Dark Bilious Vapors

As a follow up to this earlier post about the PA trial over Intelligent Design - I was finally able to save the first day’s testimony of Dr. Kenneth R. Miller (professor of Biology at Brown University) into a format to reconfigure and cut and paste the arguments and KOOL scientific information he provided.

The first day’s transcripts of that proceeding (available online at the National Center For Science Education webpage at this link.

In a nutshell, this opening *broad-side* into the illogical and falsified arguments of the I.D. proponents.

It illustrates, via current and previous scientific work, how Darwin's basic theory of Evolutions and descent from common ancestry are supported by the genetic sciences. Additionally, how contemporary evolutionary theory provides the conceptual framework in which these puzzles can be addressed and points towards a way to solve them. Also that every single scientific society in the United States that has taken a position on this issue has taken a position against intelligent design and in favor of evolution.

The issue being that there is no controversy within science over the core propositions of evolutionary theory, Intelligent design, on the other hand – and many of the specific factors cited by Michael Behe in various publications and books (like his "Darwin's Black Box" and "Of Pandas and People" which are NOT peer reviewed scientific papers or publications) claiming to describe “irreducibly complex systems” have been falsified - Proved False – by scientific studies that either preceded his claims (and which he could have been aware of) or have since been shown to be incorrect.

Mr. Miller, testifying for the plaintiff’s against the I.D. proponents, covers the blood cell clotting cascade, the bacterium flagellum, and cites new scientific studies that bolster and confirm evolutionary theory of common descent.

The heading of the topic matters and text emphasis is mine. Also these segments are not in the same order as the transcript testimony and have been slightly edited to remove extraneous comments, but otherwise they are a fair rendition of the testimony provided.

To read the click on the “more” button to see further of the Direct Exam by Mr. Witold J. Walczak of Dr. Miller. [These are long pieces... but are well explained as to the theory and the KOOL science.]

The “Common Descent Theory” of Evolution using the Hemoglobin molecule

Dr Miller Answer: Hemoglobin is the protein that makes your blood red. It's the oxygen-carrying protein found in red blood cells…It's made up of four parts. Those parts are called polypeptides, but we can think of them essentially as four subunits. It has two copies of a part called alpha-globin and two copies of a part called beta-globin.

Now, what modern molecular biology has enabled us to do is to look at exactly where the instructions are that specify these. And you'll notice that the beta-globin -- excuse me, the 12 alpha-globin instructions are specified on Chromosome Number 16 and the beta-globin instructions are specified on Chromosome Number 11.

And as our genome does for many genes, we have multiple copies of these, so we have backups. We've got extra copies of the alpha-globin genes and extra copies of the beta-globin genes, and they have very interesting physiological functions, these multiple copies, which are not relevant right now and therefore we won't get into. But there's something very interesting about these, and it enables us to test evolution right down to the level of the molecule.

And I want to point that out by looking at the beta-globin genes Chromosome Number 11. … I've zeroed in on the six copies of the beta-globin gene sequence. Each of these copies is a set of instructions for how you build this polypeptide. Five of them work, but one of them doesn't. It's given the Greek letters psi, beta, and then the number one. And the psi-beta-1 sequence isn't a gene. It doesn't work. It's a pseudogene, and a pseudogene is recognized as a gene because it's so similar to the other five in its DNA sequence, but it has some mistakes. It's broken, and it has a series of molecular errors that render the gene non-functional.

Now, I'd like to show you exactly what those molecular errors are in the next slide. This is a blow-up of the pseudogene. These are the portions that actually do the coding, if it was coded in red here. And you'll notice that there are six distinct mistakes in this gene.

… but in a very simple way, the altered initiator means that the signal that exists at the front of the gene that says "copy me" is missing. And therefore RNA preliminaries, the molecule that copies genes, can't bind, and it never gets expressed. But even if it did get expressed, it has five other errors that would keep this, the RNA copy of this gene, from being translated. It's missing the start signal. It's got stop codons that would cause the synthetic apparatus to grind to a halt. It's just a mess.

Now, the reason that this is important in evolution is actually very simple, and that is, these errors appear in a gene, they have no functional purpose. And you might ask yourself, what would I do, what would you do if we were to find another organism that didn't just have similar genes but also had a pseudogene in the same spot and had the same set of errors? There's no reason why evolution would produce a duplicate set of mistakes in two copies of things. It must mean that these two organisms are descended with modification from another organism that had the same set of mistakes.

…what I'd like to show you are three organisms, the gorilla, the chimpanzee, and the human being that share the exact same set of molecular mistakes.

Now, why is this significant?

One of the core principles of evolution is common descent. One could always argue that because the three species that I've depicted on this slide are all African species, that's where they all come from, they're all primates and they all probably started out living in similar environments, that the functional parts of this gene locus, they might work the same. But you cannot argue that the mistakes should match.

And the fact that all three of these species have matching mistakes leads us to just one conclusion, and that's the same conclusion that Charles Darwin predicted almost a century and a half ago, and that is that these three species share a common ancestor. Matching mistakes are evidence of common ancestry.

Q. And are there other animals that share the same mistakes?

A. Well, we actually don't know, because there are two great apes in which we're waiting on the genome sequence. Those are the orangutan and the Bonobo, pygmy chimpanzee. And if I had to make a friendly bet, I'd bet that they do. But other primates and other mammals, cats, dogs, horses, they don't have these mistakes. These mistakes are unique to the lineage that shows common ancestry of us and these other organisms.

