibly complex.

Defense against pathogens has a very long evolutionary history, going back at least to bacteria and archea. Adaptive (or "acquired") immunity is the tip of the iceberg, very effective, yet built upon and integrated with the earlier "innate immune system." Indeed, it should be mentioned at the outset that there is no inherent reason to split up "adaptive immunity" and "innate immunity," as they are both "parts" of an integrated system. Evolution and convenience are the reasons for splitting the "two systems" up, for only gnathostomes (jawed vertebrates) and agnathans (jawless vertebrates--now down to only hagfish and lampreys) have full adaptive function added onto the immune system that we share (not without considerable evolved differences, of course) with the rest of multicellular eukaryotic life. It is an interesting and meaningful phenomenon--unless one subscribes to ID/creationism, in which case it is meaningless--that gnathostomes and agnathans have very different, evolutionarily distinct, systems of adaptive immunity.

As I have previously noted, immune functions have emerged in the familiar cladistic patterns, adding complexity to the immune systems as evolution continues--in essentially the way that evolutionary theory predicts. It would be well, though, to lay out some of the details of the evolution of immunity, and not only with respect to adaptive immunity, but as immunity has evolved roughly since before the Cambrian "explosion". To start out, phylogeny is very important in demonstrating that (unguided) evolution occurred, and it sets out the framework for understanding the particulars of the evolution of adaptive immunity.

Scroll past the sequence data below to "part C," which shows the phylogeny of Toll and Toll-like receptors, not only of "higher animals," but of a plant, a nematode, and a sponge. There, an abbreviation for each organism is used, so here is the key to the abbreviations: MEDTRU=Barrel medic, a legume plant, CAEL=C. elegans, a nemotode worm, SUBDO=a sponge, DROME=a fruit fly, TRICAS=the red flour beetle, DANIO=zebrafish, HOMO=human, MUS=mouse, GALLUS=chicken.

In the link above, MEDTRU=Barrel medic, a legume plant, CAEL=C. elegans, a nemotode worm, SUBDO=a sponge,</div>
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