IN THE UNITED STATES DISTRICT COURTFOR THE MIDDLE DISTRICT OF PENNSYLVANIAHARRISBURG DIVISIONTAMMY KITZMILLER, et al., : CASE NO.Plaintiffs : 4:04-CV-02688vs. :DOVER SCHOOL DISTRICT, : Harrisburg, PADefendant : 17 October 2005...........................: 1:20 p.m.TRANSCRIPT OF CIVIL BENCH TRIAL PROCEEDINGSTRIAL DAY 10, AFTERNOON SESSIONBEFORE THE HONORABLE JOHN E. JONES, IIIUNITED STATES DISTRICT JUDGEAPPEARANCES:For the Plaintiffs:Eric J. Rothschild, Esq.Thomas B. Schmidt, III, Esq.Stephen G. Harvey, Esq.Pepper Hamilton, L.L.P.Two Logan Squareth & Arch StreetsPhiladelphia, PA 19103-2799(215) 380-1992For the Defendant:Patrick Gillen, Esq.Robert J. Muise, Esq.Richard Thompson, Esq.The Thomas More Law CenterFranklin Lloyd Wright DriveP.O. Box 393Ann Arbor, MI 48106(734) 930-7145Court Reporter:Wesley J. Armstrong, RMROfficial Court ReporterU.S. CourthouseWalnut StreetHarrisburg, PA 17108(717) 542-5569APPEARANCES (Continued)For the American Civil Liberties Union:Witold J. Walczak, Esq.American Civil Liberties UnionAtwood StreetPittsburgh, PA 15213(412) 681-7864I N D E XKitzmiller vs. Dover Schools4:04-CV-2688Trial Day 10, Afternoon SessionOctober 2005PROCEEDINGSPageDEFENSE WITNESSESDr. Michael Behe:Continued direct by Mr. Muise 4P R O C E E D I N G S

THE COURT: Be seated, please. All right.We return, and Mr. Muise, you may continue.DIRECT EXAMINATION CONTINUEDBY MR. MUISE:

Q. Thank you, Your Honor. Dr. Behe, I want toask you some questions about the term theory andits understanding in the science community. Asthe record has shown so far that the statementthat is read to the students in this case usesthis definition, "A theory is defined as a welltested explanation that unifies a broad range ofobservations." Is that a good definition of atheory?

A. Yes, it seems to be.

Q. Are you aware of the National Academy ofSciences' definition of the word theory?

A. Yes, I've heard it.

Q. Let me see if this is what yourunderstanding of that definition is. Inscience "a well substantiated explanationof some aspect of the natural world that canincorporate facts, laws, inferences, and testedhypotheses." Do you agree with that definition?

A. Well, that's certainly one definition ofthe word theory, but you have to be sensitiveto the fact that the word theory can be used inother senses as well.

Q. It can be used in other senses in thescientific community?

A. Yes, in the scientific community itself.

Q. Now, using the National Academy ofSciences' definition of theory, does thatmean a theory is almost certainly right?

A. No, it's not. And that might surprise somepeople unless you, until you start to think ofa couple of examples, and perhaps I'd like todiscuss two examples of a well substantiatedtheory that was widely held, but nonethelesswhich turned out to be incorrect. The first --

Q. I'm sorry, and you prepared a slide to makethis point?

A. I did, but first let me mention somethingelse. Before -- let me ask, let me mention anolder example that most people are familiarwith, and that's the example of geocentrism, the

idea that the earth is the center of the solarsystem, the center of the universe, and that thestars and sun circle around the earth. Now, itturns out that was very well substantiatedbecause people could look up and watch the starsand the sun circle around the earth.So they had very good evidence to supporttheir view. Furthermore, that theory was usedfor ages to help sailors and so on navigate theseas. So it was pretty well substantiated.Nonetheless, of course as everybody knows itturned out to be incorrect, and Copernicusproposed that in fact the sun is the center ofthe solar system and that the earth, whilerevolving on its axis, travels around the sun.So again that's an old example, but nonethelessit shows that a well accepted theory nonethelessis not necessarily correct.

Q. And you have an example of that in moremodern times?

A. Yes, a more modern example from the late19th century is something called the ethertheory of the proposition of light, and that'sshown on this slide here. I pulled off anarticle from the web describing ether theoryfrom the Encyclopedia Britannica, and they saythat, "The ether theory in physics, ether is atheoretical universal substance believed duringthe 19th century to act as the medium fortransmission of electromagnetic waves, much assound waves are traveled elastically such asair. "The ether was assumed to be weightless,transparent, frictionless, undetectablechemically or physically, and literallypermeating all matter and space."Now, this theory arose from the fact thatit was known that light was a wave, and likewaves in the ocean and waves in air that weperceive as sound, waves need a medium to travelin. But if light is a wave, what does it travelin in space? Ether. Ether was the mediumthrough which light traveled.

Q. Who was it that was the proponent of thistheory?

A. Well, it's a good thing we use this articlefrom the Encyclopedia Britannica, because on thenext slide we see that a man named James ClerkMaxwell, who was arguably the greatest physicistof the 19th century, wrote an article for theNinth Edition of Encyclopedia Britannica in the70's, the title of which was Ether. And youshould keep in mind when he wrote this for thispublication, this was not going to be read not

only by the general public at large, but by allphysicists as well.So he was writing of the idea as it wascommonly held at that time in the highest levelsof physics, and he wrote the following:"Whatever difficulties we may have in forminga consistent idea of the constitution of theether, there can be no doubt that theinterplanetary and interstellar spaces are notempty, but are occupied by a material substanceor body which is certainly the largest andprobably the most uniform body of which we haveany knowledge."Now, later on Einstein's work causedphysics to abandon the ether theory. Physicistsno longer believed that the ether does in factfill space, but let's look further on the nextslide. This is a copy of James Clerk Maxwell'sarticle taken from a collection of his papers,his article on the ether, and I want toconcentrate on the lower portion down here andI think on the next slide that's blown up alittle bit.I'm not going to read this, I'm just goingto point out that you can observe that he'susing a lot of precise numbers about the energyof light by the sun, and it turns out he's usingthat to do calculations, and in the calculationshe is deducing the properties of the ether. Forexample, these large red arrows are pointing tothe coefficient of rigidity of ether, which isgiven by the formula Ro V squared, which is2.8.The next red arrow points to a line labeleddensity of ether, which is equal to Ro, which isequal to 9.36 times 10 to the minus 19th power.Now, the point I want to make using this slideis that James Clerk Maxwell, the greatestphysicist of his time, whose equations forelectricity and magnetism are still ought tophysics students today, was using his wellaccepted theory to do precise calculationsand deduce precise physical properties of asubstance that did not exist. And so the pointis that even a well accepted theory, even afeature which seems to be required by somethingelse such as the wave nature of light, cannonetheless be inaccurate and turned out to benot only wrong, but utterly imaginary.

Q. Again I guess that would demonstrate thenature that scientific theories are tentative,is that correct?

A. Yes, I think that it helps to make thatclaim that scientific theories are tentativemore than just a hypothetical claim. The

history of science is replete with examples ofwhat seemed to be correct explanations whichturned out to be incorrect.

Q. Now, is Darwin's theory of evolution atheory in the sense of the National Academyof Sciences' definition?

A. Well, it partly is and partly isn't.

Q. Did you prepare a slide to demonstrate thatpoint?

A. Yes. A slide here is an excerpt from abook written by a man named Ernst Mayr, who,Ernst Mayr was a very prominent evolutionarybiologist, who died just I think last year atthe age of 100, and was privy to a lot of thedevelopment of what's called neo-Darwiniantheory in the middle of the 20th century, and hewrote a book entitled One Long Argument, and init he makes the case that Darwin's theory is notsome single entity, and let me just quote fromthat.He says, "In both scholarly and popularliterature one frequently finds references toDarwin's theory of evolution as though it werea unitary entity. In reality, Darwin's theoryof evolution was a whole bundle of theories,and it is impossible to discuss Darwin'sevolutionary thought constructively if one doesnot distinguish its various components. Thecurrent literature can easily lead one perplexedover the disagreements and outrightcontradictions among Darwin specialists, untilone realizes that to a large extent thesediffers of opinion are due to a failure of someof these students of Darwin to appreciate thecomplexity of his paradigm." So you have torealize that Darwin's theory is not a singleclaim. There are multiple claims within what'scalled Darwin's theory, and they can be, theycan have different levels of evidence behindthem.