Q. Could you give us another example?

A. Sure, I'm very happy to. … this is another test of the evolutionary hypothesis of common ancestry. We have, as I'm sure most people know, 46 chromosomes in our human cells. That means we have 23 pairs of chromosomes because you get 23 from mom and you get 23 from dad, so we've all got 46 total. We've got 23 pairs.

Now, the curious thing about the great apes is they have more. They have, as you can see from the slide, 48 chromosomes, which means they have 24 pairs. Now, what that means, Mr. Walczak, is that you and I, in a sense, are missing a chromosome, we're missing a pair of chromosomes. And the question is, if evolution is right about this common ancestry idea, where did the chromosome go?

Now, there's no possibility that that common ancestry which would have had 48 chromosomes because the other three species have 48, there's no possibility the chromosome could have just got lost or thrown away. Chromosome has so much genetic information on it that the loss of a whole chromosome would probably be fatal.

So that's not a hypothesis.

Therefore, evolution makes a testable prediction, and that is, somewhere in the human genome we've got to be able to find a human chromosome that actually shows the point at which two of these common ancestors were pasted together. We ought to be able to find a piece of Scotch tape holding together two chromosomes so that our 24 pairs -- one of them was pasted together to form just 23. And if we can't find that, then the hypothesis of common ancestry is wrong and evolution is mistaken.

Now, the prediction is even better than that. And the reason for that is chromosomes themselves have little genetic markers in their middles and on their ends. They have DNA sequences, which I've highlighted in here, called telomeres that exist on the edges of the chromosomes. Then they have special DNA sequences at the center called centromeres, which I've highlighted in red. Centromeres are really important because that's where the chromosomes are separated when a cell divides. If you don't have a centromere, you're in really big trouble.

Now, if one of our chromosomes, as evolution predicts, really was formed by the fusion of two chromosomes, what we should find is in that human chromosome, we should find those telomere sequences which belong at the ends, but we should find them in the middle. Sort of like the seam at which you've glued two things together, it should still be there. And we should also find that there are two centromeres, one of which has, perhaps, been inactivated in order to make it convenient to separate this when a cell divides. That's a prediction. And if we can't find it in our genome, then evolution is in trouble.

Well, lo and behold, the answer is in Chromosome Number 2.

This is a paper that -- this is a facsimile of a paper that was published in the British journal Nature in 2004. It's a multi-authored paper. The first author is Hillier, and other authors are listed as et al. And it's entitled, The Generation and Annotation of the DNA Sequences of Human Chromosomes 2 and 4. And what this paper shows very clearly is that all of the marks of the fusion of those chromosomes predicted by common descent and evolution, all those marks are present on human Chromosome Number 2.

[As a reminder] of what that prediction is. We should find telomeres at the fusion point of one of our chromosomes, we should have an inactivated centromere and we should have another one that still works. And you'll note -- this is some scientific jargon from the paper, but I will read part of it.

Quote, “Chromosome 2 is unique to the human lineage of evolution having emerged as a result of head-to-head fusion of two acrocentric chromosomes that remain separate in other primates. The precise fusion site has been located, the reference then says exactly there, where our analysis confirmed the presence of multiple telomere, subtelomeric duplications."

So those are right there. And then, secondly, during the formation of human chromosome 2, one of the two centromeres became inactivated, and the exact point of that inactivation is pointed out, and the chromosome that is inactivated in us -- excuse me, the centromere that is inactivated in us turns out to correspond to primate Chromosome Number 13.

So the case is closed in a most beautiful way, and that is, the prediction of evolution of common ancestry is fulfilled by that led-pipe evidence that you see here in terms of tying everything together, that our chromosome formed by the fusion from our common ancestor is Chromosome Number 2.

Evolution has made a testable prediction and has passed.

Q. So what you're testifying here is that modern genetics and molecular biology actually support evolutionary theory?

A. They support it in great detail. And the closer that we can get to looking at the details of the human genome, the more powerful the evidence has become.

Dr. Miller Answer: …The first respect is that, Dr. Behe, although he praises the arguments of William Paley in several areas of his book, argues that the argument from design, as Paley's argument is known, is made most effectively at the level of the cell, at the level of the molecule.

So [Behe] basically has attempted to update Paley's argument, not by looking at large organ systems, but by looking at biochemical machines that exist inside individual living cells. And the second way in which his argument differs from Paley is that, Dr. Behe, after coming to the same conclusion, that there had to be an independent designer, a creative force that created these machines, these pathways, and put them into being, Dr. Behe is unwillingly to name the identity of that designer.

And I believe he suggests that the designer, of course, could be a divine force, but it could be super intelligent space aliens from Mars or perhaps time traveling cell biologists going into the past from the future and causing the structures to be put together.

Q. And have you actually heard Dr. Behe use these examples?

A. Yes, sir, I have. Dr. Behe and I have discussed and debated this issue a number of times, and these are examples that he has used in those discussions.

Q. Now Dr. Behe advances an idea known as irreducible complexity. Can you explain to us what that idea consists of?

A. Sure. The idea of irreducible complexity starts with the observation that living cells contain complex biochemical systems and machines. They are composed of many parts. He then suggests that, that complexity is irreducible. What he means by irreducible complexity is, if we start to take a few parts away to see if we that we can't, that a machine stops functioning. Now I've prepared a few demonstratives with quotes from Dr. Behe's work to sort of illustrate this …we have the bacterial flagellum.

