Logan Gage (DI) analogizes DNA with our evolved, undesigned, natural languages

On the DI’s weblog, Logan Gage quotes a Dr. Story (from Christianity Today), then proceeds to rapidly get matters quite wrong:

Rana, like Behe before him, may be commended for providing a layman’s description of a number of astonishingly intricate cellular processes. But his portraits of cellular workings will fail to convince most mainstream scientists for the same reason that Behe’s book has been roundly dismissed: The analogy between manmade machines and cells is a poor one at best. Cellular components, although machine-like in some respects, do not behave like manmade machines. They self-assemble and self-manufacture, and they are able to transform available energy sources such as light to fuel metabolic activity.

Now what’s wrong with this reply? Didn’t we all learn from Hume that arguments from analogy are inherently weak? 

….  How anyone who has seen a bacterial flagellum could think there is not a strong resemblance to an outboard motor in both appearance and function is, I admit, beyond me. Behe’s Critics Fail to Understand Analogies and Design Detection

Actually, while Dr. Story is right enough in what he does mention, there are much better reasons not to accept Behe’s “arguments,” such as the fact that Behe manages to explain nothing about the lack of “common authorship,” after lines have diverged, of the various vertebrate wings, and of the two adaptive immune systems.  But the poor analogy of life’s machinery with designed machinery is certainly not a negligible argument, particularly because of the self-assembly that does not exist in human-made productions (one could argue that we now have harnessed self-assembly somewhat.  That it is nothing like life’s self-assembly is certain, however).

Moving to Gage’s response, I have never once understood the claim that there is a strong resemblance of the bacterial flagellum to an outboard motor.  The latter is made of metal, and is a heat engine (except for electrics, which also fail to work like a flagellum does).  The former’s materials are constrained by evolution, as is its chemical fuel.  And the parts do not look much the same at all, except in the rather misleading very mechanistic-looking illustrations that IDists are fond of using (there is nothing misleading about the figure to which he linked in normal science instruction, but it is misleading where one is claiming a strong resemblance between outboard motors and flagella).  Aside from rotary motion, I know of nothing closely or moderately analogous between an outboard motor and a flagellum, and that rotary motion is produced in a very different manner, while also propelling a very different sort of rotor.

Here, at figure 2, is an actual photomicrograph of a bacterial flagellum. It is somewhat machine-looking, all right (it is considered to be a machine, by today’s definition), but it looks far less like one of our mechanisms than the illustration to which Gage linked.

Gage moves on to the fact that self-assembly is disanalogous, but claims analogy all the same, because reproduction of bacteria means that their machinery is “MORE complex” than our own. Which suggests that he is playing fast and loose with words and definitions.  See for yourself:

According to Story, “Cellular components, although machine-like in some respects, do not behave like manmade machines. They self-assemble and self-manufacture, and they are able to transform available energy sources such as light to fuel metabolic activity. The cell can also replicate itself and copies of its parts, given energy and simple raw materials.”

But what does this show? Only that while cellular components are similar in many ways, they are also different in that…cells are actually much MORE complex than human-made machines! And therefore, it is likely that the process by which the cells originated is at least as complex as the process by which human-made machines appear (which we know involves intelligent design). What, after all, would we conclude if we stumbled upon a factory where machines not only worked with amazing efficiency but, before wearing out, actually reproduced themselves with astounding accuracy and converted energy from their environment into usable fuel so that they never needed electricity or gas?

In sum, if Rana is indeed making an argument from analogy, I think he escapes Story’s criticism unscathed.  Behe’s Critics Fail to Understand Analogies and Design Detection

Gage is apparently confused by Behe’s “complexity argument,” thereby being unable to notice that reproduction is hardly analogous with our non-reproductive machines, and indeed, reproducing robots and factories of our design are expected to have to reproduce very differently from how bacteria do.

Paley also made this argument, that reproduction of his example, the watch, would imply even greater intelligence behind it.  Which might be reasonable for Paley, because he did not recognize the reproduction is exactly what evolution needs, and, one might argue, even “predicts.”  Moreover, the reproductive methods of both eukaryotes (often with eukaryotic flagella getting the sperm to the egg) and of prokaryotes only make sense in evolutionary context, for IDists have never come up with a “design explanation” for the existence of sex and of bacterial conjugation.  The fact is that clades distribute according to clonal (with conjugation) patterns, and to sexual patterns, quite as one would expect from evolutionary predictions, and do not exhibit intervention by any “designer.”

Gage failed to support the analogy, and to show that reproduction is anything but a source of evidence that evolution occurred without any reason to suppose that any intelligence intervened.

Gage again:

What is worse for Dr. Story is that Behe does NOT make an argument from analogy, anyway. The arguments proffered by both Behe and other design theorists like Dembski and Meyer focus on the properties humanly designed objects and biological objects actually share, not properties that have some analogous resemblance.  Ibid.

Actually, Behe rests almost all of his “arguments” on faulty analogies, although he does base his “irreducibly complex argument” on faulty assumptions–these assumptions being both the “purpose” for which he never provides evidence, and the silly notion that complexity sans the design characteristic of rationality is evidence of intelligent intervention.

I wrote the post linked here before the present one, so that I could refer back to it.  Behe’s acceptance of the molecular clock as a viable possibility, and the evidence of common descent–which likewise depends upon non-intervention by a designer–demonstrate that Behe is not resting his “argument” upon similarities with human designs, he is trying to claim that non-teleological evolutionary expectations are the result of a designer.  It was Paley who argued that life really was made like an architect or artificer would produce, while Behe refuses all tests of design, mainly because he has no evidence for design.

Those who worry about “interference” should relax.  The purposeful design of life to any degree is easily compatible with the idea that, after its initiation, the universe unfolded exclusively by the intended playing out of laws.  Michael Behe  The Edge of Evolution, 232

This is Behe with his get-out-of-jail-free card.  In the end, his ID predicts absolutely nothing (though in other places he claims otherwise), including intervention (which contrasts with his interventionist view of the “Cambrian Explosion” in DBB).  This is completely contrary to what Gage said above, although it is also completely contrary to most of what Behe wrote in his books as well.  Yet in this place, he is (if he understands the implications of this statement) pointedly denying the “shared properties” of human and biological entities, for clearly, shared properties would require intervention by a designer that made objects akin to our own.

This was Gage’s supporting “argument” for the idea that Behe is discussing “shared properties” of human-made and biological entities:

For instance, these theorists often point to what is at the heart of all biological life, namely DNA. They then point out that this biological information has the SAME semantic properties that human written or spoken language has. They are not making an analogy at all.  Behe’s Critics Fail to Understand Analogies and Design Detection

I do not recall Behe making such an argument, although I would not be surprised if he has done so.  But there are two large problems for such an argument:  The first is that human languages also were not “designed,” with semantic structure apparently evolving at least part of the way prior to language, and evolving since humans began to truly speak.  It is begging the question to assume that human language was somehow “designed” apart from evolution, when all of the evidence indicates that, like nucleic codes, human language evolved.  The second problem pales by comparison, but of course the semantic structure of DNA is not that of a “natural language” at all.

I suppose that Gage is trying to claim that because human language (which he assumes, against the evidence, was “designed” or some such thing) has semantics, and the genetic code can be understood to have semantics, that the two have the same properties.  Since the DNA code, and what is encoded by it, is not like a “natural language” used by humanity, it is the same old argument by “analogy” that is presented by Gage–at least as weak as all of the other “analogies.” 

And, as I stated above, if we actually follow the analogy we’ll end by recognizing that human language semantics evolved without guidance (save our own evolving guidance), and so did DNA with its “semantics”.  So they can have that analogy, if they want to have it, and we will understand that DNA must have evolved, instead of being intelligently designed.

How could the molecular clock work with design happening?