Q. Did he break out these five claims in thisOne Long Argument that you're referring to?

A. Yes, he did. He went on to say, well whatare those ideas that are grouped together underDarwin's theory? He called them, he identifiedfive different components, the first of which is"evolution as such." He says this is the theorythat the world is not constant or recentlycreate nor perpetually cycling, but rather issteadily changing. So what we might call changeover time.

Q. Is that a theory or is it an empiricalobservation of facts? How would you describethat?

A. Well, yeah, I myself would call that morean observation rather than a theory. We seethat the earth seems to have changed over time.The second --

Q. Go ahead.

A. The second aspect of Darwin's theory thatMayr discerned was common descent. This is thetheory that, "Every group of organisms descendedfrom a common ancestor and that all groups oforganisms, including animals, plants, andmicroorganisms, go back to a single origin oflife on earth." The third point is somethingcalled multiplication of species. This theoryexplains the origin of enormous organicdiversity.I won't read the rest of the quote there,but it's just a question why are there so manyspecies, the multiplication of species. Thefourth component of Darwin's theory according toMayr is something called gradualism. Accordingto this theory, "Evolutionary change takes placethrough the gradual change of populations andnot by the sudden saltational production ofnew individuals that represent a new type." Sogradualism, things thing gradually over time.And the last component according to Mayr isnatural selection. According to this theory,"Evolutionary change comes through the abundantproduction of genetic variation, the relativelyfew individuals who survive, owing toparticularly well adapted combinations ofinheritable characters, give rise to the nextgeneration." So this is what's commonly calledsurvival of the fittest.

Q. Is this strength of the scientific evidenceequal for each of these five separate claims?

A. No, they vary greatly in the strength ofevidence that's behind each of those.

Q. Has it been your experience that supportersof Darwin's theory of evolution and opponents ofintelligent design have conflated the evidencefor the occurrence of evolution, the change overtime, with the evidence for the mechanism ofevolution, natural selection?

A. Yes. In my experience many people confusethe various parts of Darwin's theory. They

don't make the distinction that Ernst Mayrmakes, and people see that there has been changein the world and a lot of people then assumethat because there has been change in the world,then it must have been change driven by naturalselection. And that's a mistaken conclusion.

Q. Are there other senses in which the wordtheory is used by scientists?

A. Yes. You have to realize that scientiststhemselves use the word theory in a very broad,with a very broad range of senses. Not only inthe sense that the National Academy gave to it,but scientists themselves use it to indicatemany other things.

Q. Now, you did a search of Pub Med searchingfor the term theory, is that correct?

A. Yes, that's right. In order to illustratehow scientists themselves use the word theory,I did a search in a database called Pub Med,which is maintained by the National Library ofMedicine, which is a division of the NationalInstitutes of Health of the federal government,and this is a database of abstracts and titlesof almost all biological articles that arepublished. It contains millions and millions ofarticles.

Q. And have you prepared several slides todemonstrate this point?

A. Yes, I have. In this first one, whichmight be a little bit hard for me to read, butnonetheless the red arrow down here, I certainlywon't read the whole abstract, but if you cansee the little red arrow down here, let me justread a phrase from this. This says that, "Thisstudy does not support the previous theory."And so they are using the word theory hereto mean a previous idea that has now been shownto be wrong or have evidence against it.

Q. If I may, Dr. Behe, just interrupt you herebriefly that might help you in your testimony aswell, if you go to the exhibit book that you'vebeen provided, and if you look under Tab 8 Ibelieve, there's an exhibit marked Defendant'sExhibit 203-A, as in Alpha.

A. Oh, okay. Yes.

Q. Is that the search that you conducted onPub Med in which the slides are derived from?

A. Yes, that's correct. Yes, uh-huh.

Q. And if it will help you to perhaps look atthose as opposed to trying to review it on thescreen, work between the two.

A. Okay. Thank you. And the next slide up onthe screen here is if you follow the red arrows,and those points to other occasions of the wordtheory, it says in this article, "The membranepacemaker theory of aging is an extension of theoxidative stress theory of aging." So in herethe scientists are using the word theory toexplain, or to refer to ideas that are verylimited in scope, which may or may not have muchevidence to support them.So in a much different sense than theNational Academy used in its booklet. Youcould go to -- oh, thank you for the next slide.Let me just see if I can find that one article.Here it is. Okay. If you look at this otherarticle from Pub Med, it's pointing to asentence that begins, "In theory, change inclimate would be expected to cause changeselsewhere."So again a scientist here is using theworld theory to refer to, you know, we wouldexpect this to happen, a kind of expectation.Now, I put up here a publication of my own thatI published with my dissertation advisor WalterEnglander, and if you could read the top itreads, "mixed gelation theory," and it refers tomixtures of sickle cell hemoglobin with othertypes of hemoglobin. So again we were using theword theory to describe ideas and results thathave a very limited providence.And finally on the next slide this is anarticle taken from an issue of Science Magazineseven years ago, a special issue which focusedon the question of why is there sexualreproduction. And the article was entitled "WhySex? Putting Theory to the Test," and theauthor said the following. "Biologists havecome up with a profusion of theories since firstposing these questions a century ago." Thesequestions meaning why is there sexualreproduction, and again the author here isusing the word theory in terms of competinghypotheses, competing ideas, none of which havemuch evidence behind it, none of which have wideacceptance in the scientific community.

Q. I want to return to Ernst Mayr and ask youare the parts of Darwin's theory as he's listedhere well tested?

A. No, they are not. If you look at the

top ones, evolution as such, common descent,multiplication of species, those are all welltested. The claim of gradualism is in myopinion rather mixed. There's evidence for,and some people argue against it. But thecomponent of Darwin's theory natural selectionwhich is sometimes viewed as the mechanism thatDarwin proposed for evolution is very poorlytested and has very little evidence to backit up.

Q. I want to go through in a little bit moredetail on some of these claims. Going back tothat first claim, and I believe you testifiedprobably akin to an empirical observation, isthat correct?

A. Yes, evolution as such that the worldis changed over time, and life as well.

Q. Does intelligent design refute theoccurrence of evolution?

A. No, it certainly has no argument with thiscomponent of Darwin's theory. As a matter offact I think there is a, on the next slidethere's an excerpt from Of Pandas and Peoplewhere the authors write, "When the word is usedin this sense, that is the sense of change overtime, it is hard to disagree that evolution is afact. The authors of this volume certainly haveno dispute with that notion. Pandas clearlyteaches that life has a history, and that thekinds of organisms present on earth have changedover time." And let me make the point thatErnst Mayr calls this component evolution assuch. That is the basic idea of evolution.

Q. So when you hear a claim that intelligentdesign is anti-evolution, are those accurate?

A. No, they are completely inaccurate.

Q. Returning back to the slide with ErnstMayr, the second claim, does intelligent designspeak to that second claim of common descent?

A. No. Intelligent design looks to see ifaspects of life exhibit a purposeful arrangementof parts as evidenced by their physicalstructure. It does not say how such a thingmight have happened.

Q. Is common descent nevertheless addressed inPandas?

A. Yes. I've read sections that do address

common descent.

Q. How does it fit then within intelligentdesign?

A. Well, some people point to empiricaldifficulties that they see for common descent,but common descent itself is not a claim, eitherfor or against is not a claim of intelligentdesign theory.

Q. Would it be accurate then to say it'sviewed more as a difficulty with Darwinismrather than a claim for intelligent design?

A. Yes, that's correct. Common descentapplies more to Darwinian claims, which claimdescent with modification, than it does tointelligent design, because intelligent designis focused exclusively on the question ofwhether we can discern the effects ofintelligence in life.

Q. In which of these claims is intelligentdesign focused principally upon?

A. Intelligent design focuses exclusively onthe fifth claim of Ernst Mayr, or the fifthcomponent that Ernst Mayr identified in Darwin'stheory, that of natural selection, or in otherwords what is the mechanism of evolution, howcould such things happen.

Q. Is it your view that that is where thescientific evidence for these five claims isperhaps the weakest?

A. Yes, that is in fact the most poorlysupported aspect of Darwin's theory. As amatter of fact, that's where the evidence inmy view points away from Darwin's theory.