So this is, in a way, a summary of Dr. Behe's argument. And one of the things that I think is important to make clear to the Court is that, it is absolutely true that there are many, many structures in the living cell, many biochemical pathways for which we don't have a detailed biochemical -- excuse me, a detailed evolutionary explanation. That is a point that all scientists will concede. Do Doctor –

Q. I'm sorry. Is that true just about evolutionary theory or is that true about any science?

A. That's true about anything. In cell biology, for example, I think most people and the court are aware that when a cell divides, the chromosomes that carry the genetic information of a cell are moved apart and separated into the two daughter cells. We have enormous arguments in the field of cell biology as to what theexact mechanism is by which that force is generated. We can all see it happen. Any high school student can watch the separation of chromosomes under a microscope in a high school laboratory. But we still don't know exactly what the motor or the mechanism is that moves these apart. There are many, many other unsolved problems in biology.

…. So it's important to note that Dr. Behe's argument does not say simply, well, there are complex structures within the cell for whom we do not understand the detailed evolutionary origin of, that's absolutely true. But his argument really rises to a different level. What I've shown on this slide is a diagram of the bacterial flagellum.

Now bacteria, of course, are very, very simple cells. They're found everywhere in nature. They're found, for example, in our digestive systems. They're found in the skin. They're found on the surface of the table. Some bacteria have little whip like structures called flagellum. You might almost considers them to be outboard motors. And these things whip around at very high rates of speed, and they propel the bacteria through water, or sometimes they pull the bacteria in sort of a screw like motion through the water.

So it's marvelous machines. They are acid powdered reversible rotary engines. These are marvelous little machines, and they are made of a whole series of protein parts, some of which are shown in this little diagram here. …

Now what I wrote here is that, Dr. Behe has made very clear in what I think is fairly called his biochemical argument from design, that that argument depends upon a much bolder claim than simply saying, scientists have not completely explained how this structure evolved. And that bolder claim is shown in the next animated section of this slide. And that is that, the evolution of complex biochemical structures cannot even or ever be explained in principle. And, of course, what he means by that is, there is some aspect of this complexity, which means we can say not just, we haven't figured it out yet, but we will never figure it out, and that's where the evidence for design lies.

…. I'll try to use Dr. Behe's words to explain why he holds this point of view. The reason that evolution cannot explain, he says, the origin of such structures is because they have a property, which he calls irreduciblecomplexity, or they are irreducibly complex.

I thought it best for the Court to read the description of irreducible complexity in Dr. Behe's own words.

…Quote, ”By irreducibly complex, I mean a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning. And now, from my point of view, the key part of the argument, and I'll continue to read. An irreducibly complex system cannot be produced directly by slight, successive modifications of a pre-cursor system -- and that's how evolution would have to produce it -- because any pre-cursor to an irreducibly complex system that is missing a part is by definition non-functional. So his argument is that, if you have a multi-part system, and all the parts are necessary to function, you can't produce that system five parts at a time, six, seven, and gradually build up the complex system, because there is no function possible until the last part is snapped into place. And that's why evolution cannot produce that system.”

[A]nother quote of Dr. Behe's that tries to make this point absolutely explicit as to why you need the system to be working. He points out, another quote, Darwin's Black Box, page 39,

quote, ”Since natural selection can only choose systems that are already working -- and if you remember, his contention is, if you're missing a part, you're not working -- then if a biological system cannot be produced gradually, it would have to arise as an integrated unit, in one fell swoop, for natural selection to have anything to act upon,”

closed quote.

And Dr. Behe rightly points out that, to imagine such complex systems arising spontaneously in one fell swoop is something that no serious biologist would argue could happen, and I will not argue either. So his point is, as long as irreducible complexity holds, then any system we can identify as irreducibly complex couldn't have been produced by evolution. It's a very, very coherent argument.

Q. Does he identify some organisms that he calls irreducibly complex?

A. Well, counselor, not so much organisms, but he certainly identifies some machines and some structures that he regards as irreducibly complex, one of which, of course, is the bacterial flagellum. And I pointed out, this slide contains a diagram of the flagellum. And to the right is actually sort of what we call a false color, but an electron micrograph showing a bacterium with several flagellum protruding from one end. So that is one of the principal systems to which he points.

… And I should also point out, …that Dr. Behe also says, the blood clotting cascade that [is] an example of an irreducibly complex system, the eukaryotic cilium, similar system to the flagellum, that's irreducibly complex, the vesicle targeting system that parcels out things in living cells, and also the immune system are all examples of irreducibly complex systems.

Now what I did in this slide was to prepare a graphic to make this point as clear as possible to those of us in court today. And that is to emphasize that complex biochemical machines composed of multiple interacting parts, if they work, they can have a essence of the biochemical argument from irreducible complexity, however, is that the individual parts of that machine have no function of their own. And because they have no function on their own, they cannot be produced by natural selection and, therefore, the impediment, the reason you can't get to here from there, you can't go from individual parts to the machine, is because the individual parts have no functions of their own.

Now evolutionary biology has grappled with this problem before. And the next slide shows how evolutionary biologists generally explain the evolution of complex machines.

And that is, they agree, yes, there are such machines. You need all these parts for a
particular function. But where these machines come from is, they come from pre-existing machines which have functions of their own, and that the individual parts of these machines originate in components that have different functions. So the way in which evolutionary biology picks up

Dr. Behe's challenge is to basically say, you're wrong, that the individual parts of these machines cannot have a function that is favored by natural selection. Now that, of course, in this slide, this is not evidence, of course, in the scientific sense. This is merely an argument.

But the reason I like the way that Dr. Behe has put his argument, and I like sort of describing it this way, is because it actually is amenable to a scientifictest. Something that most arguments for intelligent design are not.