The molecular clock has been vigorously debated since it was proposed, and many issues surrounding it are still contended.  Overall, however, it remains a viable possibility.  Michael Behe, DBB, 174

He is right both about questions remaining, and that it is a viable possibility.

But how could it be, if ID were correct?  From Aristotle, down to Paley and the creationists, τεχνη or design has always been marked off from “nature” (nature in the exclusive sense) or “physis”.  Indeed, Behe and most of the other prominent IDists like to suggest that the “Cambrian Explosion” is an obvious time when “design” was effected (DBB 27-28).  And yet the molecular clocks (mostly DNA, now) tick through the “Cambrian Explosion” without marking any break from the usual processes, even though it is possible that more refined methods could yet capture an uptick in change (not the break that most would expect from a designer intervening, however).

For so long the various sorts of creationists have tried to argue that intervention by God would be obvious.  Since it never has been, however, Behe increasingly writes as though no intervention can ever be observed, from any sort of mark of design, to any break in the molecular clocks.

This criticism has nothing to do with the accuracy of molecular clocks, which may in fact not be as reliable as some have claimed.  It is that Behe never expects any of the effects of intervention to be visible in life (if these were found, you can be sure that most IDists, probably including Behe, would quickly adopt them, though).  This, perhaps, is the most important change that ID has produced, since the older IDist Paley, and traditional creationists, always expected design to be observable–and generally not by christening complexity as “evidence for design,” like Behe illegitimately does.

As it happens, we could easily apply Paley’s criticisms of the evolutionary concepts of his day (before Darwin came up with a scientific theory) to Behe’s evidence-free designer/evolution-tweaking God, because a major argument of Paley’s book was precisely that design has positive evidence in its favor (arguable then, but not now), while evolutionary ideas were lacking in evidence (not entirely true, since common ancestry did comport well with evolution).  Really, anyone who wanted to show conclusively how ID avoids all legitimate tests (falsification being the best rule-of-thumb) would do so by comparing Paley’s attempts to show that design is falsifiable, with Behe’s never-ending attempts to avoid all reasonable tests of ID.

This is part of a series of posts that I am combining into one long post, which may be found at Darwin’s Black Box.

What is ID’s efficient cause?

IDists are keen to return Aristotle’s “final cause” to the sciences, or at least to biology (see Dembski, for example).  Which is rather sad, because they can give us no evidence for the purpose of organisms, instead they wish to insist that life “had to be designed” and thus has purpose.  One has to wonder what good that would be to know, since we would still need to be able to discover purpose for it to impact us, and ID has never been able to demonstrate any purpose (to be sure, nearly all IDists have sacred writings in mind to provide specific purpose, but will not admit it in their supposed science).

So OK, they want final causes (aside from those of animals such as humans), and perhaps formal and material causes as well, but where is their “efficient cause”?  That is the closest that Aristotle’s “causes” (aitia, which probably would translate better as “reasons” than “causes”) come to fitting with scientific causation in the classical realm, they do not deny the importance of efficient causes, and yet they have none whatsoever.

It should be noted that Aristotle was not one who simply called “intelligence” or “design” the cause or the reason (not of a manufactured item, that is), the aition, because intelligence is just a faculty, and design is merely a category of actions or “causes”.  Thought using intelligence might be a cause, and design may be part of a specific process, but simply invoking intelligence, thought, or design would explain nothing by themselves.  There is an apparent exception to Aristotle’s “efficient cause” as a specific cause or set of causes, which is God the unmoved mover–a very indefinite “cause”–but even IDists don’t appeal to such ancient fictions, partly because it would too readily reveal the religious motivation behind ID.

Aristotle has these things to say of the “efficient cause”:

Again (3) the primary source of the change or coming to rest; e.g. the man who gave advice is a cause, the father is cause of the child, and generally what makes of what is made and what causes change of what is changed.

…

e.g. both the art of the sculptor and the bronze are causes of the statue. These are causes of the statue qua statue, not in virtue of anything else that it may be-only not in the same way, the one being the material cause, the other the cause whence the motion comes.

…

All causes, both proper and incidental, may be spoken of either as potential or as actual; e.g. the cause of a house being built is either ‘house-builder’ or ‘house-builder building’.

…

In investigating the cause of each thing it is always necessary to seek what is most precise (as also in other things): thus man builds because he is a builder, and a builder builds in virtue of his art of building. This last cause then is prior: and so generally.

Further, generic effects should be assigned to generic causes, particular effects to particular causes, e.g. statue to sculptor, this statue to this sculptor; and powers are relative to possible effects, actually operating causes to things which are actually being effected.  Aristotle’s Physics

In a scientific sense, this is all rather imprecise.  But even Aristotle’s generic causes, such as “the art of building,” is far more precise and meaningful than anything we have gotten out of ID as an efficient cause.  Dembski even makes “efficient cause” more precise than Aristotle does:

The efficient cause is the immediate activity that produced the statue–Michelangelo’s actual chipping away at a marble slab with hammer and chisel.  Dembski

Dembski’s example of an efficient cause moves us closer to scientific causation, and is a typical example used by those who are explaining Aristotle’s “four causes”.  Despite the fact that he waffles on mechanism in that article–and attacks the strawman of design being “barred from the content of science” (has any archaeologist tried to explain pottery without intelligent agents involved somehow?)–he is still hardly consistent when he makes statements such as this one:

You’re asking me to play a game: “Provide as much detail in terms of possible causal mechanisms for your ID position as I do for my Darwinian position.” ID is not a mechanistic theory, and it’s not ID’s task to match your pathetic level of detail in telling mechanistic stories. Notorious Dembski comment

Ah yes, Dembski has neither evidence for a final cause, nor for an efficient cause.  Likewise with Behe, who pretends to take a more scientific approach than Dembski, he will not even commit to the specificity that an ancient thinker like Aristotle would:

Another problem with the argument from imperfection is that it critically depends on a psychoanalysis of the unidentified designer.  Yet the reasons that a designer would or would not do anything are virtually impossible to know unless the designer tells you specifically what those reasons are.  One only has to go into a modern art gallery to come across designed objects for which the purposes are completely obscure (to me at least).  Features that strike us as odd in a design might have been placed there by the designer for a reason–for artistic reasons, for variety, to show off, for some as-yet-undetected practical purpose, or for some unguessable reason–or they might not.  DBB, 223

What, people refuse to call something like that science?  Notice how desperate he is to claim no distinguishing marks of design (since he knows that these are lacking from life that we have not engineered) that he goes to deliberately obscure art as his “example.” 

Yet in the first and second Dembski links (to the same source), it is argued, against a strawman, that design is readily detectable.  To be sure, he misunderstands his own sci-fi analogy as the search for “complex specified information,” when in fact it was rationality behind the signal that indicated intelligence.  Dembski explaining what was detected in the movie Contact:

In this sequence of 1126 bits, 1’s correspond to beats and 0’s to pauses. This sequence represents the prime numbers from 2 to 101, where a given prime number is represented by the corresponding number of beats (i.e., 1’s), and the individual prime numbers are separated by pauses i.e., 0’s).  Dembski

Yes, that’s right, it isn’t complexity that is discovered (Dembski calls unlikely simplicity by the name “complexity,” a distortion even of the meaning of the term), it is rationality.  Even Behe gets it slightly, and ludicrously brings up rational agents:

Rational agents can coordinate pieces into a larger system (like the ship) to accomplish a purpose.  Edge of Evolution, 168

Yes, and the context from which that comes has any number of rationally-devised artifacts being discovered.  Nevertheless, note how carefully he words it, to avoid the implication that life ought to appear rationally designed if it was intelligently designed.  He’s still relying on evident “purpose,” which he deliberately tried to avoid as a test of “design” in the previous quote.  There, too, he wrote of “reasons” for design, as he denied their visibility, suggesting that he knew very well that he was denying that purpose is evident in life, while in this later quote he is trying to suggest that rationality is found exactly through evident purpose (as he had also done in DBB, prior to denying it in order to avoid predicting evident purpose in life–in response to those who noted exactly the lack of purpose in so many aspects of life).