Q. Again so does intelligent design questionall parts of Darwin's theory of evolution?

A. No. It focuses exclusively on the questionof the mechanism of evolution, and I tried tomake that clear as this picture shows. This isan issue of something called the reports of theNational Center for Science Education, whichis a group which strongly advocates for theteaching of Darwinian evolution in school, andI wrote a letter to the editor of The Reports,which was published in an issue approximatelyfour years ago.And here's an excerpt from that letterwhere I explain, "The core claim of intelligent

design theory is quite limited. It says nothingdirectly about how biological design wasproduced, who the designer was, whether therehas been common descent, or other suchquestions. Those can be addressed separately."It says, "Only that design can be empiricallydetected in observable features of physicalsystems."And I go on to say, "As an importantcorollary it also predicts that mindlessprocesses such as natural selection or theself-organization scenarios favored by Shanksand Joplin will not be demonstrated to be ableto produce irreducible systems of the complexityfound in cells." So I tried to clearly explainthat the only focus of intelligent design is onthe mechanism of evolution, or the question ofwhether or not aspects of life show the marksof intelligent design.

Q. And you said this was published in TheReports by the National Center for ScienceEducation?

A. Yes, that's correct.

Q. And that's an organization where Dr. KevinPadian is the president?

A. Yes, I understand he's the president ofthat.

Q. And Dr. Alters and Forrest are alsoassociated with this organization?

A. I think Dr. Forrest is and Dr. Milleris. I'm not sure about Dr. Alters, and alsoProfessor Pennock has a reply in that sameissue of The Reports.

Q. Now, Dr. Miller in his expert report thathe's provided in this case said that Darwin'stheory actually has many mechanisms. Do youagree with that?

A. No, I disagree, and here is a little copyof Professor Miller's expert report, and helists a number of things, including geneticrecombination, transposition, horizontal genetransfer, gene duplication, sexual selection,developmental mutation and so on, and he saysthat, "The relative importance of these andother mechanisms of evolution, these conflictscontinue to motivate."So he seems to be calling these mechanisms.He's making a mistake here. Except for sexualselection, all the other components listed in

his report, gene transfer, transposition,recombination, are simply ways that diversityis generated in nature. But diversity has to beacted upon in Darwin's understanding by naturalselection. So natural selection is the onlymechanism of Darwinian evolution. The sexualselection that he lists, that is a mechanism,but it's a subset of natural selection wherefeatures have selected value due to theconsideration of their ability to allow anorganism to attract mates or otherwisereproduce.

Q. Do other scientists agree with yourposition on this?

A. Yes, they do. Here's an excerpt froman article by a man named Jerry Coyne, whowas writing in a magazine called The NewRepublic. Now, Jerry Coyne is a professor ofevolutionary biology at the University ofChicago and a vocal opponent of intelligentdesign, as the title of the article shows.He writes an article entitled The Case AgainstIntelligent Design.Nonetheless, he disputes what ProfessorMiller has said, the idea that he had talkedabout, Jerry Coyne says the following, "Since59 Darwin's theories have been expanded, andwe now know that some evolutionary change can becaused by forces other than natural selection.For example, random and nonadaptive changes inthe frequencies of different genetic variance,the genetic equivalent of coin tossing, haveproduced evolutionary changes in DNA sequences,"and here is an important point."Yet, selection is still the only knownevolutionary force that can produce the fitbetween organism and environment, or betweenorganism and organism, that makes nature seemdesigned." So Professor Coyne was saying thatwell, there can be random genetic changes inorganisms, but the only mechanism pertinent tothe discussion of whether there is design innature or not is Darwin's idea of naturalselection.

Q. Do any other scientist besides intelligentdesign proponents question the ability ofnatural selection to explain various aspectsof life?

A. Yes, a number of scientists who are notdesign proponents also question the ability ofnatural selection to account for features oflife, and one example is shown on this slide,a man named Stewart Kauffman, who is a professor

of biology at the University of Toronto now, in93 wrote a book called The Origins of Order:Self organization and Selection in Evolution,and that was published by Oxford UniversityPress, and in the introduction to his book hewrote the following, "Darwin's answer to thesources of the order we see all around us isoverwhelmingly an appeal to a single singularforce: natural selection. It is this singleforce view which I believe to be inadequate, forit fails to notice, fails to stress, fails toincorporate the possibility that simple andcomplex systems exhibit order spontaneously."So in this quotation Professor Kauffmanis summarizing his view that the Darwinianmechanism of natural selection is inadequateto explain some features of biology.

Q. Does Dr. Kauffman still maintain that view?

A. Yes, he does. He also contributed anarticle to the book Debating Design, to whichI and others also contributed, which waspublished by Cambridge University Press lastyear in which he reiterates his views aboutself-organization and complexity. He wrote inthe underlying bold portion, "Much of the orderin organisms I believe is self organized andspontaneous. Self-organization mingles withnatural selection in barely understood ways toyield the magnificence of our teeming biosphere.We must therefore expand evolutionary theory."In other words natural selection is notsufficient. We have to expand evolutionarytheory to include something else other thannatural selection if we want to explain whatwe see in biology.

Q. Sir, you've already shown that the theoryof evolution does not consist of a single claim,and you testified that proponents of the theoryof evolution tend to conflate evidence for oneclaim to support another claim, and also youtestified that opponents of ID, intelligentdesign, claim that it's anti-evolution, and youshowed a slide of Pandas which refutes thatparticular claim. Now, when we say, when we usethe term Darwin's theory of evolution, what isthe common understanding for that?

A. Well, the common understanding is thatnatural selection has driven all of the changein the world, we see in the biological world.

Q. Now, the evolution as such, understandingthat life is changed over time, that wasunderstood before Darwin's time, is that

correct?

A. Yes. People have been proposing suchthings for I think a couple of hundred yearsbefore Darwin's day. Darwin's distinctivecontribution to this discussion was the proposalof natural selection. It was he who hadproposed what people considered to be acompletely unintelligent mechanism for theproduction of the complexity of life.

Q. With that understanding, sir, is Darwin'stheory of evolution a fact?

A. No. No theory is a fact.

Q. Are there gaps and problems with Darwin'stheory of evolution?

A. Yes, there are.

Q. Is there one principal contention you havewith the explanatory power of the theory ofevolution that's is particularly relevant forintelligent design?

A. Yes, I think the major overwhelming problemwith Darwin's theory is what I summarized in myexpert report. I stated the following, "It ismy scientific opinion that the primary problemwith Darwin's theory of evolution is the lack ofdetailed, testable, rigorous explanations forthe origin of new complex biological features."

MR. ROTHSCHILD: Your Honor, objection, justto the extent I just want to make sure that theexpert report is not coming into evidence. Idon't object to the slide as long as that'sclear.MR. MUISE: The report is not coming, YourHonor. It's just for demonstrative purposes todemonstrate his opinion.THE COURT: I'll consider that just to be aclarification objection.MR. ROTHSCHILD: Thank you, judge.THE COURT: There's no need for a ruling.You can proceed.BY MR. MUISE:

Q. Dr. Behe, do scientists who do not adhereto intelligent design share your opinion ofthis?

A. Yes, they do. A couple of examples areshown next. Here is an excerpt from a book by aman named Franklin Harold, who's an emeritusprofessor of chemistry at Colorado State

University, and four years ago he published abook entitled The Way of the Cell with OxfordUniversity Press, and he quote, "We must concedethat there are presently no detailed Darwinianaccounts of the evolution of any biochemicalsystem, only a variety of wishful speculations."So he also seems to share that view.

Q. Has Dr. Miller acknowledged such problems?

A. Yes. Dr. Miller himself wrote in hisexpert statement, "Living cells are filled ofcourse with complex structures," and let's skipdown to the underlying bold statement, hecontinues, "One might pick nearly any cellularstructure, the ribosome for example, and claimcorrectly that its origin has not been explainedin detail by evolution." So again everybodyagrees that Darwinian theory has not given anexplanation of many, many features of life.

Q. With that in mind, sir, I have somespecifics I want to ask you. Has the theoryof evolution, in particular natural selection,explained the existence of the genetic code?