Q. I'm sorry. This is -- is Dr. Behe's argument for irreducible complexity, is that an argument directly for design?

A. That's a good point. The answer is, no, it's not. It really is an argument that says why such systems are not produceable by evolution. So it's a negative argument against evolution. It is in itself not evidence. Even if the argument were correct, it's not evidence of a designer, it's not argument for design, it simply is an argument that the evolutionary mechanism wouldn't work in this case.

Q. So that's why this argument is testable?

A. That is correct. As I mentioned earlier, one of the problems with intelligent design is that it doesn't make any testable predictions. This actually isn't a testable prediction of design either. This is simply an argument as to why evolution wouldn't work. And that can be subjected to a test.

…. [T]he nature of the test that I or any other scientist would propose is pretty simple.

If you animate the slide, you'll see that Dr. Behe's prediction is that the parts of any irreducibly complex system should have no useful function.

Therefore, we ought to be able to take the bacterial flagellum, for example, break its parts down, and discover that none of the parts are good for anything.

If evolutionary theory holds, however, and we can animate again, and we'll show that in the right-hand side, evolution makes an extremely straight forward prediction. And that is, when we look at these irreducibly complex structures, we ought to be able to find parts of those systems that actually do have useful

So we can do a very straight forward either/or test to distinguish between these two alternatives….[F]rom a review article showing some of the proteins involved in the construction of the bacterial flagellum. Now the individual names of the gene products need not concern us. They often begin with FL for flagellum. But as you can see, just as Dr. Behe says, this is a complex multi-part biochemical machine.

Now the test that I would propose…And if Dr. Behe is correct, if we take away even one part, there should be no function.

But I'm going to propose that we take away not one, not two, I'm going to propose we take away 30 parts. And what I'm going to propose to do is, take 30 of these proteins away and see what is left. And the slide that I set up is animated, and what we have done is -- actually, could you go back for the animation and then do it again?

… And you can see the parts that I have removed are on the outside and the inside, and what are left are 10 proteins that span the inner and outer membrane. These bacteria, any of them are surrounded by two membranes. These 10 remaining parts are shown in the next diagram, which will come up on the slide. And this is a diagram showing where these 10 parts are. They exist at the very base of the flagellum near one of the cellular
membranes.

Now the prediction that is made by Dr. Behe in his book is extremely straight forward, which is, since this was an irreducibly complex machine, and we've taken away most of its parts, what's left behind should be non-functional because, you remember, he wrote, any pre-cursor to an irreducibly complex machine that is missing a part is, by definition, non-functional.

This guy is missing 30 parts.

… Well, it turns out that what is actually left behind when we take those parts away is a
little structure with those 10 parts, which is known to microbiologists as the type III secretory system. And I can see, Mr. Walczak, you're saying, why, of course, it's the type III secretory system.

The Court: That certainly was on my mind.

Dr. Miller: Exactly. Now I was expecting a question of, how do you know it's not type II or type IV? The type III secretory system is a little molecular syringe that some of the nastiest bacteria in all of nature have. Yrsinia pestis, for example, which is the organism that causes bubonic plague, is a type III secretor. And what it does is, it gets inside our boy, crawls up alongside, and uses this syringe to inject poisons into a human cell.

And in the lower left-hand corner of the slide, I have some diagrams showing the operation of a type III secretory system.

Now the connection between this and the flagellum is that the type III -- the 10 proteins in the type III system are almost a precise match for the corresponding 10 proteins in the base of the bacterial flagellum.

So it's very clear that a subset of those proteins has an entirely different function, a beneficial function, not for us, but for the bacterium, and a function that can and is favored by natural selection. … So the summary of this example is really very straight forward. When we take this complex multi-part system, which is the bacterial flagellum, the prediction made by Dr. Behe from irreducible complexity is when we break the parts apart, we should have no useful functions. Anyone missing a part is, by definition, non-functional.

We follow that up. We do break it apart. And lo and behold, we find -- actually, we find a variety of useful functions, one of which I have just pointed out, which is type III secretion. What that means, in ordinary scientific terms is that, the argument that Dr. Behe is made is falsified, it's wrong, it's time to go back to the drawing board.

Q. And does Dr. Behe focus on just one type of cell? I'm sorry if I'm using the wrong terms here.

A. No, he doesn't. His arguments extend to a wide variety of cells and a wide variety of systems that he identifies as irreducibly complex.

Q. But the reasoning, the analysis that you just went through is -- applies in the same fashion to these other examples, is that correct?

A: Yes.

Dr. Miller Answer: …Pandas (written by Michael Behe - Professor of biochemistry at Lehigh University) also, in their discussion of molecular similarities, talks about what is known as the blood clotting cascade. And in this particular case, all of us … have blood that clots properly. And what that means, of course, when we cut ourselves, we don't just bleed and bleed and bleed and bleed, but that cut eventually seals with a blood clot.
…
Now, blood clotting is, biochemically, an enormously complicated process. … Everyone agrees that this is complicated… Pandas describes this system, and … it tells students, As we shall see, such interactive systems as illustrated here by the mechanism for a blood clotting are very strong arguments for intelligent design and are virtually impossible to explain in terms of Darwinian evolution, unquote.

Now, it's interesting to look into Pandas and say, why is it that this is an argument for design and impossible to explain by evolution?

… Here is a page from Pandas describing the blood clotting cascade … the essence of the argument that students are given in Pandas.