The fact of the matter is that both Dembski and Behe do not wish “design” to be tested by evidence of purpose, for they know that, for instance, malaria pathogens do not seem to fit any kind of evident purpose.  They bring up purpose in order to ignore efficient causation and the rationality typically evident behind such causation (even if some art is hard to figure out, the rationality of the frames betrays intelligence via rational efficient causation).  Likewise, they totally avoid efficient causation, for as I previously argued, they have no causes at all, only unconstrained accident (or whim).

Evolution is also fraught with accident (see link above), but these are “lawful accidents,” of the kind that are permitted and even (probabilistically) predicted.  We have “efficient causation,” or more exactly, scientific causation.  And what is interesting to note is that while Dembski and Behe contradict themselves and each other with their “arguments,” primarily because they can show no “intelligent design” causation whatsoever, earlier ID really did mean to find the marks of intelligence and rationality in life:

…We allege, that the same principle of intelligence, design, and mechanical contrivance, was exerted in the formation of natural bodies, as we employ in making of the various instruments by which our purposes are served […]. William Paley

Paley was looking for efficient cause (see also pp. 8 & 233 of the above link for his criticisms of explanations lacking in efficient causes), and for observable purpose.  Behe and Dembski contradict themselves on these matters, while generally trying to smuggle “purpose” in via “complexity.” 

Paley’s ID was tolerably close to a scientific hypothesis–which Darwin took seriously.  By avoiding all causes (even the ones they bring up, like “purpose”–Aristotle’s “final cause”), the current crop of IDists cannot even match Paley’s now-failed “science,” nor even keep from contradicting themselves as they both claim that purpose and rationality are evident, and that they are not.

This is part of a series of posts that I am combining into one long post, which may be found at Darwin’s Black Box.

Evolutionary history of tuberculosis deciphered

Or more exactly, the evolutionary history of Mycobacterium tuberculosis complex has been deciphered, indicating that there are two clades:

ScienceDaily (Oct. 22, 2008) — The evolutionary timing and spread of the Mycobacterium tuberculosis complex (MTBC), one of the most successful groups of bacterial pathogens, remains largely unknown. Here, using mycobacterial tandem repeat sequences as genetic markers, we show that the MTBC consists of two independent clades, one composed exclusively of M. tuberculosis lineages from humans and the other composed of both animal and human isolates.

The latter also likely derived from a human pathogenic lineage, supporting the hypothesis of an original human host. Using Bayesian statistics and experimental data on the variability of the mycobacterial markers in infected patients, we estimated the age of the MTBC at 40,000 years, coinciding with the expansion of “modern” human populations out of Africa. Moreover, the diversification of the oldest EAI and LAM populations took place during plant and animal domestication. Science Daily

It’s a somewhat interesting story, particularly due to its relevance to understanding tuberculosis as a disease.

One just has to wonder, in addition, how IDists propose to decide that this branch indicates normal processes of evolution (as at least most self-identified “IDists” would), while another branching happens to be due to design, despite the fact that it reveals no substantially different patterns.  Of course I have brought this up several times already, however it’s worth bringing up yet again, because it is important to understanding diseases like malaria (how adaptable are pathogens?), and because this aspect puts IDists squarely in the camp of creationists and their inability to tell “design” apart from “Darwinism.”

To put it more starkly than I have previously–the methods used for determining clades do not differ substantially across the taxa.  Some of the details change, of course, but the principles, the standards, are the same going back to the Cambrian and beforehand.  Furthermore, they do not differ meaningfully for “suddenly evolving” immunity genes like TCR and BCR (at least parts of which exist in the agnathans–hagfish and lampreys, but are much more diversified and important to jawed vertebrates–the gnathostomes–which use them in their adaptive immune systems, unlike agnathans with their adaptive immune systems), or the apparently far more sedately-changing Toll and Toll-like receptor genes.

Surely it is (in any “design” sense) a mystery of how malaria, tuberculosis, and humans, along with their ancestors, can be phylogenetically analyzed in essentially the same manner no matter whether we study their “designed” parts or their “evolved” parts.  Meaning that there is no obvious difference in causation of evolution across the taxonomic groups (and there is no definite way to assign the taxonomic categories, other than species, although the cladistic branches are not at all arbitrary), and no reason at all to think that design makes any difference to understanding the relationships of pathogens and hosts.  This is important to recognize when analyzing disease and our immune system, as well as when we recognize that Plasmodium spp. are vulnerable to certain drugs precisely because of their very different “lawfully accidental” evolutionary history–which means that drugs targeting the Plasmodium apicoplast have a good chance of being non-toxic to humans.

Then again, in a sense it’s somewhat silly to be discussing the IDist inability to distinguish “design” from “normal evolution” when they have no ability even to show that resistance to chloroquine (which Behe goes on about) actually evolved, rather than be the result of a miracle, or a series of miracles.  The fact is that the IDists attempt to empty science of any and all of the meaning that science gains by matching up cause and effect, and by understanding that similar effects have similar causes (unless, of course, another identifiable cause producing similar effects has been found–IDists only claim that it has, by refusing to differentiate the effects of “design” from those of evolution).

So it’s fail all the way, actually.  Of course they can’t say how “designed clades” differ from “evolved clades,” because they can’t ever rule out “design” with their (lack of) standards.

Malaria has evolved cold tolerance

To put matters in perspective, consider a related problem that has stumped malaria.  Although malaria is a ferocious parasite, quite willing to eat anything that gets in its path, P. falciparum needs a warm climate to reproduce.  If the temperature falls below about 65°F, the parasite slows down.  When the temperature gets to 61°F, it can’t reproduce  It’s stymied.  If a mutant parasite appeared that was tolerant to somewhat lower temperatures–not to freezing conditions, just to cool temperatures–it would be able to invade regions that are now closed to it.  Edge of Evolution, 82

Behe seems to think that P. falciparum is the only malarial parasite that infects humans.  P. falciparum is restricted to quite warm regions, but P. vivax has indeed invaded much cooler regions, including London in past centuries.  P. vivax tolerates temperatures of five degrees Celsius cooler, which amounts to nine degrees Fahrenheit cooler:

Compared with the more virulent Plasmodium falciparum, P. vivax tolerates a wide range of temperature environments (minimum: 16°C vs. 21°C for P. falciparum), which may explain its broader distribution. Host Switch Leads to Emergence of Plasmodium vivax Malaria in Humans

Then too, since Behe has no idea of what temperatures P. falciparum endured in the past, he does not know that it has not evolved to tolerate lower temperatures than it could initially.  Regardless of that, it is unsurprising that a Plasmodium species can live in cooler regions than can P. falciparum.

And when one species can survive in a region in which a related species cannot, competition often prevents evolution to fit the competitor’s adaptation.  After all, it may require several changes to endure cooler temperatures, and they may initially come with costs which make the species less fit.  When one species already can endure cooler temperatures it is not particularly likely that another species will, and especially not in the rather short time period in which P. falciparum has been infecting humans.  Nevertheless, P. vivax suggests that it could happen in other species, particularly if somehow P. vivax went extinct.

Behe could always ask why P. vivax can’t endure 6°C, or -6°C, or cryogenic temperatures.  And who knows, maybe he will.   But as I have previously argued, it is not for us who accept the constraints of science and evolution to explain why evolution is not all-powerful, it is for him to try to explain why his omnipotent god fails to reveal omnipotence in “his designs.” 

