Archive for September 2008

Behe and language origination

September 30, 2008

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.

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.


Behe denies all avenues to understanding the evolution of pathways

September 29, 2008

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.

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.

More confusion from Luskin

September 29, 2008

It would take too much time to deal with all of the errors in Luskin’s latest attack on the evidence of evolution.  So I’ll just hit on several of the problems.   Here’s a paragraph, revealing his typical blithering and ignorance:

Clearly, Darwin’s public relations team has invested much rhetorical capital into this fossil. If past experience is to be our guide, the only event that might cause Darwinists to criticize Tiktaalik would be the publishing of a fossil that was claimed to better document evolution. In the past, I have called such events, evolutionist “retroactive confessions of ignorance.” And with a recently published re-analysis of the fish Panderichthys, Darwinists are now praising Panderichthys for having features that are “much more tetrapod-like than in Tiktaalik,” and are retroactively confessing weaknesses in their precious Tiktaalik, which is now admitted to be a fossil with a “quality” that was “poor.”  Luskin

He seems to be deliberately (one is never certain just exactly how the mixture of stupidity and dishonesty of Casey maps out to be) confusing the problem of “poor quality”  of the Tiktaalik specimens with the idea that it must be poorly demonstrating evolution.  Of course the “poor quality” to which the Nature paper is referring only directly affects the digits of Tiktaalik, which was not exactly the most important issue for which it was being studied.

And as usual, he both treats science like the conformity to dogma that his appalling “science” is, as if “Darwinists” (another problem, but let’s just mark it and go on) are some monolithic group, not a bunch of people who disagree on the details while using essentially the same evolutionary model.  He even contradicts this disingenuous insinuation later on where he writes:

In fact, as reported in a National Geographic (NG) news article, not all evolutionary paleontologists are convinced that these bones were the precursors to real tetrapod digits:

Michael Coates, an evolutionary biologist at the University of Chicago, called the new findings “intriguing” but is not convinced that the digit-like structures in Panderichthys’s fin are the equivalent of our fingers. 

For one thing, they seem unusually flat for radial bones, Coates said.  Luskin

So let’s see, the “Darwinists” are retroactively confessing to ignorance, which of course they never did (Luskin’s too ignorant to understand the situation that existed or exists), except that they’re also disagreeing with exactly the fossil, Panderichthys–which they’re also praising.  The idiot can’t keep a single idea straight throughout his very short article.  Plus, he has no idea of what Tiktaalik is about (since he only reacts against it), which is to fill in a rather large piece of the puzzle of tetrapod radiation.  Casey appears never to have learned that we’re not simply looking for “the one and true missing link,” rather we almost certainly never find representatives of the ancestral species (with the likely exception of Homo erectus, but that’s a very recent transitional), and are looking for various representatives of the transition which gave rise to later groups, including ourselves. 

Way back when, I made essentially those points, as well as complaining about the very real hype surrounding Tiktaalik:

Tiktaalik is a beauty, a triumph of predictive paleontology which relied on evolutionary factors to pinpoint where a fish-to-amphibian transitional might be found. However, it was not just any old transitional they were looking for, they wanted evidence whcih would show how the shoulder girdle evolved. After all, they already had fish-to-amphibian transitionals, Elpistostege, Ichthyostega and Acanthostega. Some even consider Tiktaalik to be, in effect, a better-preserved version of Elpistostege.

I wish that the reporting in the media, and even in the NOVA program, were more clear about these matters. Sure, it’s great that Tiktaalik (hardly the vision one would have of an intelligently designed machine, merely a fish adapting to quadrupedal locomotion) was found near the height of the circus that is ID, however there has not been any excuse for denying non-teleological evolution on the supposed lack of transitionals, for all vertebrate classes have had transitional forms known for decades.  Forum @ Dawkins’ site

Everyone who actually knows enough about science recognizes that hype is common both within and without the scientific community, especially from the people who discovered something new (like Tiktaalik) and wish for it to appear as important as possible.  The point is that someone like myself discounts it, while Casely Luskin simply blithers stupidly on, without comprehending, learning, or, seemingly, ever caring whether or not his account is an honest one.

I know that putting another “Casey lies” observation under “News” is questionable, yet it is another permutation of his dishonesty, so it fits well enough.

The cilium evolved into part of the “irreducibly complex” chordate eye

September 27, 2008

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.

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.

ID has problems with keeping its dogma straight

September 25, 2008

But in fact, DNA isn’t exactly like a blueprint.  Only a fraction of its sections are directly involved in creating proteins and building life.  Most of it seems to be excess DNA, where mutations can occur harmlessly.  Edge of Evolution, p. 66

The above is a rather unexceptional statement by Behe, a reasonable inference from past data, if possibly it is being superseded by later research results. 

But one of the more persistent, if typically bizarre (particularly in light of how IDists typically deny that “design” has any expectations, other than irreducible complexity and the like), claims of IDists is that ID predicts that most “junk DNA” has uses.  Somehow, one of their “leading lights” failed to recognize this “prediction,” quite possibly because it cannot be derived from the vague claims of “ID theory.”

Of course evolution doesn’t really make predictions either way about “junk DNA,” other than that nothing in evolution precludes junk DNA from existing in genomes (very little apparent junk DNA exists in most prokaryotic organisms, while tandem repeats, duplications, and transposons almost certainly produce some true junk DNA in eukaryotes).  This hasn’t prevented IDists from claiming that “neo-Darwinism” insists that much of our genomes has to be junk.  Here’s a recent example from the ignorant Casey Luskin:

Study Challenges Two Icons of Evolution: Functional Junk DNA Shows “Surprising” Genetic Differences Between Humans and Apes

These sources promoting the classic “junk DNA” icon of neo-Darwinism need updating, as a Yale University news release from earlier this month recalls the fact that “[i]n the last several years, scientists have discovered that non-coding regions of the genome, far from being junk, contain thousands of regulatory elements that act as genetic ‘switches’ to turn genes on or off.” In this case, the junk triggered genes that control human thumb and foot development.

Most studies that have claimed that humans and apes have nearly identical genomes have primarily looked at the gene-coding portions of the genome, not the non-coding DNA (formerly claimed to be “junk”). Perhaps as biologists study the non-coding regions of our genome, they will find evidence that challenges two icons of evolution: Not only does “junk” DNA have function, but humans aren’t as genetically similar to apes as was once thought.  [bolding added] Casey Luskin lying for the DI

I guess if you have nothing honest to say, just pick your favorite lie and call it an “icon of evolution,” never bothering to consider why it is that Behe repeats “the classic “junk DNA” icon of neo-Darwinism,” being oblivious both to its “neo-Darwinian” status and to any “prediction” of ID that “most junk DNA” will be found to have a purpose.

The only apparent reason for the constant drumbeat about how “junk DNA” really does have function, and that ID is supposed to predict that it does while “neo-Darwinism” is supposed to predict otherwise, is that IDists are desperate to come up with any kind of evidence for their claims.  That they have none is adequately shown by the fact that one of ID’s “leading theorists,” Behe, fails to recognize either assertion in his most recent book, in spite of his own eagerness to fault “neo-Darwinism” at every turn.

You’d think that people who just make up things as they go along would have the sense to get together to get their stories straight.  ID fails even to design its own propaganda intelligently.

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.

Common descent is demonstrable only when causes are known

September 24, 2008

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.

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.

Eukaryotic flagella are derived from intracellular transport systems

September 23, 2008

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.

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.