[Q]uote, ”Only when all the components of the system are present and in good working order does the system function properly,”

unquote. ..It talks about the various proteins in the clotting pathway, and it says, quote,

"Some of them -- these are the clotting proteins -- share discrete regions of their sequences with some others. Does that mean that they derive from one another? It may. But consider that even if this were the case, all of the proteins had to be present simultaneously for the blood clotting system to function,”

unquote. And the emphasis here is mine.

So the argument made by Pandas is that the reason this is an example of design is because it's a multi-part system, and all of the parts have to be put together, presumably by a creator/designer before the system will work. .. Well, that's a scientific statement in the sense that it's a claim that all the parts have to be present for the system to work. And because that is a scientific claim, we can investigate it scientifically and see if it is valid.

…A standard and simple and straightforward scientific test of the claim that all parts must be present for this to work is simple. Eliminate one of the parts, see if the blood will clot. If it won't clot anymore, the claim might be right. If it will clot, the claim could be wrong.

Well, fortunately nature has actually done that experiment for us. And if you could advance the slide, I'm going to show right now, essentially here's the pathway, and I'm going to propose an experiment which is that we eliminate one of the important factors known as factor 12. That's right here. So there's my experiment. …We have just eliminated factor 12, and the question now before the Court is, will blood clot or will it not?

…It turns out that whales and dolphins have done this experiment for us already. Whales and dolphins, in 1969, well before Pandas was published, were shown to lack factor 12. And the slide contains a reference to an article by Robins, Kasting, and Aggeler from Science Magazine, Volume 166, Page 1420, 1969. And you will note a quotation from the abstract of this article saying, "The dolphin intrinsic cascade lacks factor 12,"unquote.

Now, this is from ancient history, as far as we molecular biologists might be concerned today, because 1969 is pre-molecular. So one might wonder, has that result held up? Also in the lower left-hand corner of the slide I have pointed out that a paper published in 1998 by Semba, et al., confirms using genome analysis, that whale Hageman factor 12 basically is now a pseudogene in the whale genome. That's why it is not produced. It is, indeed, missing from the clotting cascade. Whales face many problems on this planet. They're overhunted, they're overfished, but they don't have any problems with their blood clotting. So blood clots just fine, despite missing the factor. So the scientific prediction from Pandas turns out to be wrong.

Q. And the prediction was -- this was known in 1969 is what you're saying?

A. Absolutely, that's correct. So certainly the people writing it should have known. But interestingly, in recent years, you might say the situation has gotten worse.

Q. I'm sorry, worse in what sense?

A. Worse in the sense that the case that Pandas is trying to make has become even farther removed from scientific reality. …

Here again is my representation of the various components of the blood clotting cascade. And this time I'd like to propose that we take away not one part, but three. …The proposal is that we take away the three parts which are known as the contact phase system. Now, that includes factor 12, which we talked about a second ago, but also factor 11 and also the factor that catalyzes the conversion of 12 to the active form.

… Those are the three parts that I propose eliminating. …. There they go. They're gone. It turns out these three parts are missing in a vertebrate known as the puffer fish. And I have placed in the left-hand part of the slide a reference to a paper Jiang and Doolittle, 2003. The title of the paper is, The Evolution of Vertebrate Blood Coagulation as Viewed from a Comparison of Puffer Fish and Sea Squirt Genomes.

It appeared in the proceedings of the National Academy of Sciences, a very eminent scientific journal, Volume 100, Page 7527. And the relevant point here is that they are missing three parts of the system and their blood clots perfectly well. …

Q. So the prediction in Pandas and what Pandas teaches students has, in fact, been invalidated, refuted by the scientific evidence?

A. It was refuted by the scientific evidence in 1969 that was confirmed by genome studies of the whale, and it has been further refuted by Jiang and Doolittle's study of the contact phase system.

Q. I asked you, in preparation, to select a third example, and that was the immune system. What is the immune system?

A. Well, it's a very good question, because we all depend for our very lives on a functioning immune system. It's a system of our body that is widely distributed. We have cells from our immune system sort of engaging in patrol, floating throughout the blood stream and the tissues. And it's a system that enables us to identify, defend against, and to repel foreign invaders. …[C]hicken pox is a virus when invades the human body, the immune system recognizes the code proteins on the virus, makes cells that can continue to recognize it, and produces proteins called antibodies that will bind to the surface of the virus.

[Once someone has] the chicken pox, …[They] would be permanently immune to the chicken box. This is a very important realization for medicine to have because, of course, most of us in this room have received vaccinations designed to stimulate our immunity from diseases far worse than chicken pox such as, for example, polio and diptheria and whooping cough in an effort to stipulate our immune systems to make sure we never get sick from those diseases.

I thought I would start by pointing out an essential protein of the immune system. You can't work without it. That essential protein is sometimes -- it is called by researchers an immunoglobulin, but it is more commonly called an antibody. These are the essential molecules of the immune system.

…It basically is a little Y shaped molecule with two binding sites. And you'll notice in those binding sites are labeled foreign particle binding sites. I hope I have antibodies circulating in my bloodstream against chicken pox. So if I get chicken pox virus in my body, that foreign particle binding site on my chicken pox antibody will bind to the surface of the virus. Another one will bind to the other site. And gradually, the virus will be cross linked into a mesh world, which my immune system recognizes, eliminates from the circulation, and destroys.

[A] diagrammatic view of this molecule. It's made up of four parts.

These are each polypeptides, and they're diagrammed. And you'll notice that part of these -- each of the polypeptides is colored blue, and another part is colored red. The red says, variable region.

The antibodies in my body against polio differ from the antibodies I have against diptheria in the variable regions. They have a different shape because the viruses or the bacteria have different molecules on the surface.