Evolving to live at lower temperatures has not “stumped malaria,” as he claims.  In fact, with P. vivax living at lower temperatures, P. falciparum‘s lack of evolution to tolerate lower temperatures is in line with evolutionary expectations, considering the relatively short time in which it has has to evolve.  So there you are, malaria seems to fit evolutionary expectations quite well, and Behe fails in this detail as well.

This is part of a series of posts that I am combining into one long post, which may be found at The Edge of Evolution

ID’s problem is not particularly poor design, but the evident cause of “poor design”

…The key to intelligent-design theory is not whether a “basic structural plan is the obvious product of design.” Behe, DBB, 223.

Let’s try this idea out on real science:  The key to evolutionary theory is not whether a basic structural form is the obvious product of evolution.

What?  Could anything be less scientific than claiming that finding the “obvious product” of design (or evolution) is not the key to ID (or to evolutionary theory)?

The context indicates that Behe just wants to insist over and over again that “irreducible complexity” is evidence for design, which, if it was, would mean that intelligent people would never have accepted evolutionary theory.  More importantly, if “irreducible complexity” indicated any sort of design, surely it would be accompanied by the obvious products of design–if by “design” we mean anything that is at all within our sphere of observation.  Back when ID was honest, if not especially coherent or cogent, Rev. William Paley wrote something quite the opposite of what Behe wrote:

Ought it then to be said, that though we have little notion of an internal mould, we have not much more of a designing mind?  The very contrary of this assertion is the truth.  when we speak of an artificer or an architect, we talk of what is comprehensible to our understanding, and familiar to our experience.  We use no other terms, than what refer us for their meaning to our consciousness and observation… Natural Theology

But you know, since design is not a comprehensible explanation, Behe et al. have to reverse Paley, and insist that the incomprehensible (as they portray the mere gaps in our knowledge) is the mark of design, thus easily putting ID into the same category as “internal moulds” and Lamarckist conceptions of evolution.

A little later than the quote that begins this post, Behe is complaining that Ken Miller demands perfection from “the designer,” and suddenly finds human design to be analogous (showing how incoherent he is).  That is, humans often make designs which are not optimized, so why not build the retina of the eye backwards in vertebrates (Miller was arguing that the backward retina is contrary to design), even though it is the “right direction” in cephalopods?  Well, apart from the fact that the IDists’ “designer” is God, clearly any entity having the intelligence to design the immune system could surely think well enough to put the retina in properly, instead of backwards.

Nevertheless, I do not especially like the “backward retina” argument against design, mainly because that fact means almost nothing except that the eye was not designed.  While it is well and good to point out that life was not designed, ID has never once had any scientific argument, nor any realistic shot at fooling more than a few biologists into thinking that it was.  Both for public relations, and for maintaining the integrity of science, what we have to do is to show that evolutionary theory explains life.  The “backward retina” is not readily shown to be the result of evolution (evidence from the time when it was fixed is scant, at best), while other “poor designs” are.

 In this linked post I made the point that pterosaur and bat wings are “poorly designed” next to bird wings. Again, though, that is only the minor issue pointing to the greater issue, which is that, for example, bat wings are simply the way that they are because of the constraints imposed by (unguided) evolution upon the modification of mammal forelimbs into wings.  The problem that IDists need to explain is why “design” follows constraints of evolution, not the constraints of any known intelligence, when it produces bat wings.  Any number of factors might cause a designer to produce a less than stellar design, of course, so the important question is why the only identifiable factors behind “poor design” in organisms are the constraints of unintelligent evolution.

Moving beyond that post, however, it is important that “poor design” is found rather more often just where one would expect in evolution, during the transitional periods.  Archaeopteryx has many of the advantages of birds, including the feathers which are sculpted into the wonderful avian aerfoil wing.  Yet it is not at all as efficient or “well designed” as modern birds are, whether because of its heavy teeth and jaw (by comparison to modern birds’ light bills, that is), its bony tail, or the fact that it lacked the “ligament-based force balance system” (Nature) that makes modern bird flight less work than it was for Archaeopteryx.

One could look at any of the major changes in form and lifestyle and see there fulfilled the predictions of evolution that “incomplete optimization” during the transitional period of complex is inevitable, whether it is the transition of fish to tetrapod, tetrapod to whale, or dinosaur to bird (actually, genetic evidence suggests that bats flew prior to evolving sonar, so this too would be an incomplete transition at least for the sonar-using bats.  Without fossils of the transition, though, I only include this likely example parenthetically).  Obviously I could belabor the point and dig up the details of the transitions, however these would not add much to the argument. 

The fact is that while human designs do undergo transitions in which they are not optimized, there is nothing in human design like the millions of years of suboptimal “design” which afflict evolutionary transitions.  Their designer-God certainly would not be expected to be troubled by the trial-and-error methods that humans utilize.  Only evolution is expected to transition between modes of life via often-poor, evolutionarily constrained “body plans,” and only it could predict that bat wings will not show any kind of “common authorship” with bird wings subsequent to bird and bat lines diverging.

It is no wonder that Behe tries so hard to ignore the many practical tests of evolution, and to replace these with impractical tests which require lost evidence in order to work.  What else can he do?  He cannot point to any “obvious product of design” in life (save what we have genetically or otherwise modified), nor can he explain anything via “design” that evolution not only explains, but predicts–from the lack of common authorship of changes after divergence in (primarily) vertical-inheritance organisms, to the enduring “poor design” of bat wings, and on to the “poor designs” of Archaeopteryx which are based on the fact that it was still a dinosaur that was yet evolving its flight abilities.

There does not seem to be any other pseudoscience which tries so hard to bypass all of the reasonable tests of both itself and its “rival.”  Perhaps this is because no idea held by millions of people has been debunked in so many ways, and with so many examples, as ID/creationism has been.

This is part of a series of posts that I am combining into one long post, which may be found at Darwin’s Black Box.

Horizontal transmission of a transposon in animal species

Here is the core of the article, in my opinion:

The fact that invasive DNA was seen in a bush baby but not in any other primates, and in a tenrec but not in elephants, hints that something more exotic than standard inheritance is going on.

However, this patchy distribution by itself does not rule out the traditional method, as some of the species could have lost the transposon DNA throughout evolutionary history.

So the team looked at the position of the hAT transposon – if it had been inherited from a common ancestor it would have been found in the same position, with respect to other genes, in each species. But they could not find a single case of this.

Since first entering the genome, the hAT has been able to reproduce dramatically – in the tenrec, 99,000 copies were found, making up a significant chunk of its DNA. Feschotte speculates that this must have had a dramatic effect on its evolutionary development.

“It’s like a bombardment”, he says. “It must have been evolutionarily significant because the transposon generated a huge amount of DNA after the initial transfer.”

Feschotte says he expects many more reports of horizontal gene jumping. “We’re talking about a paradigm shift because, until now, horizontal transfer has been seen as very rare in animal species. It’s actually a lot more common than we think.”  New Scientist

“More” is probably a good bet, all right, but horizontal transmission of genes is still not all that common in animals, so far as we can tell.  Still, 99,000 copies is bound to have made a difference in the evolution of the tenrec.

I thought the story itself was interesting, but it also has elements in its discovery that demonstrate how out-of-the-ordinary animal genetics can be and is discovered.  IDists sometimes like to point to the fact that this or that scientist agrees that design could be detected. 

But that’s their entire problem, it could be detected and it never is.  Meanwhile, science continues to find “non-canonical” changes and evolutionary patterns, such as this gene being laterally transferred into animal genomes.  It is entirely a matter of what has evidence and what does not.  Vertical transmission is by far the dominant form of gene transmission in, say, vertebrate species, as indicated by both conserved genes and by the lack of commonality after taxa diverge.  Horizontal transmission occurs, and is identifiable by its “lawfully accidental” appearance in unrelated species, as well as by the fact that the gene is not found in the same places in the genomes of the animals having a particular gene.