A. No.

Q. Has the theory of evolution, in particularnatural selection, explained the transcriptionof DNA?

A. No.

Q. Has the theory of evolution, in particularnatural selection, explained translation of "M"RNA?

A. No.

Q. Has the theory of evolution, in particularnatural selection, explained the structure andfunction of the ribosome?

A. No.

Q. Has the theory of evolution, in particularnatural selection, explained the structure ofthe cytoskeleton?

A. No.

Q. Has the theory of evolution, in particularnatural selection, explained nucleosomestructure?

A. No.

Q. Has the theory of evolution, in particularnatural selection, explained the development ofnew protein interactions?

A. No.

Q. Has the theory of evolution, in particularnatural selection, explained the existence ofthe proteosoma?

A. No.

Q. Has the theory of evolution, in particularnatural selection, explained the existence ofthe endoplasmic reticulum?

A. No.

Q. Has the theory of evolution, in particularnatural selection, explained the existence ofmotility organelle such as the bacterialflagellum in the eucaryotic syllium?

A. No.

Q. Has the theory of evolution, in particularnatural selection, explained the development ofthe pathways for the construction of the sylliumand flagella?

A. No.

Q. Has the theory of evolution, in particularnatural selection, explained the existence ofdefensive apparatus such as the immune systemand blood clotting system?

A. No.

Q. Sir, is it fair to say that under thisbroad category of difficulties that we justreviewed lies much of the structure anddevelopment of life?

A. Yes, that's correct.

Q. Does this cause you to question whether aDarwinian framework is the right way to approachsuch questions?

A. Yes, it does, because if Darwinian theoryis so fruitless at explaining the veryfoundation of life, the cell, then that makesa person reasonably doubt whether it's, whethersome other explanation might be more fruitful.

Q. Sir, in your expert opinion is there aproblem with falsification of Darwin's theory?

A. Yes, there's a big problem with that.Falsification is roughly the idea that thereis some evidence which would make somebodychange his mind that a theory was right or notright. In many instances Darwinian theory isextremely difficult to falsify, and let me giveone example. On the next slide is shown afigure of vertebrate embryos taken from abiochemistry textbook by Voet and Voet, and thisis the biochemistry textbook that is used widelyin colleges and universities across the UnitedStates.The figure here is drawn after a figurethat was first drawn in the 19th century by aman named Ernst Haekel, who was an embryologistand supporter of Darwin's theory. As you see inthe figure, the vertebrate embryos all begin bylooking virtually identical, very extremelysimilar, and yet in the course of theirdevelopment they develop into completelydifferent organisms. A fish, reptile, bird,amphibian, human, and so on. And Ernst Haeckelthought it was exactly in accord with whatDarwin expected.And the reasoning is illustrated by aquotation on the next slide from a book entitledMolecular Biology of the Cell, which was writtenby Bruce Alberts, who I mentioned earlier waspresident of the National Academy of Sciences.One of his co-authors is James Watson, the Nobellaureate who with Francis Crick won the prizefor discovering the double helical shape of DNA,and other illustrious authors. And in thetextbook they explain those embryological factsby saying the following, "Early developmentalstages of animals whose adult forms appearradically different are often surprisinglysimilar."Such observations are not difficult tounderstand. The early cells of an embryo arelike cards at the bottom of a house of cards.A great deal depends on them, and even smallchanges in their properties are likely to resultin disaster." So if I can summarize theirreasoning here, the authors were saying theseextremely similar embryos are exactly what weexpect, because in vertebrates the basic bodyplan is being laid down in the earlygenerations. And if you upset the foundationof a structure, that's likely to essentiallydestroy it.So what we expect is for later stages ofdevelopment to be dissimilar, but the earlierstages to be very, very similar. Nonetheless,

it turns out that those drawings were incorrect,and a number of years ago in the late 1990's thejournal Science ran a story about a study thathad been done to try to reproduce Haeckel's,results, and it turns out they could not bereproduced. And the story was entitledHaeckel's Embryos: Fraud Rediscovered, and ifyou look at the illustration in the news story,on the bottom row one sees the drawings ofembryos as Haeckel produced them, and on the toprow you see photographs of embryos which weretaken by a modern team of embryologists, lookingvery, very much different.And on the next slide are excerpts fromthe news story. It was written, it says,"Generations of biology students may have beenmisled by a famous set of drawings of embryospublished 123 years ago by Ernst Haeckel.'The impression they give that the embryos areexactly alike is wrong,' says MichaelRichardson, an embryologist at St. George'sHospital Medical School in London," and he wasthe lead author of the study which showed theincorrectness of Haeckel's results."Not only did Haeckel add or omit features,but he also fudges the scale to exaggeratesimilarities." Now, here is the point withrespect to the topic of falsification. Sincethese studies have appeared, no Darwinianbiologist that I'm aware of has decided thatDarwinian biology is incorrect. But if atheory, Darwin's theory, can live with oneresult, and its utter opposite with virtuallyidentical embryos and with significant variationin the embryos, then it says nothing about thattopic.It doesn't predict anything. It will livewith whatever result experimental science comesup with, which means that Darwin's theory hasnothing significant to say about a major featureof life, embryology, because if you think aboutit, if one kind of organism is to give rise toanother kind of organism over time, then theembryological plan for building that firstorganism has to change into the embryologicalplan to build the second kind of organism, andyet how that could happen is a topic thatDarwin's theory of evolution does not address inthe least.

Q. Sir, if I could direct your attention tothe exhibit book, under Tab 16, Defendant'sExhibit 271?

A. Number 16 did you say?

Q. Tab 16, that's right. Is that a copy of

that article, it's an on-line version ofHaeckel's Embryos: Fraud Rediscovered?

A. Yes, it's a copy of the article that doesnot have the illustrations in it.

Q. Was the article written by Elizabeth --

A. Pennisi.

Q. Pennisi, the one you've been referring to?

A. Yes.

Q. Does the bacterial flagellum in the Type 3secretory system, and we're going to be talkingabout these in a little bit greater detaillater, but is there an analogy also with regardto the falsifiability that you could --

A. Yes. As I'll discuss later, againDarwinian theory can't decide whether theType 3 secretory system might have arisen fromthe flagellum, the flagellum from the secretorysystem, whether both developed independently,or other pertinent questions. So again thequestion of falsifiability, if it doesn't, can'tpredict any of those, then it has nothing to sayabout those features.

Q. Now, does Darwin's theory have difficultyexplaining what we see in nature regardingsexual reproduction?

A. Yes, turns out that it does. It wasrealized not long after Darwin published histheory, it was realized by a man named AugustWeisman that Darwinian theory actually predictsthat most organisms should reproduce asexuallybecause, one reason is because Darwinian theory,one goal of an organism, goal in the terms of abetter evolutionary result, is to get more ofthe organism's genes into the next generation.If an organism reproduced asexually by clonalreproduction, the offspring would contain all ofthe genes of the organism. But during sexualreproduction, for each offspring reproduced theparent gets only half of its genes into the nextgeneration.And this has been a conundrum that has beenunsolved in Darwinian theory for over a century,and during that time scientists have not justbeen sitting around. They've been trying veryhard to come up with explanations for that, andas a matter of fact they've come up with so manysuggestions, so many theories, that in 1999 aman named Kondrashov published an article in the

journal Heredity entitled Classification ofHypotheses on the Advantage of Amphimixis, andfor amphimixis read sexual reproduction. Therewere so many competing ideas that he had toclassify them into groups to try to keep bettertrack of them, and he --

Q. This was written in 1993?

A. Yes, in 1993, about ten years ago. Let mejust read the first sentence here, "After morethan a century of debate, the major factors ofthe evolution of reproduction are stillobscure."

Q. If I could direct your attention again toyour exhibit book, Tab Number 9, and it's listedas Defendant's 270, is that the article you'rereferring to?

A. Yes, that's the one. And if I couldcontinue the quote after the bolded text, hecontinues, "During the past 25 years, hypotheseshave become so numerous and diverse that theirclassification is a necessity. The time isprobably right for this. No fundamentally newhypothesis has appeared in the last five years,and I would be surprised and delighted if someimportant idea remain unpublished." So he wasexpressing his view that an exhaustive look hadbeen done and that we have not yet come up withan answer.

Q. Do you have additional slides and articlesto demonstrate this point?

A. Yes, that's right. This was in 1993. Inthe year 1998 Science, the journal Scienceissued a special issue which focused on theevolution of sex, and in that the leadoffarticle of a number of articles in that issuewas the one entitled Why Sex? Putting Theory tothe Test. Now, notice the word theory is notbeing used in the sense that the NationalAcademy gives to it.And if you look at this little abstractwhich is, or this little blurb up on theleft-hand corner I think on the next slidethat's enlarged, it stated that, "After decadesof theorizing about the evolutionary advantagesof sex, biologists are at last beginning to testtheir ideas in the real world." So let notice acouple of things about that.Again they're using theory, theorizing, ina sense like brainstorming. Furthermore, theysay that this brainstorming, this theorizinggoes on ahead of the activity of testing it.