The genius, if you will, of the immune system, is that it can produce an antibody that will attach to, stick to, identify, and destroy just about anything. So one of the most important things in our immune system is the ability, basically, to produce antibodies against any conceivable molecule that might get inside our body. …

Now about 20 years ago, a scientist working at MIT named Susumu Tonegawa … determined exactly how antibodies had the ability to produce such diversity. And that is, it turns out to be a system in the genes of cells in the immune system known as a VDJ recombination system. And this system is not at all unlike a point in development, parts of DNA, in a variety of genes, are literally shuffled. They're tossed from one side to another, and they are rearranged to form a final gene. Now some elements of this shuffling are random just like you hope the dealer, when you go to Las Vegas, is shuffling those card randomly so you don't know what you're going to get.

But it's in that random shuffling that our immune system develops the ability to produce an antibody to just about anything. That shuffling is at the heart of why the immune system works. If anything goes wrong with this process, the individual in which it goes wrong loses the ability to make diverse antibodies, they get very sick, and they're in big trouble when they start to see foreign organisms.

… Where did this system come from?

That's the question that people interested in evolution always try to answer. About 10 years ago, a number of scientists, including Nobel Prize winner David Baltimore, speculated that this process, which is called VDJ recombination, might actually have evolved from a system known as transposition, a system in which genes jump around.
...

[From a] reference to the Baltimore group's paper in the proceedings of the National Academy of Sciences is a quotation from this paper illustrating his hypothesis. They, and he means the gene shuffling system, could have been part of retrotransposons and had a DNA rearrangement function this their previous life. It's possible that the ancestors of these genes, they're called RAG genes, may have been horizontally transferred into a metazoan multi-cellular animal lineage at a recent point in evolution.

So he argued, he suggests there might be an evolutionary way to explain where this system came from. It's a very interesting suggestion. And as I wrote in the slide, perhaps the three part system arose from a type of mobile genetic element known as a transposon.

It's a hypothesis, but the important point, and the reason it's useful is that, it is a testable hypothesis.

…Now Dr. Behe was aware when he wrote Darwin's Black Box of the speculations of the Baltimore lab.

Q. I'm sorry, what year was Black Box written?

A. That was written in 1996.

Q. And the Baltimore article was?

A. 1994.

Q. So Dr. Behe addressed that. And he regarded this as mere speculation. And he also basically told researchers, don't bother. And the reason you shouldn't bother is actually given in the bottom of the slide. On page 130 of Darwin's Black Box, he wrote, and I quote,

”In the absence of the machine -- that's the gene shuffling machine -- the parts never get cut and joined. In the absence of the signals for where to cut, it's like expecting the machine that's randomly cutting paper to make a paper doll. And, of course, in an absence of the message for the antibody itself, the other components would be useless,”

closed quote.

So he basically argues, because this is a multi-part system and all parts had to be together for it to work ahead of time, you're not going make any progress. A few pages later, he's even more explicit about that. On page 139, he wrote, quote,

”As scientists, we yearn to understand how this magnificent mechanism came to be, but the complexity of the system dooms all Darwinian explanations to frustration. Sisyphus himself would pity us. I hope you're up on your classical mythology.”

Q. That's what Dr. Behe wrote in his book in 1996?

A. That is correct, sir. He basically told scientists, don't bother to try to investigate the
evolution of this because it's irreducibly complex, it's multi-part, you cannot solve it with evolution.

Q. So what's happened since then?

A. What's happened since then is, I think, very interesting. Can I have the next slide? This is the quote from Dr. Behe. The complexity of the system dooms all Darwinian explanations to frustration.
…
In 1996, the same year that Darwin's Black Box came out, very strong biochemical similarities were found between this shuffling process, the VDJ recombination, and the way in which retroviruses shuffle their DNA, very suggestive.

Q. Now when you say, found, where was this found?

A. The -- well, the report is in the journal Science. This particular case, I believe, was found in a prokaryotic system because retroviruses can go into all sorts of systems. But the important point is, these investigators noticed there were biochemical similarities between the way the genes are shuffled in the immune system and the way that retroviruses go into other cells.

Q. This is a publication that has been peer reviewed?

A. That is correct. This is the journal Science, one of the best scientific publications in the United States. And, obviously, this was peer reviewed research.
…

…Two years later in the journal Nature, …it turns out that the cutting and transposing enzymes that are normally used for these transposable genetic elements can be replaced by the RAG enzymes, which do the cutting and pasting in the immune system. So that's suggested a further biochemical similarity between these two systems published in 1998 in the journal Nature. Also, of course, peer reviewed. …

In 2000, the RAG enzymes were shown to cause transposition in mammalian cells. What this meant was, not only can they shuffle the immune system pieces of DNA, they can shuffle other pieces of DNA as well.

So little by little, we're beginning to understand that elements of the Baltimore hypothesis are being born out by published research in peer review journals.
…
Once again, the quote that we've been talking about, if you could advance it, in 2003, the VDJ recombinase was shown to cause transposition -- in other words, shuffle DNA around -- not just in mammalian cells, but in human cells as well. The next animation, please, will show the transposases were discovered in nature not associated with the immune system that are a perfect mimic for the way the immune system gene shuffling machine works in human cells. And this was in the journal Nature.

And finally, the last part of this puzzle was put together in the last year, and that is the actual transposic from which these enzymes and insertion sequences evolved were identified by a paper printed in the public library of science, which is a brand new, but very highly regarded peer review journal, and this is Kapitonov & Jurka in 2005.