Now if we could ever find the commonality of authorship in any evolutionary development, such as older IDists predicted, ID would at last have some evidence in favor of it.

There’s a reason why all vertebrate wings are modified legs of their terrestrial ancestors

But don’t ask the IDists to explain it.  They can’t, and as usual, they avoid addressing anything (other than to complain that “it’s too complex too evolve”) that shows up their claims, which is just about every complex biological organ or system.

I am posting about vertebrate wings and how they are all as divergent from each other–and dependent upon unlikely “design” choices–as evolution predicts, in order to drive home the point of yesterday’s post, as well as many of the earlier posts.  The strangeness of the “designs” claimed by IDists are too often let go by without much argumentation, yet it is truly odd from a design standpoint that the two adaptive immune systems share none of the same parts except the genes inherited from the vertebrate ancestors from which the two lines diverged, and that evidence of “similar authorship” of subsequent change is completely absent (as predicted by evolution).  Vertebrate wings are just another example of the fulfillment of this evolutionary prediction, only the “physical precursors” (DBB, 45) are patently unpromising from a design standpoint–and clearly some vertebrate wings are rather better than are others.

Pterosaur, bird, and bat wings are all homologous, of course, but only through their shared ancestry of reptilian forelimbs and feet. Here is a source showing the morphologies of pterosaur, bird, and bat wings.  All vertebrate wings are analogous as well, but all had to evolve from legs, and not from the wings of unrelated animals.  Pterosaur wings evolved from archosaur legs, and bird wings did as well.  Only, by the time birds evolved, the archosaurs had evolved into dinosaurs (and other organisms), so that bird wings evolved from dinosaur forelimbs.  Bat wings evolved from mammal forelimbs.

And how does this compare with design?  Well, however strange it may seem to IDists, the Wright brothers studied bird wings, not mammal or reptile forelimbs, to assist their own attempts at achieving flight.  They also used “first principles” and empirical studies, so that their airplane’s wings were hardly mere modifications of bird wings.

Yet we are to believe that a “designer” capable of creating extremely complex systems–of the kind that humans cannot presently create–went back again and again to legs in order to design vertebrate wings.  Which is just as evolution predicts, in the tetrapod context.  Would anybody ever expect that of an alien?  Really, no, because it does not fit with our conception of rationality and intelligence.  Legs (forelimbs, anyhow) only have some of the musculature and skeletal strength needed for wings, they have none of the shape or detailed structural components needed for wings.

To be sure, birds were fortunate to evolve their own wings, rather than to copy the previously-existing pterosaur wings.  The latter were not at all bad structures, but they were unlikely to do well with a tear.  Even more importantly, presumably, the evolution of feathers provided birds the chance to evolve truly superb airfoils.  Birds have come near to optimizing aerodynamics, thanks to the fact that they inherited from dinosaurs the ability to grow feathers at varying lengths and in different morphologies.

Ah, well, maybe the designer was learning, after all.  However bizarre such an “argument” may be, IDists will try anything out to save their beliefs, so we’ll go through this “hypothetical” as well.  Pterosaurs came first, then birds, and last of all, bats.  The designer could have tried out pterosaurs, then bettered itself by inventing birds.

As anyone reading this must have anticipated, that is hardly the way to save “design” of bird wings, even if we neglect the unlikely starting points, namely, the unpromising terrestrial forelimbs.  Because, clearly, the bat wing is not an improvement on bird wings, in fact it is step back from the wonderful aerodynamics of birds with their feathers.  Bats fly well enough, but one reason they hang upside-down to sleep is because they do not have the flying power to simply take off from a perch, as a bird does (yes, birds also “jump” into the air, yet that is nothing mammals could not evolve to do as well).  Bats are not the fliers that equivalently sized birds are, not only because evolution deprived them of feathers, also because they do not have the efficient breathing apparatus that birds evolved from dinosaurs. 

At least bat wings are less likely to suffer badly from tears than pterosaur wings were, which hardly makes them equal to bird wings in flight ability.  Modifying legs into wings is as unpromising a “design strategy” as any unprejudiced person would assume at first, but it was the only route open to the evolution of vertebrate wings (unless we count “flying fishes,” but their “wings” are modified pectoral fins, from which tetrapod forelimbs evolved, so nothing substantively changes by imagining their evolution of true flight (surely it could happen)).

I have asked several IDists, including Paul Nelson, to explain this extremely odd “design strategy,” and of course I was met with absolutely no answers to the “riddle,” although I was often “treated to” irrelevant and repetitive ID claims.

I think that this particular focus puts the evolution of adaptive immunity into perspective.  At this point we really cannot point to either agnathan (hagfish and lampreys) or to gnathostome (jawed vertebrates) and say that one of them has the “best” adaptive immune system.  In fact, at the present time they appear to be fairly comparable, at least in numbers of recombinations possible to “adapt” to the threatening pathogen.  Vertebrate wings, however, are fairly easily compared, and the comparison produces a true winner in bird wings.  Furthermore, we know how designers have gone about making wings by looking at organisms, and they neither stuck anywhere nearly as rigidly to their organic “prototype” as IDists claim that their god did, nor did they look to legs as promising wing material.

This, then is the primary lesson of adaptive immunity.  The point is less what system is “better than the other,” but is more that organisms fit the only causes available to unguided evolution in every respect.  To put it in “authorship” terms, no designer could be convicted in a court of law for copying the design of one vertebrate wing to another vertebrate wing, or of one adaptive immune system to another one, for no similarities (other than limitations of inheritance and of physics–homology and convergence, that is) exist between them.  Adaptive immune systems and vertebrate wings share homologies, due to common ancestry, but no similar thoughts from the same mind is responsible for the modifications of their respective common inherited genes, in either vertebrate wings, or in the two adaptive immune systems.

If one were really interested in predicting that organisms were designed, one would insist that a common intelligence behind various designs would leave its mark upon organisms.  And it is because evolution passes all realistic tests of its predictions, including the lack of “common authorship” of the modifications occurring in divergent organisms, that Behe demands virtually supernatural knowledge of the specifics of evolutionary developments that took place so long ago, and for which so much of the evidence has been lost.  Behe’s problem with evolution is avoiding the fulfilled predictions of unguided evolution, along with avoiding any realistic predictions of design.

This is part of a series of posts that I am combining into one long post, which may be found at Darwin’s Black Box.

Evolution of Adaptive Immunity V–Complexity evolves, isn’t copied

Behe has basically one arrow in his quiver–life is really complex. Unfortunately for him, complexity is hardly diagnostic of design.  Still, it is fair to say that evolutionary theory must address complexity.  Considered collectively, indeed, life is far more complex than it would ever have to be if it were designed.  That is because evolution is very good at coordinating complex simultaneous and sequential changes.  And it has no ability to do what a designer can do, which is to take what works in one organism and copy it (with any necessary modifications) to work in another organism. 

While horizontal gene transfers are the exception to the rule that evolution does not copy from distantly-related taxa, such transfers can generally be inferred from the evidence, and these events typically do not affect metazoan evolution much.  So although the transposon genes which gave rise to RAG1 and RAG2 genes in gnathostomes (jawed vertebrates) may have transferred from bacteria into eukaryotes, evolution of adaptive immunity had to rely almost entirely upon genes that were vertically transferred, or at least that had been for a very long time.

The adaptive immune system of the agnathans (jawless vertebrates–lampreys and hagfish) is not nearly as well characterized as is the adaptive immune system of gnathostomes.  That it is very different from our immune system is well-understood, however, and some of its evolutionary origins can be understood as well.  Both adaptive immune systems developed largely out of the innate immune sytem, and are highly integrated with innate immunity (the integration is more an educated guess in the case of agnathan adaptive immunity, but well-demonstrated in the case of our own).  And what we see with agnathan adaptive immunity is the ability of evolution to evolve new systems over and over to meet an important need (immunity is one of the most important requirements), and its utter inability to copy anything complex if lateral transfers of genetic material are rare to non-existent.