And furthermore that the testing can be put offdecades from when the theorizing takes place.

Q. If I could direct your attention again tothe exhibit book under Tab 10 and there's anexhibit listed, Defendant's Exhibit Number 269,is that a copy, it looks like an on-line versioncopy of the article that you're referring to?

A. Yes, that's right.

Q. I believe you have another slide you'd liketo cite?

A. Yes. There's an excerpt from this articlewhich is on the next I think -- oh, yes, I'msorry. Yes, this is kind of a repeat of onethat I've done already, "Biologists have come upwith a profusion of theories since first posingthese questions a century ago." So clearly thisis an idea that has stumped science for a verylong time. Another excerpt from the article isshown on the next slide. The author writes,"How sex began and why it thrived remains amystery. Why did sex overtake asexualreproduction?" I'm going to skip down here,and the author continues, "Sex is a paradox inpart because if nature puts a premium on geneticfidelity, asexual reproduction should come outahead. All this shuffling is more likely tobreak up combinations of good genes than tocreate them. Yet nature keeps reshuffling thedeck."

Q. And if I could just so the record is clear,those last two quotes that you read from werefrom which articles?

A. They were from the article Why Sex? PuttingTheory to the Test by Bernice Wuethrich.

Q. Again do you have another slide to makethis point?

A. Yes, I do. This is a quotation of a mannamed George Williams. George Williams is aprominent evolutionary biology at the Stateuniversity of New York at Stonybrook, and hewrote a book in the mid 1970's entitled Sex andEvolution, and a part of that book was quoted ina book recently by Richard Dawkins of OxfordUniversity, and the quotation is this. "Thisbook," that is George Williams' book, "this bookis written from a conviction that the prevalenceof sexual reproduction in higher plants andanimals is inconsistent with currentevolutionary theory. There is a kind of crisis

at hand in evolutionary biology," and Dawkinscomments on this quotation on the next slide.Richard Dawkins, an evolutionary biologistat Oxford University, Dawkins says, this isDawkins speaking, "Maynard Smith and Hamilton,"which refers to two prominent evolutionarybiologists, "said similar things. It is toresolve this crisis that all three Darwinianheroes along with others of the risinggeneration, labored. I shall not attempt anaccount of their efforts, and certainly I haveno rival solution to offer myself."So the point is that this problem is stillunresolved, and yet this goes to the very heartof evolutionary theory, or a theory of evolutionthat expects that most species would reproduceasexually can be likened to a theory of gravitythat expects that most objects will fall up.And in either case a reasonable person mightwonder if the theory is missing some large pieceof the puzzle, and certainly I think as aneducator students should be apprised of factslike these.

Q. Sir, does Darwin's theory account for theorigins of life?

A. No, Darwin's theory does not even addressthe origin of life.

Q. Is this an unsolved scientific problem?

A. Yes, it certainly is. And it also poses,it poses a large problem for Darwin's theoryas well, and --

Q. What is that problem?

A. I think I have a little excerpt from myexpert report in which I dealt with thatquestion, and I said the following, "The problemthat the Origin of Life poses for Darwin'stheory is the following. If the beginning oflife required something extra, something inaddition to the unintelligent operation ofnatural processes that Darwin's theory invokes,then it would be fair for a curious inquirer towonder if those other processes ended with thebeginning of life, or if they continued tooperate throughout the history of life," andI'll stop there, close quote. So the point isthis. If we cannot explain the origin of lifeby unintelligent processes, and if intelligentprocesses were in fact involved with that, thenwe might wonder did they continue throughout thehistory of life, or did they stop at that point.

Q. Sir, do you have an additional slide tomake this point regarding the questions of theorigins of life is left unresolved?

A. Yes, I do. Just a couple. It's easy tofind scientists involved in a study of theorigin of life who are very willing to say thatwe have not a clue as to how life started, andhere's a convenient source, this was aninterview by PBS with a man named Andrew Knoll,who is an eminent professor of biology atHarvard who studies the early development oflife, and one of the topics they wanted to speakwith him over was, "Why it's so devilishlydifficult to figure out how life got started."And on the next slide they put the questionto Andrew Knoll, they say, "How does life form?"And Professor Knoll says, "The short answer iswe don't really know how life originated onthis planet." And skip a bit, "We remain insubstantial ignorance." Next slide, they askedanother question, the interviewer asked, "Willwe ever solve the problem of the origin oflife?"And Knoll says, "I don't know. I imaginemy grandchildren will still be sitting aroundsaying that it's a great mystery." So thathere's a person involved in studying the originof life who says quite frankly that we don'tknow what's going on and he doesn't have anyparticular expectation that our grandchildrenwill understand the origin of life.

Q. Sir, if I could direct your attention tothe exhibit book under Tab 12, Defendant'sExhibit Number 267, is that the interview thatyou've just been testifying to?

A. Yes, it is.

Q. I'd like to direct your attention to whatI have put up on the screen here is an excerptfrom a booklet entitled Science and Creationismwhich was put out by the National Academy ofSciences in 1999, and if you could please readthat quote?

A. Yes. The National Academy wrote, "Forthose who are studying the origin of life, thequestion is no longer whether life could haveoriginated by chemical processes involvingnonbiological components. The question insteadhas become which of many pathways might havebeen followed to produce the first cell," andI'll stop there, close quote.

Q. Do you have any problems with this

statement?

A. Yes. I find it very disturbing, becausein that statement you don't see any referenceto the results of workers in the field. Youdon't see any reference to the data of whatpeople have come up with. Instead, in thispublication they focus on the attitudes of thescientists involved, and while the attitudesmight be an interesting sociological phenomenon,they do not go to the question of whether wecan explain the origin of life.And furthermore, this booklet is writtenfor teachers and indirectly then for theirstudents, and by advising teachers or lettingteachers or by saying this to teachers, it seemsto me the National Academy is encouraging themto have their students think of this problem inthe same way that workers have been doing forthe past fifty years in the same way that hasproved fruitless for over half a century.

Q. Sir, is there a scientific controversyregarding intelligent design in evolution?

A. Yes, there is.

Q. And what leads you to that conclusion?

A. Well, in addition to, you know, thearticles and counterarticles and things thathave been mentioned earlier in the day, andbesides the conferences and symposia that I haveattended, there have also been a number ofpublished books and articles debating design,and a good example of that is shown on thescreen here, this is the cover of the bookentitled, excuse me, Debating Design: FromDarwin to DNA ,and it was edited by two people,William Dembski, who's a philosopher andmathematician and intelligent design proponent,and Michael Ruse, who's a professor of thephilosophy of science and a student of Darwinianthought, and in this number of academicscontributed chapters arguing not only aboutintelligent design and Darwinism, but alsocomplexity theory, self-organization, and otherviews as well.

Q. And I believe you testified previouslythat some of the experts that are testifyingon behalf of plaintiffs in this case have alsocontributed chapters to this particular book?

A. That's correct. Kenneth Miller has achapter in there. I think Robert Pennock hasa chapter in there as well.

Q. And I believe you also testified duringthe qualifications portions that you contributeda chapter to a book that was written by RobertPennock, scientists debating the question ofintelligent design?

A. That's correct, published by MIT Press.

Q. And there was also a similar book –

MR. ROTHSCHILD: Objection, Your Honor.I think it's mischaracterizing the title.MR. MUISE: Your Honor, I didn't say whatthe title was. It's what the --MR. ROTHSCHILD: I think he did say it,Your Honor.MR. MUISE: The nature of the book. I don'tbelieve I stated the title. If I stated thetitle --THE COURT: How did he mischaracterize it?MR. ROTHSCHILD: He called it scientistsdebating intelligent design, or something tothat effect. He used the word scientists. It'sactually Intelligent Design and Its Critics, ifit's the Pennock edited book.MR. MUISE: Okay. I don't see much adistinction with that, Your Honor, but --MR. ROTHSCHILD: It think it's a loadedquestion.THE COURT: Well, for the record you don'tdoubt, Mr. Muise, that's the correct title, ordo you? Let's just be clear.MR. ROTHSCHILD: Sorry, Intelligent Design,Creationism, and Its Critics, I am corrected.MR. MUISE: I believe that's the correcttitle, Your Honor. I'm just verifying.(Brief pause.)MR. MUISE: Let's go back to your --THE COURT: Just so we're --MR. MUISE: I do have it here, Your Honor,and I just want to make it clear what the titleis, and I believe Mr. Rothschild is accurate.THE COURT: All right. Then there's no needfor a ruling on it. You can just clarify it forthe record.BY MR. MUISE:

Q. The book by Robert T. Pennock was entitledIntelligent Design, Creationism and Its Critics:Philosophical, Theological and ScientificPerspectives, is that correct?