It's worth noting how these researchers described facsimile of the paper, and also has a quotation from the abstract. Now this is absolutely filled with technically latent language, but it shows how thoroughly researchers have explored this particular -- this particular hypothesis.

… I'm going to read, starting at the quotation marks, and I will skip over some of the technical terminology. Quote,

”The significant similarity between the transib transpases and RAG core, the common structure of these transpases and others, as well as the similar size of these basically catalyzed by these enzymes directly support the 25-year-old hypothesis of a transposon related origin of the VDJmachinery.

And the researchers then point out, there have been other hypotheses that have been considered. Previously, the RAG transposon hypothesis was open to challenge by alternative models of convergent evolution. Because there were no known transpases similar to the gene shuffling ones, the RAG ones found, it could be argued that our gene shuffling enzymes, the RAG1 independently developed some transposon-like properties rather than deriving them from a transposable element encoded transpases.

These arguments can now be put to rest.

And they're very straight forward about saying, we have solved the puzzle of where this system came from. It came from evolution. And it came from a transposable element system.

…So the summary of what we have just gone through, and this is a tree analysis of these transposons and humans and mammals are right down where it says, mammals, is that the summary is that between 1996 and 2005, each element of the transposon hypothesis has been confirmed and, furthermore, when the enzymes that do this gene shuffling are actually put to an analysis to see how closely related they are to see if they themselves match the evolutionary predicted tree, they
match that tree perfectly.

So we've got it.

And as I was getting ready to pack up and come to Harrisburg for this trial, I happened to glance over the Internet at the latest issue of the journal Nature, which has actually not yet appeared in print. I'm still waiting for my copy in the mail. But fortunately, you can on look at things on the Internet several days ahead of time.

The VDJ recombination system is not the only important part of the immune system. There is another important part known as the compliment system. And in this case, compliment does not mean, say something nice about somebody. Compliment in this case is a system that compliments or completes part of what's known as the immune response. And it consists of a series of proteins that target and destroy. And they destroy, in a molecular sense in a most vicious way possible, foreign invaders, especially bacteria and foreign cells. One of the key elements of this is a compliment component now as C.. this article reported, and this is from Jansen et al. It's from a combined Dutch and candinavian group. And again, it's in the latest issue of Nature.

They, for the first time, worked out the detailed structure of compliment C.. and the structure of compliment C. Immediately told them how this compound must -- how this protein must have evolved. It was made up of a series of modular units of exactly the sort that one would expect to arise by gene duplication, and the molecule had unmistakable sites in which pieces of another gene became recombined with it to produce the complete molecule. Hence, they title this work structures of compliment component C. Provide insights into the function and evolution of immunity.

So the entire idea of evolutionary theory is providing a fruitful avenue of investigation into every aspect of the immune system, not just the gene shuffling that I've talked about, but into this other area known as compliment.

Q. So Sisyphus isn't that envious?

A. I don't think so.

Q. I'm listening to the arguments that you have described Dr. Behe is making, that these components are irreducibly complex, and that science cannot explain them. And in some cases, he's been shown wrong. But is that essentially the argument, that scientists currently can't explain some aspects of evolution?

A. In essence, that is the argument. It is what a philosopher might call the argument from ignorance, which is to say that, because we don't understand something, we assume we never will, and therefore we can invoke a cause outside of nature, a supernatural creator or supernatural designer.

Q. And is this not a completely negative argument? I mean, it sounds like this is an attack on evolution? A. This is in every respect a completely negative argument. And if one combs the pages Of Pandas and People or, for that matter, if one looks at Dr. Behe's book or if one looks at the writings of other people who consider themselves to be intelligent design advocates, all that one finds is example after example, argument after argument, as to why evolution couldn't produce this, didn't make that, and doesn't provide an explanation for the following.

I have yet to see any explanation, advanced by any adherent of design that basically says, we have found positive evidence for design. The evidence is always negative, and it basically says, if evolution is incorrect, the answer must be design. Never considers
an alternative idea.

Q. Now let me just stop you. Just because science today cannot explain something, does that mean it can never be explained?

A. Of course not. And if it did, no one would do scientific research. What attracts scientists to research is the lure of the unknown. There is nothing more dreadful than to wake up one morning and think that all the fundamental problems in your field has been solved. On the day that I think all fundamental problems in cell biology have been resolved, I will retired to Sussex and keep bees, as Sherlock Holmes once said.

You want unsolved problems. You're attracted to them. I'll just give you a very simple example.

Proteins are built by hooking together strings of amino acid, almost like beads on a string. The machine that does that building is called a ribosome. We have worked for years to understand the detailed molecular structure of the ribosome.

As a result of work that's been published in the last couple years, we know the internal structure of the ribosome down to the atomic level. We can now look inside it, and we can see the molecular details of how these two amino acids are brought into very close
proximity.

But do you know what? There's still an unsolved problem. We still don't understand the chemistry that forges the link between those two beads on a chain. There was a very popular hypothesis that was put forward by Peter Moore at Yale University. But in the last year, a number of experimenters, including Al Dahlberg at my own university, has shown that Moore's ideas are wrong.

So what scientists everywhere realize is, there's a great prize to be won. That's very exciting. To find the mechanism by which these are joined together. What no one is doing is to say, we'll never solve it, we're going to attribute the formation of the bond between amino acids to an unseen outside force operating beyond nature and, therefore, any chemical explanation is doomed to failure.

That's something we never say in science, because if we did, it would be a research stopper. It would tell us, give up, go home, we'll never figure it out.