And of course the usual predictions of evolution (which are not predictions of design, naturally), that similarities between each adaptive immune system which date back to before we diverged from the agnathan line, along with considerable differences arising since then, are to be found when the two immune systems are compared.  I have already quoted the text below in a previous post, but I do so again to establish here the homologies between agnathan and gnathostome immune systems:

Many of the genes for transcription factors involved in gnathostome lymphocyte development can be found in agnathans. SPI-B, IKAROS, EBF, GATA, PAX-2/5/8, and BACH2 gene relatives have all been identified in the lamprey (Rothenberg and Pant, 2004).  Since many of the signaling pathways involved in inflammatory responses, such as the NF-κB pathway, exist in insects, it is not surprising that lymphocyte-like cells in lampreys possess NF-κB and STAT signaling-cascade components. Many additional genes that our lymphocytes use for activation purposes are expressed by lamprey lymphocytes (Mayer et al., 2002 and Pancer et al., 2004b).  These include genes for the CD45 transmembrane protein tyrosine phosphatase, SYK protein tyrosine kinase, Src family members, and the HS-1 adaptor molecule. Lamprey lymphocyte-like cells also express relatives of the CXCR4 chemokine receptor and its SDF-1 ligand, the cytokine interleukin 8 (IL-8) and its receptor, and the IL-17 receptor.  The Evolution of Adaptive Immunity

In my last post, and in many others, I pointed to Behe’s correct statement that Darwinian evolution requires “physical precursors” (DBB, 45), and noted in the last post how gnathostome immunity meets this test (which Behe fails to apply).  Clearly agnathan adaptive immunity meets this test as well, and is thus beholden to inherited accidents.  The flip side of evolutionary prediction states that further development of lines that have diverged will not follow the same pathways, that they are subject not only to natural selection, but also to the contingencies and accidents of mutation–and even of selection (natural selection is also variable).  Which means that anything as complex as gnathostome adaptive immunity essentially could not re-evolve in agnathans, or vice-versa.  However and in whatever sequence the two adaptive immune systems evolved, at least one of the divergent lines simply missed out on the evolution of immunity in the other, and even though the two adaptive immune systems are considered to be “convergent,” they are very different since the two systems diverged.

Here is a diagram and caption explaining the very different recombinatorial functions of agnathan and gnathostome adaptive immune systems. Very simply, the difference is that instead of rearranging V(D)J sections of the TCR/BCR genes, a VLR (variable lymphocyte receptor) gene with three coding segments separated by large non-coding sites (introns) is translated, and–this is one of the most important aspects–LRR (leucine rich repeats) are randomly incorporated into the germline VLR gene.  See the above link, and The Evolution of Adaptive Immunity for a more full explanation, as it is the evidence for the evolution of a very different complex system that is to be discussed here.

While the exact phylogenetic relationships between the LRR-containing genes has not been untangled, many are associated with “innate immunity”, and these include Toll-like receptors in our immune system.  One might expect LRR-containing genes from innate immunity to be the source for the agnathan VLR gene, and of course this may be the case.  The following would tend to suggest as much:

An abundance of ancestral LRR genes were available for the evolutionary development of the VLR recombinatorial immune system seen in lampreys and hagfish. LRR proteins are found in unicellular organisms and throughout the animal and plant kingdoms, where they are used for a variety of purposes, including microbial invasion and host defense responses (Buchanan and Gay, 1996). Well-known examples include the bacterial internalins (Cabanes et al., 2002), plant disease-resistance R proteins (Dangl and Jones, 2001), and Toll-like receptors of the innate immune system (Akira et al., 2006). Due to the large interaction areas provided by their elongated and curved shape, LRR proteins may bind their ligands with very high affinities. These favorable structural and functional characteristics, coupled with the presence of a large number of LRR genes in cephalochordates (Pancer and Cooper, 2006), would have made the different LRR modular units an attractive substrate for generating diversity given the development of a recombinatorial mechanism for randomly assembling them in an agnathan ancestor.  The Evolution of Adaptive Immunity

However, one of best of the currently-known evolutionary links is with vertebrate platelet receptor glycoproteins.  See:  Evolutionary link between agnathan VLRs and vertebrate platelet receptor glycoproteins (From: Evolution and diversification of lamprey antigen receptors: evidence for involvement of an AID-APOBEC family cytosine deaminase, Nature Immunology).  A more recent study finds that same glycoprotein, hagfish VLRB.59 (unsurprisingly), and a human Slit protein to be most closely related to a particular lamprey VLR-antigen complex (Byung Woo Han, et al. “Antigen Recognition by Variable Lymphocyte Receptors,” 26 Sept. 2008 Science  321:1834-1837).

The same source states:

So far, only the binding mode of the TLR[Toll-like receptor]4-MD2 complex is similar to that of antigen recognition by VLRs, in that residues on the concave surface of the N-terminal and central domains of TLR4 interact with MD2.  However, no interaction is seen between LRRCT [C-terminal leucine-rich receptor capping region] of TLR4 and MD2 as observed between the highly variable insert in LRRCT of VLRs and antigens.  Because we do not yet have sufficient VLR [variable lymphocyte receptor] and TLR [Toll-like receptor] complex structures to make statistically significant conclusions, and the number of LRR modules in TLRs is much greater than in VLRs, it may be too early to infer evolutionary relationships between VLRs and TLRs.  (Ibid.)

The general link between the evolution of VLRs and genes containing LRRs seems to be beyond any reasonable doubt, however.

Once again, the predicted evolutionary patterns play out in the evolutionary histories of the two adaptive immune systems.  Homologies exist between the two systems via the “physical precursors” which must exist for “Darwinian” evolution to occur.  Without much lateral transfer of genes, however, accident and contingency interact with natural selection to make quite different adaptive immune systems after the two diverge. 

Mindlessly, the IDists complain that evolution “can’t predict” future evolution, apparently without realizing that one of the predictions of evolution is that much of evolution is not predictable.  This should be understood as an extension of chaos theory, wherein complexity cannot be predicted.  Nevertheless, causal factors can be predicted to produce different patterns.  Design of any type we know would use rationality for a purpose, and would be unhindered by the genetic barriers between taxa, hence would be expected to transfer the design of one organism to another one without any “physical transfer” (actually, as we understand design scientifically, the physical transfer would take place via the designer, but IDists like to pretend that intelligence is non-physical).

Evolution cannot do this, but it can evolve different types of complexity again and again.  Both evolution’s unpredictability vis-a-vis the specific forms that will evolve, and its predictability regarding the homologies that will nevertheless exist via common ancestry, point to only one mechanism, that of evolution.  As Isaac Newton put it:

Rule I. We are to admit no more causes of natural things than such as are both true and sufficient to explain their appearances.

To this purpose the philosophers say that Nature does nothing in vain, and more is in vain when less will serve; for Nature is pleased with simplicity, and affects not the pomp of superfluous causes.

Rule II. Therefore to the same natural effects we must, as far as possible, assign the same causes.