A. That's correct.

Q. And that book was published by the MITPress?

A. That's correct, yes.

Q. You contributed an article makingscientific arguments for intelligent designin that book?

A. That's correct, I did.

Q. I should clarify, you submitted a chapter,is that correct?

A. Yes that's, right.

Q. Were there other scientists who submittedchapters in that particular book?

A. Yes. There were several arguing againstmy ideas and several others arguing on otherpoints.

Q. Were these scientists making scientificarguments in that book?

A. Yes.

Q. Again similarly I believe there was a bookthat was edited by John Campbell and Steve Meyerentitle Darwinism: Design in Public Education,is that correct?

A. Yes, that's right.

Q. Published by Michigan State UniversityPress?

A. Yes, that's correct.

Q. And several scientists and otherscontributed articles for that particularbook, is that correct?

A. Yes, that's right.

Q. If I could direct your attention to theexhibit, Tab 13, marked as Defendant's Exhibit6.

A. Yes.

Q. Do you know what that, what is Defendant'sExhibit 266?

A. It is a publication in the journalTheoretical Biology by two authors, RichardThornhill and David Ussery entitled AClassification of Possible Roots of Darwinian

Evolution.

Q. And who are Thornhill and Ussery?

A. They are two scientists, David Ussery isat the Institute of Biotechnology and TechnicalUniversity of Denmark and, Technical Universityof Denmark, and Thornhill I'm not quite sure of.

Q. Is that an article that was published ina scientific journal?

A. Yes, the Journal of Theoretical Biology isindeed a scientific journal.

Q. What was that article about?

A. As its title implies, it was trying togroup, put into groups possible pathways thata Darwinian evolutionary pathway might take,and it was particularly concerned with theproblem of irreducible complexity.

Q. Did it particularly refer to irreduciblecomplexity?

A. Yes, it did. It refers to irreduciblecomplexity by name I'm certain, virtuallycertain, and it makes reference to my bookas well to illustrate the problem.

Q. So would it be fair to say based on thesearticles and books and symposia that you've beenattending that scientists are debating thisissue in scientific and academic circles?

A. Yes, that's what I would say.

MR. MUISE: Your Honor, I'm about to startinto another area. I know we've only been goingfor an hour, but I'm not sure how that'll workout.THE COURT: No, keep going.MR. MUISE: Okay.THE COURT: Because we've not been at itlong enough to take a break.BY MR. MUISE:

Q. Dr. Behe, I'd like to return to the conceptirreducible complexity, which you testified wasa term that you coined in Darwin's Black Box, isthat correct?

A. Yes, that's right.

Q. Now, you testified that the designarguments speaks of the purposeful arrangement

of parts. Are there any other aspects of thedesign argument?

A. Yes, and that's correct. There are otheraspects, and they're shown on the next slide.Just like Ernst Mayr showed that there wereseveral aspects to Darwinian theory, there areaspects to the intelligent design argument. Theintelligent design argument itself, the positiveargument for it is the purposeful arrangement ofparts, as I have described.However, in an inductive argument, ifsomebody else offers a counterexample to theinduction, then one has to address that to makethe inductive argument stand. So there's alsoa negative argument which says that despiteDarwinian claims that the inductive positiveargument is unrefuted, that is that Darwinismcannot account for the purposeful arrangementof parts.

Q. So that's your argument against theplausibility of a Darwinian explanation fordesign, is that correct?

A. Yes, that's right.

Q. Do you have several slides that furthermake this point?

A. Yes. Now, what would make Darwinianexplanations seem implausible? Well, CharlesDarwin himself wrote how his argument could berefuted. In his writings in his book On theOrigin of Species he wrote that, "If it could bedemonstrated that any complex organ existedwhich could not possibly have been formed bynumerous successive slight modifications, mytheory would absolutely break down," adding,"but I can find out no such case."In this passage Darwin was emphasizing thathis was a gradual theory. Natural selection hadto improve things slowly, in tiny steps overlong periods of time. If it seemed that thingswere improving rapidly, in big leaps, then itwould start to look suspiciously as if randommutation and natural selection were not thecause.

Q. Have other scientists acknowledged thatthis is an argument against Darwin's theory ofevolution?

A. Yes. In his book Finding Darwin's GodKenneth Miller has written that, "If Darwinismcannot explain the interlocking complexity ofbiochemistry, then it is doomed."

Q. I believe we have a quote from anotherprominent scientist?

A. Yes. Richard Dawkins in his recent bookThe Ancestor's Tail, from which I quotedrecently, wrote "That it is perfectly legitimateto propose the argument from irreduciblecomplexity, which is a phrase I use, as apossible explanation for the lack of somethingthat doesn't exist, as I did, for the absenceof wheeled mammals." Let me take a second toexplain Dawkins' reference.He's saying that this problem is a problemfor biology, but nonetheless he thinks thateverything in biology has a Darwinianexplanation. So that whatever we do see inbiology necessarily is not irreducibly complex,and I think in my opinion that's an example ofbegging the question. But he does recognize theconcept of irreducible complexity.

Q. Sir, I'd like at this point for you todefine irreducible complexity, and we have aslide here.

A. Yes, in my article from the journal Biologyand Philosophy, I defined it this way. "Byirreducibly complex, I mean a single systemwhich is necessarily composed of several wellmatched interacting parts that contribute to thebasic function, and where the removal of any oneof the parts causes the system to effectivelycease functioning."

Q. Now, you have up there "necessarily"in italics. Is there a reason for that?

A. Yes, the definition that I gave in Darwin'sBlack Box did not have those italicized wordsnecessarily, but after the books came out and anevolutionary biologists at the University ofRochester named Allen Orr pointed out that itmay be the case that if you had a system thatwas already functioning, already doing somefunction, it's possible for a part to comealong and just assist the system in performingits function, but after several changes perhapsit might change in such a way that the extrapart has now become necessary to the function ofthe system but that could have been approachedgradually.And I, in thinking about it I saw that hewas thinking of examples that I did not havein mind when I wrote the book. So I kind oftweaked the definition here in this article totry to make it clear and try to exclude those

examples that I didn't have in mind.

Q. Is it a common practice within the sciencecommunity for a scientist to adjust, modify, ortweak their theories based on criticisms thatthey get from other scientists?

A. Oh, sure. That's done all the time.Nobody is perfect, nobody can think ofeverything at once, and a person is alwaysgrateful for criticism and feedback that helpsto improve an idea.

Q. Does criticism undermine the idea thatyou were trying to convey by irreduciblecomplexity?

A. No, it didn't. It clarified it, and afterhis, after reading his SI I saw that he wasthinking of things that I did not have in mind.So I tried to clarify that.

Q. You have this system in underlyingcapitalized and in red. What's the purposefor that?

A. Well, that to me has turned into a pointof confusion because some people, includingProfessor Miller, have been focusing thediscussion on the parts of the system and sayingif one removes a part and then can use the partfor some other purpose, then they say that meansthat it's not irreducibly complex, but that isnot the definition I gave to irreduciblecomplexity, that is not the concept ofirreducible complexity that I described inDarwin's Black Box. I said that if you takeaway one of the parts from the system, thesystem, the function of the system itself ceasesto work, and whether one can use the part foranything else is beside the point.

Q. So then it is fair to say Dr. Miller's usesthe wrong definition of your concept and thenargues against that different definition toclaim that your concept is incorrect?

A. Yes. It's a mischaracterization, yes.

Q. Now, Dr. Padian testified on Friday thatthe concept of irreducible complexity appliesabove the molecular level, is that correct?

A. No, that is incorrect. In Darwin's BlackBox I was at pains to say that the concept ofirreducible complexity applies only to systemswhere we can enumerate the parts, where we can

see all the parts and how they work, and I saidthat in biology therefore that necessarily meanssystems smaller than a cell, systems whoseactive molecular components we can elucidate.When you go beyond a cell, then you'renecessarily talking about a system, an organor animal or any such thing, that is so complexwe don't really know what we're dealing with,and so it remains a black box, and so the termirreducible complexity is confined to molecularexamples.