Q. What is Dr. Behe's argument?...Dr. Behe's argument is consistent with the arguments made in Pandas, I believe you testified before?

A. Yes, sir, that's exactly what I testified. The term irreducible complexity, which is a feature of Dr. Behe's book, does not appear in Pandas. But the core idea behind irreducible complexity, which is in these complex systems, all parts must be assembled in order to have function, that is at the heart and soul of the arguments which are in Pandas.

Q. Now what I've heard are these negative arguments about evolution. What is the evidence in Pandas? Let's start with Pandas. What is the affirmative evidence for a designer?

A. I'm not aware that there is any affirmative evidence for a designer anywhere in that book.

Q. And what about in Dr. Behe's work?

A. As far as I can tell, there is no affirmative evidence for a designer in Dr. Behe's book either. Both books rely entirely on negative inferences by saying that, if evolution has problems, if evolution is wrong, if evolution cannot provide complete explanations, then we can go ahead and say it's a designer.

Q. So how do they make that argument? I mean, even if there's no evidence? What's the rationale? What's the reasoning for getting to that designer?

A. Well, with all due respect, I believe I've already answered that question, which is, I don't find there is any reasoning in that area at all. It's the sort of logical fallacy in which you might say, well, I have theory A, and I have theory B. And I can prove theory B by showing theory A is wrong.

And in science, you say, excuse me, just a minute. Besides theory B, there's an infinite number of other possible theories. So you don't, quote, prove one by showing that another one is wrong. If you show another one is wrong, you've shown that it's wrong. All other alternative theories are now equal contenders.

So the logic of picking out intelligent design, which is inherently untestable, and saying that any evidence against evolution is evidence for intelligent design employs a logical fallacy that I think most scientists reject.

Q. So the argument is that, if science can't explain it, that default is, a designer?

A. That is the argument, as I understand it, and as it is expressed in both of these books.

Q. Has the scientific community taken a position similar to yours about intelligent design not being science?

A. Well, the scientific community, of course, is large and diverse, and I'm sure there are a few people who are enamored of intelligent design. As I mentioned earlier, the largest scientific organization in the United States, the one organization that probably can fairly be said to speak on behalf of the scientific community in this country is the American Association for the Advancement of Science, or AAAS. I know they have indeed taken a position on this issue.

…. Quote,

”Whereas ID, intelligent design, proponents claim that contemporary evolutionary theory is incapable of explaining the origin of diversity of living organisms, whereas to date, the ID movement has failed to offer credible scientific evidence to support their claim that ID undermines the current scientifically accepted theory of evolution, wheres as the ID movement has not proposed a scientific means of testing its claim, therefore, be it resolved that the lack of scientific warrant for so-called intelligent design theory makes it improper to include it as a part of science education,”

closed quote.

Q. That is the official position of AAAS?

A. That is correct, sir.

Q. That is the largest association of scientists in North America?

A. That is absolutely correct. And this is the organization that really speaks on behalf of the scientific community in our country.

Q. Now has the National Academy of Science taken a position on intelligent design?

A. Yes, sir, I believe it has

Q. Could I ask you to take a look at Plaintiff's Exhibit 192? This is the publication we viewed earlier today?

A. Yes, sir, it is.

Q. Could you turn to page 25, please? And could we highlight the third paragraph on that page, please? And this is from the conclusion of this publication, Dr. Miller?

A. Yes, sir, I believe it is.

Q. Could you please read for the record the highlighted text?

A. Quote,

“Creationism, intelligent design, and other claims of supernatural intervention in the origin of life or of species are not science because they are not testable by the methods of science.

These claims subordinate observed data to statements based on the authority, revelation, or religious belief.

Documentation offered in support of these claims is typically limited to the special publications of their advocates. These publications do not offer hypotheses subject to change in light of new data, new interpretations, or demonstration of error.

This contrasts with science where any hypothesis or theory always remains subject to the possibility of rejection or modification in the light of new knowledge,”

close
quote.

Q. Are you aware of any scientific organizations that have taken a position that intelligent design is science?

A. I am not aware of any scientific organization that has taken a position that intelligent design is science, not one.

Miller Answer: …Quote, intelligent design means that various forms of life began abruptly through an intelligent agency with their distinctive features already intact, fish with fins and scales, birds with feathers, beaks, and wings, et cetera.

Q. Is that science?

A. No, not at all. And, in fact, anyone would recognize that in a flash as a form of special creation, because what we have here is intelligent design means the various forms began abruptly, and I might add separately, which is what the previous quote implied, and everything was intact. In other words, organisms were created by an intelligent force instantaneously with all of their features present.

… Of Pandas and People, and you can see that what is presented here is Pandas -- or the view of the fossil record and natural history that Pandas wishes to show to students, and that is that every single organism began its existence on earth as a result of a creative process with the information inserted into it, as it says, by an intelligent agent. It lasts for a certain time on earth, and then it vanishes due to extinction.

So what we have basically is a series of separate creative events required to bring each individual type of organism into existence. If one wished to understand whether or not Pandas is consistent with the idea of common descent, one look at this graphic tells you huh-uh, because what Pandas clearly shows in this graphic is separate descent of every single basic type of organism.

Q. And is that similar to creation science as it was practiced in the 1980s?

A. It is -- the notion of separate descent is identical to creation science, and the only difference that I can see is that in Pandas the creative events are presumed to be spaced out over time, whereas in creation science, those creative events were presumed to have occurred at the same time or the same six-day period. Other than that, I don't see much to differ them.

Karen on 10.04.05 @ 01:49 PM CST