As to respiration in a man and in a beast, the descent of stones [meteorites] in Europe and in America, the light of our culinary fire and of the sun, the reflection of light in the earth, and in the planets.  From Principia Mathematica

I went with Newton because, as a theist, he clearly is not trying to do away with God with his rules.  But using just those two rules, we could hardly allow that anything other than unguided evolution gave us the forms of life (building upon the starting form(s) of life, of course), since we cannot bring in extra causes when we have sufficient cause–and especially we cannot bring in causes which are not expected to result in the effects we observe.  Even more, via Rule II, we cannot assign different causes to similar effects, so that when we ascribe homologous “physical precursors” and unrelated accidents and natural selection producing the hierarchies and homologies that we see in “microevolution,” we can only conclude that the same causes produced essentially the same patterns and results in “macroevolution.”  At least this is true if one knows of no causes that give similar effects as unguided evolution, and of course intelligence is presumed by any reasonable person to produce quite different results than do unintelligent processes (indeed, IDists want this to be so by insisting on a “designer,” but they completely fail to scientifically differentiate between the results of design and those of unguided evolution).

Others have dealt more closely with Behe’s “challenge” regarding adaptive immunity.  I have been far more focused on demonstrating that nothing in adaptive immunity is what one would expect of design, and upon facts like the one that we can follow the apparently gradualistic evolution of a myriad of biochemicals involved in innate immunity as they came to serve adaptive immunity.  Furthermore, genes coding for biomolecules specifically performing the adaptive functions of gnathostome recombination, like TCR genes and part of the BCR gene, along with RAG1, exist in organisms related to gnathostomes, like lampreys and lancelets.  Correspondingly, the LRRs of the agnathan VLR gene have numerous counterparts both inside and outside of innate immunity.

That is how science is done, by identifying similar causes by observing similar effects.  It is no wonder that Behe is on record at Dover wishing to change science, because by no means is finding similar patterns of homology via the last common ancestor of a group of organisms, plus dissimilarity since they diverged (again, where the organisms do significantly laterally share genes), in “microevolution” and in “macroevolution”, to be ascribed to different causes.  Doing so would make a mockery not only of science, but of the processes of justice (akin to claiming that the expected similarities of father’s and child’s genes were due to the miracle of the Holy Spirit).

The fact is that of all of the fundamental biochemical pathways, adaptive immunity is especially good at confirming the predictions of evolution–that complexity evolves due to accidents of heredity, mutation, and environment (selection itself is contingent, but non-accidental in crucial ways), and it is not copied into groups like agnathans and gnathostomes.  Copying would be indicative of design in such a case, and we never find copying where a designer would have to be the cause of such replication.

This is part of a series of posts that I am combining into one long post, which may be found at Darwin’s Black Box.

Evolution of Adaptive Immunity IV–“Lawful”* accidents of heredity visible in adaptive immunity

I should add at the outset that it may not be merely accidents of heredity (along with the many other factors) that are so visibly behind adaptive immunity, but that horizontal transfer may play an important role as well, even if heredity is responsible after the putative horizontal transfer.

Certainly many of the accidents of heredity have been mentioned previously in my discussions of this subject, from Toll-like receptors ultimately triggering adaptive immunity, to the considerable evolution of the molecular families involved in “innate immunity” and “adaptive immunity” since adaptive immunity arose, mentioned here. However, mostly that evolutionary evidence is not specific to adaptive immunity, and even though I am totally unwilling to pretend that the integrated “adaptive” and “innate” functions are separately evolving systems, it is important that adaptive immunity, as separately conceived, should be evolutionarily understood as far as possible. And, fortunately, quite a lot regarding its evolution is known, while conjectures filling some of the gaps also have supporting evidence behind them.

I would just note that in this post I am primarily discussing the evolution of adaptive immunity in gnathostomes (jawed vertebrates), and not the separately evolved (and basically unrelated) adaptive immunity of agnathans (hagfish and lampreys).   Yet for understanding gnathostome immune system evolution in context, the evolutionarily-derived similarities are important for showing what existed prior to the evolution of gnathostome and agnathan immune systems.  Here is a passage highly revealing of the “physical precursors” (Behe rightly insists that “physical precursors” are essential for “Darwinian evolution” in DBB, but fails to mention that these are generally found) to adaptive immunity:

Cells with phagocytic and other innate-immune-defense capabilities are present in many invertebrate species, but none of them have been shown to be long-lived migratory cells with clonally diverse anticipatory receptors and adaptive-immune-response capabilities. On the other hand, cells with the characteristic morphological features of lymphocytes and much of the molecular machinery possessed by gnathostome lymphocytes have been found in lampreys and hagfish (Uinuk-Ool et al., 2002, Mayer et al., 2002, Najakshin et al., 1999 and Nagata et al., 2002), the only two living agnathan representatives. These findings suggest that lymphocyte progenitors evolved in the most basal vertebrates, or possibly a protochordate ancestor.

Many of the genes for transcription factors involved in gnathostome lymphocyte development can be found in agnathans. SPI-B, IKAROS, EBF, GATA, PAX-2/5/8, and BACH2 gene relatives have all been identified in the lamprey (Rothenberg and Pant, 2004). Since many of the signaling pathways involved in inflammatory responses, such as the NF-κB pathway, exist in insects, it is not surprising that lymphocyte-like cells in lampreys possess NF-κB and STAT signaling-cascade components. Many additional genes that our lymphocytes use for activation purposes are expressed by lamprey lymphocytes (Mayer et al., 2002 and Pancer et al., 2004b). These include genes for the CD45 transmembrane protein tyrosine phosphatase, SYK protein tyrosine kinase, Src family members, and the HS-1 adaptor molecule. Lamprey lymphocyte-like cells also express relatives of the CXCR4 chemokine receptor and its SDF-1 ligand, the cytokine interleukin 8 (IL-8) and its receptor, and the IL-17 receptor. In keeping with their apparent lack of MHC genes, agnathans possess only the preduplication genes for each of the three proteasome subunit pairs needed for gnathostome immunoproteasomes to produce peptides that fit into the cleft of MHC class I molecules (Klein and Nikolaidis, 2005). The identification of this constellation of cellular components in lampreys suggested that, given the ability to make diverse anticipatory receptors, agnathan lymphocyte-like cells are potentially capable of mediating adaptive immune responses.  The Evolution of Adaptive Immunity

The linked source above is quite a good relatively brief source for understanding the evolution of both systems of adaptive immunity.

Especially interesting is the situation that the crucial lymphocytes would appear to have evolved well before adaptive immunity did, and that even those apparently have counterparts in invertebrates today, but without the long-lived migratory ability of lymphocytes.  There is, of course, the possibility (though I cannot think it all likely) that either of the two adaptive vertebrate immune systems evolved independently after the earlier one already existed, but, even then, leukocytes would have already existed for at least one of the systems.

At the heart of gnathostome adaptive immunity, however, is the recombination of the V(D)J gene segments of immunoglobulins by prototypic T and B lymphocytes, which is initiated by RAG1 and RAG2.  The V(D)J gene segments are found in the TCR and BCR genes, and provide the components for T antibodies and B antibodies respectively.  This description is terribly abbreviated, but links provide the necessary background information, while I only mention these facts in order to point out why TCR, BCR and RAG1and RAG2 are considered for phylogenetic studies, along with MHC class I and class II genes.

The excerpt above notes that agnathans evidently lack the MHC genes.  Yet MHCs use the Ig domains of the Immunoglobulin superfamily (IgSF), so have a broad ancestral linkage in that way, as do the BCR and TCR genes.  IgSF proteins are found in insects, and some of these may have immune functions (The Evolution of Adaptive Immunity). 

More interesting from the standpoint of observing a rather exact record of the evolution of adaptive immunity is the fact that agnathans have one TCR-like gene and a VpreB-like gene (one of the “surrogate light chains” of BCR), despite the lack of agnathan use of these genes for their own adaptive immune systems.  In addition, the TCR-like gene actually has the V- and J-like sequences used in gnathostomes, only these are within “a single V region exon,” so would not operate in proper gnathostome fashion (The Evolution of Adaptive Immunity).