Q. Well, I want to read to you severalsections, passages from Pandas that Dr. Padianreferred to as claiming that this is the conceptof irreducible complexity, and I'd like yourcomment on each one of those as I go through.The first one, "Multifunctional adaptationswhere a single structure or trait achieves twoor more functions at once is taken as evidenceby the proponents of intelligent design of theirtheory," and the reference is page 72 of Pandas.

A. Well, if -- I'm sorry, what is the questionthen?

Q. The question is, is that a definition oris that within your concept of irreduciblecomplexity?

A. No, that's not the way I define the term,and I'm not quite sure what he has in mind.

Q. And the second example is, "Proponentsof intelligent design maintain that only aconsummate engineer could anticipate soeffectively the total engineering requirementsof an organism like the giraffe." That's acitation from page 71. Is that a referenceto the concept of irreducible complexity?

A. No, it isn't. Again, irreduciblecomplexity focuses on the cell and systemssmaller, because we have to elucidate all theparts, and you have to keep in mind that theparts of a biological system are molecularparts, even though most people commonly thinkof large organisms. Let me just say that, youknow, that you should keep in mind thatDarwinism has other problems beyond irreduciblecomplexity. So Pandas might have been pointingto those.

Q. Two more such examples. The third one, twomore of out of four, this is the third out offour, "But it has not been demonstrated thatmutations are able to produce the highly

coordinated parts of novel structures neededagain and again by macroevolution." And again,is that referring to the concept of irreduciblecomplexity?

A. Well, again unless he's referring to themolecular level, then no, that is not correct.It turned out that molecular changes, smallchanges in DNA can actually cause large changesin an organ. You might lose the finger or get aduplicate of a finger or some such thing, so youhave to apply the concept of irreduciblecomplexity to the molecular revel.

Q. And the last example, "Design theorysuggest that various forms of life beganwith their distinctive features already intact,fish with fins and scales, birds with feathers,beaks, and wings," that's a reference to page 25of Pandas. Is that a reference to the conceptof irreducible complexity?

A. No, it is not. Again one more time, theconcept of irreducible complexity applies tothe molecular level simply because in biologythe molecular level is where changes are takingplace. There are active components. That'swhere the rubber meets the road in biology.So one has to restrict one's self to that level.

Q. Is that the level where we can identify thecomponents of the systems?

A. Yes, that's the critical thing. We haveto see how things are working so we can realizewhat's going on and decide whether or not anexplanation is plausible.

Q. So it would be fair to say those fourexamples I read to you may illustrate orhighlight other difficulties with Darwin'stheory, but they're not specifically addressedin the concept of irreducible complexity?

A. Yes, that's right. Just becauseirreducible complexity is a problem, thatdoesn't mean that it's the only problem.

Q. Now, again can you give us an example of anirreducibly complex biochemical system?

A. Yes, an excellent example is again thebacterial flagellum, which uses a large numberof parts in order to function, and again if youremove the components, if you remove thepropeller, if you remove the hook region, ifyou remove the drive shaft or any multiple parts

of the flagellum, it does not work. It's ceasesto function as a propulsive device.

Q. Now, Professor Miller has testified thatthe flagellum is not irreducibly complex. Doyou agree with him?

A. No, I don't.

Q. I'd like for you to go through and explainyour objections to his claim.

A. Okay. This is a slide from ProfessorMiller's presentation on the flagellum.Let me just first read through the slidecompletely and then I want to point to severalmischaracterizations that are contained on theslide. He writes, "The observation that thereare as yet no detailed evolutionary explanationsfor certain structures in the cell, whilecorrect, is not a strong argument for specialcreation, 'design.' As Michael Behe has madeclear, the biochemical argument from designdepends upon a much bolder claim, namely thatthe evolution of complex biochemical structurescannot be explained even in principle."This has three mischaracterizations I'dlike to point out in turn. The first one iswhat many people considered to be an informallogical fallacy, and that is called poisoningthe well. It is given the reader a, leading thereader to suspect the other person's argument.It's kind of a version of an ad hominemargument. When he uses the term specialcreation and quotation in design, that looks tome like he's indicating to the reader that thepeople who make these arguments are trying tomislead you into thinking that this is design,but it's really special creation.What's more, again the word creation hasvery negative overtones and is used as apejorative in many academic and scientificcircles. Furthermore, the phrase specialcreation occurs nowhere in Darwin's Black Box.I never used the phrase special creation inany of my writings except perhaps to say thatintelligent design does not require this. Andso again I think it is a mischaracterizationand it appears to me an attempt to kind ofprejudice the reader against this, against myargument.The second point is this. The secondmischaracterization is this. He says, "Theobservation that there are as yet no detailedevolutionary explanations for certain structuresin the cell, while correct, is not a strongargument for special creation that is 'design.'"

Here Professor Miller is doing something moreunderstandable. He's essentially is viewing mytheory through the lens of his own theory. Soall he sees is essentially how it conflicts withhis own theory and thinks that that's all thereis to it.But as I have explained throughout the daytoday, if we could go to the next slide, thatan inability to explain something is not theargument for design. The argument for design iswhen we perceive the purposeful arrangement ofparts, the purposeful arrangement of parts suchas we see in the flagellum, such as we see themolecular machinery such as described in thatspecial issue of Cell and so on.We can go to the next slide, this is a copyof the first slide of Professor Miller's, thethird mischaracterization is this. He says, "AsMichael Behe has made clear, the biochemicalargument from design depends upon a much bolderclaim, namely that the evolution of complexbiochemical structures cannot be explained evenin principle." This is a mischaracterization.It's essentially absolutizing my argument.It's making overstating my argument in order tomake it seem brittle, to make it more easilyargued against.

Q. Have you addressed such a claim in Darwin'SBlack Box?

A. Yes, if you read Darwin's Black Box yousee that I say the following, "Even if a systemis irreducibly complex and could not have beenproduced directly, however one cannot definitelyrule out the possibility of an indirectcircuitous route. As the complexity of aninteracting system increases though, thelikelihood of such an indirect route dropsprecipitously."So here I was arguing well, there's a bigproblem for Darwinian theory. These thingscan't be produced directly, but nonethelessyou can't rule out an indirect route, butnonetheless building a structure by changingits mechanism and changing its componentsmultiple times is very implausible and thelikelihood of such a thing, the more complexit gets, the less likely it appears. So thepoint is that I was careful in my book toqualify my argument at numerous points, andProfessor Miller ignores those qualifications.

Q. Do these qualification also demonstratethe tentative nature in which you hold yourtheories?

A. Yes, that's right. I always -- well, I tryto state it in what I thought was a reasonableway and in a tentative way as well.

Q. I believe we have a couple of more slidesfrom Dr. Miller that you --

A. Yes, this is essentially a continuation.These will be slides number 2 and 3 from hisslides on the flagellum. This is just acontinuation of his overstated arguments.He says, "The reason that Darwinian evolutioncan't do this is because the flagellum isirreducibly complex," and he quotes mydefinition of irreducible complexity fromDarwin's Black Box, and continue on the nextslide.And he states that, "That claim is thebasis of the biochemical argument for design."But again that is not the basis for thebiochemical argument for design. The basisfor the biochemical argument for design is thepurposeful arrangement of parts. Irreduciblecomplexity shows the difficulties for Darwinianprocesses in trying to explain these things.

Q. Now, Dr. Miller claims that naturalselection can explain the flagellum. Doyou agree with that claim?

A. I'm sorry, can you restate that?

Q. Dr. Miller claims that natural selectioncan explain the bacterial flagellum. Do youagree with that claim?

A. No, I disagree, and we go on to the nextslide, which is another one of ProfessorMiller's slides from his presentation on thebacterial flagellum, and he tried to explainmolecular machines using kind of simple conceptsto try and make it more understandable to abroad audience. So for example on theright-hand side which he labels "Evolution,"he has little colored hexagons, which are exist,which are separated, and then he has thehexagons forming little groups and arrowspointing between the hexagons and the groups ofhexagons, and finally there is kind of a largeaggregation of hexagons.On this, which he labels "Design," hehas the colored hexagons separate and arrowspointing to a larger aggregation of hexagons.Now, I'm sure Professor Miller was trying toget across a concept which is difficult, but inmy viewing and my understanding and presentingit this way, this overlooks enormous problems

that actual molecules would encounter in thecell.