 It is stunning from any “design” sense to see our relatives, the agnathans, with genes that could almost effect the actions of our adaptive immunity.  It is essential to, and predictive of, evolution that genes able to be modified through relatively slight changes exist in ancestors prior to the existence of adaptive immunity, and hagfishes and lampreys preserve the record of at least some of these necessary genes.  This is in addition to the previously-established fact that adaptive immunity comes from, and is integrated into, innate immunity, which would be necessary for the evolution of such a complex biochemical pathway.

There is more, however.  The core of RAG1 has also been found to have a homologs in animals which have diverged from our own common ancestor.  These homologs are Transib transposases, whose functions are to break DNA up in order to insert transposons into the genome.  Because RAG1 and RAG2 perform very similar actions as the transposases in order to rearrange the V(D)J segments, it was hypothesized that their genes would derive from transposase genes.  There are “RAG1 Core–Like Sequences in the Sea Urchin, Lancelet, Starlet Sea Anemone, and Hydra Genomes,” as my source indicates.  The homolog in the lancelet is presumably the most important relationship to our adaptive immune system, since the lancelet is a chordate, as are the vertebrates.  See RAG1 Core and V(D)J Recombination Signal Sequences Were Derived from Transib Transposons.

Unfortunately for Behe, his little consideration of the actual science of the evolution of adaptive immunity includes this gem:

…It’s on thing to say an organism has a completed, functioning system, and another to say how the system developed.  The authors certianly realize this.  They note that

immunoglobulin and TCR genes both require RAG proteins for rearrangement.  On the other hand, RAG proteins require specific recombination signals to rearrange immunoglobulin and TCR genes

(RAG is the component that rearranges the genes.)  They make a valiant stab at accounting for the components, but in the end , it is a hop in the box with Calvin and Hobbes.  The authors speculate that a gene from a bacterium might have luckily been transferred to an animal.  Luckily, the protein coded by the gene could itself rearrange genes; and luckily, in the animal’s DNA there were signals that were near antibody genes; and so on.  Darwin’s Black Box 137

Ah, yes, the attempt to fault evolution for actually accounting for what happened across the taxa.  It is, as I have stated, an accident of heredity that we ended up with the TCR and BCR genes which provide the gene segments which are then rearranged by RAG proteins, and of course it is also an accident of heredity that we ended up with a proper transposase core that could rearrange the V(D)J pieces.  But we account for the accidents in our theory, for evolution can only occur with relatively likely accidents. 

There is nothing particularly odd about transposases in a genome, TCR and BCR genes–that these, or their homologs, exist in organisms lacking adaptive immunity shows that to be the case.  The accidental nature of evolution is simply that those particular genes ended up in our ancestors, so again, the accident is in the particulars of heredity.  What would be strange is for a designer to go around seeding organisms that lack adaptive immunity with exactly the genes needed for their relatives to evolve heredity, even though they have no need for these particular genes, as opposed to genes with similar functions.

No, paradoxically, the ancestral transposase genes and the TCR and BCR genes were not accidentally within the vertebrate genome at all, that is, not in the sense that Behe claims that they were.  They were there because vertical genetic transfer dictates that the accidents of evolution will be substantially preserved (subject to evolutionary change, naturally) in the genome, and it will be these preserved elements that provide the basic resources for further evolutionary changes. 

To elucidate further, there are different kinds of accidents.  Science recognizes the endless production of accidents, within the constraints of “natural law”* and other known regularities.  These types of accidents are abundant throughout, and are conclusive evidence for, biological evolution.  The accidents of a TCR-like gene, and part of a BCR-like gene in agnathans, and the accident of the RAG1 core gene in our chordate ancestor, are the “lawful”* sorts of accidents that are unavoidable in evolution, hence are predicted by evolutionary theory.

What Behe wants us to believe is that the “lawful” acquisition, and causal transferral via heredity, of the accidents of our evolutionary ancestors are in fact accidents of the unexplainable, spooky (supernatural) kind.  While he certainly missed the mark on the RAG1 gene, his usual fallback position has been that homologous genes simply “indicate heredity,” and nothing else.  No, that’s missing the heart of evolutionary processes, for evolution is constrained by present and past accidents.  RAG1 is not at all a “lucky” occurrence (not at the inception of the evolution of adaptive immunity, that is), it is one of the few genes that unguided evolution could possibly use to evolve a crucial function of adaptive immunity, hence its evolutionary modification into immune functionality is “law-like”*–which sorts of actions traditional Catholics have credited to God.

In later writings (namely, EoE), Behe brought up the possibility of “design” by God choosing a universe out many that would produce the requisite mutations for a desired outcome.  This is too bizarre, however, because this is essentially a kind of multiverse concept used not to explain how the conditions of life came to be right, but one in which incredible accidents are selected by God to account for the entire course of evolution.  In other words, rather than crediting God for purpose (other than the one existing behind the chosen “possible universe”), rationality, and evident design, God is responsible for incredible and unlikely accidents, a sort of hyper-accident in the operation of the universe, yet a fine-tuning of the underlying laws of the universe.

In one way, then, he credits God for order and “lawfulness”, and in the other he credits God for extremes of accident, neither reconciling the two opposite notions, nor explaining why God didn’t opt for the malaria-free universe, or the one that gave us super-intelligence, radio communications, and the ability to fly (surely all of these are possible in an infinite number of evolutions of life).  The result is an incoherent God, let alone one lacking in benevolence.

Getting back to the core of this post–after that little excursion into the strange and irrational “saves” that Behe is forced to invoke–I wish to point out that not all of the genes of adaptive immunity have been found to have homologs in our agnathan, non-vertebrate chordate, or invertebrate relatives–notably the RAG2 gene .  Questions of how adaptive immunity evolved abound, certainly.  But unless we are willing to embrace the extremely unlikely accidents of Behe’s later “thought,” or the strange accidents that “designed” our relatives to retain evidence of a number of the needed precursors for “lawful” evolution, we will stick to the “lawful”* accidents which evolution must utilize in modifying life and its systems.  For it is an accident that we had the particular genes we did before we evolved adaptive immunity, yet it was not at all accidental that we would have the functions of TCR-like, BCR-like, and RAG1-like genes before  our particular type of adaptive immunity arose. 

Nature, and thus evolution, continue to operate according to “law-like” regularities, much as traditional theists have claimed.  Many theists did suppose that there was an early intervention, to produce life.  However, few considered pure accident or unknowable intervention to be at work through the course of earth’s history–for that would make our intelligence unable to reliably make sense of what we observe, quite like Behe’s claims fail to make sense out of observation.

We accept the accidents of evolution because they do not deviate from the processes that we observe, and because the same patterns in “microevolution” exist in “macroevolution.”  “Lawful accidents” are all that we ever propose to exist, and to explain the patterns of “microevolution” and of “macroevolution.”  Behe would have us believe that incomprehensible accident, or unknowable intervention (it is not sensible, knowable “complexity” that Behe claims to be the mark of design, quite unlike Paley’s contention), is responsible for the “law-like”* patterns discovered to underlie the appearance, and relatedness, of gnathostome innate immunity. 

Unfortunately for him, this means not only that science is worthless, but so is rational thought.  According to him, we are the result, and the observers, of the incomprehensible accident (at least from our unprivileged viewpoint) that this universe is said by Behe to be.  The problem for the IDists is that “design” itself no longer has any meaning in such a universe, and we can only be left in an existential nightmare of appearances without any kind of truth existing behind these.  As a matter of intellect, it becomes the worst possible world, for no observation of regularities (such as we find in “macroevolution”) is reliable in the IDist universe.

*I use quote marks around “lawful” and related words, because modern science and philosophy understand “nature’s laws” to be the result of inductive reliable observational regularities, and not as absolute and unquestionable verities such as one might credit to God.

This is part of a series of posts that I am combining into one long post, which may be found at Darwin’s Black Box.