Q. Have you addressed these claims in otherwritings that you have done?

A. Yes. Professor Miller has presentedexactly the same argument in several othersettings, and I have addressed it severaltimes, most recently in my chapter in DebatingDesign, and if you go to the next slide --

Q. Is this a figure from that book, DebatingDesign?

A. Yes, this is Figure 2 from that chapter.And the slide is entitled "An irreduciblycomplex molecular machine, can it arise fromindividual functional precursors." I used littlecolored squares instead of hexagons, butnonetheless the concept is kind of the same.The colored squares are supposed to representindividual proteins which perhaps existed inthe cell already, there is six different ones,and the complex molecular machine now issupposed to be an aggregate of all six proteinswith a new function that the system has that theindividual parts did not have. Unfortunatelywhile this illustrates, you know, something, itleaves out many concepts which are critical toevaluating the likelihood of such a thing. MayI continue?

Q. Yes, go ahead.

A. For example, proteins, the components ofmolecular machines are not little coloredsquares. They are not little colored hexagons.They are very complex entities which we will seein a second. Additionally, notice this redsquare. The red square with the little arrowplaces it against the green square and theyellow and the blue. Why is it there? Whydidn't it go down there? Why is it sticking toB and C and D? Why doesn't it float away?None of those questions are answered, thisis an oversimplified way to look at a verycomplex problem. For example, let me just makeone more comment. Notice that in machines inour common experience, if you put a part in aplace different from where it usually is, thatoften times breaks the machine. If in anoutboard motor you took the propeller and youput it on top instead of down by the rotor, thenthe machine would not function. And it's theexact same way for molecular machines.

Q. Have you prepared some slides todemonstrate some of the more complexityof these parts?

A. Yes, I'm afraid we're going to have togo a little bit into the complexity of thesemolecular systems.

THE COURT: Do you want to break here,Mr. Muise?MR. MUISE: That would be wonderful, YourHonor.THE COURT: Why don't we do that, let's takea 20-minute break here, and we'll return andwe'll pick up with those slides at the end ofthe recess. We'll be in recess.(Recess taken at 2:48 p.m. Proceedingsresumed at 3:13 p.m.)THE COURT: Be seated, please. You can pickit up where you left off, Mr. Muise.CONTINUED DIRECT BY MR. MUISE:

Q. Thank you, Your Honor. Dr. Behe, before webroke we were talking about how proteins aren'tsimply colored squares or hexagons, that theyare far more complex than that, including whatmakes them stick together in any particularorder, and I want to return back to that. Weput up a slide which has some indication Ibelieve of proteins, and I'd like you to explainwhat you meant, that they're more complex thanjust these colored hexagons.

A. Yes, sure. Let me preface my explanationby saying this, that in talking about thesematters there's kind of, an intelligent designproponent and a Darwinian theorist who havedifferent goals. A Darwinian wants to persuadehis audience that evolution isn't all thatdifficult, it's doable, and so will not alwaysattend to all the complexity of a system,whereas in order to show the difficultiesfor undirected unintelligent processes, anintelligent design proponent has to show allof the very severe complexity of systems, andthat's often times hard to do because peopleoften times don't have the patience to attendto it, but I apologize in advance but I have toattend to some of the complexities here.So on this slide there are three figurestaken from a biochemistry textbook by Voet andVoet of the protein, of the same protein, aprotein named hemoglobin. Hemoglobin is theprotein that binds oxygen and carries it fromyour lungs and dumps it off in peripheraltissues such as your fingers and so on. Now,this is a rendering of the structure of

hemoglobin, and actually this rendering itselfdoes not show the full complexity of hemoglobin.Let's focus --

Q. You're referring to Figure 8-63 on thisslide?

A. Yes, that's correct. Let's focus on thisyellow glob here. You'll notice a number ofcircles. They represent atoms in one of whatare called the protein chains of hemoglobin,but the amino acids in that protein chain areactually different. So if it was actuallyrendered in more detail you would see a lot ofdifferent colors of atoms, indicating differentgroups and so on, and the identity of all theseamino acids is also frequently very critical tothe function of a protein.Hemoglobin itself consists an aggregate offour proteins designated here by the blue andthe green and the light blue colors, and it isthe aggregate of the four protein chains, thatis the active molecular machine in this cellthat carries oxygen from your lungs to yourtissues. Nonetheless, a drawing like this ofsuch a complex system is often times bewilderingto students, and so artists with the properpurpose of getting across some conceptual pointsto students will draw simplified renditions ofthe same figure.For example, in the lower left here thisis also supposed to be a rendition of the sameprotein hemoglobin. But in here the only atomsthat are represented are things called the alphacarbons of each amino acid, and the artist haskind of shaded it to show the differentdirections in which the protein chain isheading. One can also to make a legitimatepoint to students simplify the drawing evenfurther, and here's another rendering ofhemoglobin in Voet and Voet.Here each very, very complex protein chainis rendered as a simple square, and the O sub 2represents the oxygen that each protein issupposed to be carrying. Now, all of theseare legitimate renderings of the proteinhemoglobin, but when we discuss these mattersand we discuss difficulties with evolution andwe discuss arguments for intelligent design, wehave to keep in mind that this is the actualprotein, this is the actual machine in the cell,and so these are the things that we have to dealwith.

Q. Again that last figure you're referring tois 8-63?

A. That's right, uh-huh.

Q. And the two previous, the one just previousto that was Figure 10-37 and the one prior tothat 10-13?

A. That's correct. Now, let's considera further point. We have this yellowconglomeration of circles representing theatoms of the protein chain, with this blue oneand this green one and this light blue one. Whydo they stick together? Why don't they justfloat away? How come they are in thearrangement they are? Why don't we have theyellow one over here? The green one down here?Well, it turns out that proteins arrangethemselves. Molecular machines are actuallymuch more sophisticated than the machines ofour common experience, because in our commonexperience with things like say outboard motors,an intelligent agent assembles the parts ofthose machines. But in the cell the molecularmachines have to assemble themselves. How dothey do that? They do it by having surfaceswhich are both geometrically and chemicallycomplementary to the proteins to which they'resupposed to bind, and I think --

Q. Do you have a slide to demonstrate thatfor us?

A. Yes, I do. I think it's the next one.Okay, remember here's another little cartoonversion which gets rid of some complexity ofthe system in order to make an important pointto students. This is also a figure taken fromthe biochemistry textbook Voet and Voet. Thisis meant to convey why two molecules, why twoproteins bind to each other specifically in thecell. This one up here is supposed to representone protein. The second one is supposed to bethis greenish area, and it's supposed to have adepression in it in which the yellowish proteinbinds to and sticks.Now, let me point out a couple of things.You'll notice that the shapes of the proteinsare matched to each other. They'regeometrically complementary, kind of like ahand in a glove. But not only are theygeometrically complementary, they're alsochemically complementary. You see these littlecircles and NH and this thing here? Well, theseare chemical groups on the surface of the twobinding proteins, and they attract each other.Certain groups attach other groups.I think the easiest to understand is theone right here, there's a red circle marked with

a minus sign in it. That indicates an aminoside chain of a protein that has a negativecharge. When it binds to the larger one, noticethat on the surface of the larger proteinthere's this blue circle with a plus sign in it.That is taken, that is meant to indicate anamino acid side chain with a positive charge.Negative and positive charges attract. Sotherefore these guys stick together.If this were a negative charge these twoproteins would not stick together. They wouldfloat away from each other. It's not sufficientto have just one group in the protein becomplementary to another group in a protein.Usually proteins have multiple amino acids thatstick together and cause them to bind to eachother. For example, look up here, this littlecircle labeled H. H is supposed to stand forsomething called hydrophobic, which essentiallymeans oily. It doesn't like to be in contactwith water.It lines up with another H on the greenprotein so that the two oily groups can sticktogether and avoid water. So it's kind of likeoil, you know, oil and water, they don't mix.If they're in this configuration the two oilygroups can stick together and be away fromwater, and there are other groups, too, whichI won't go into which exhibit things callhydrogen bonding which also help the proteinsstick together.So in molecular machines, in aggregatesof proteins, all of the proteins which aresticking together have to have all thesecomplementary surfaces in order for them tobind their correct partners. If they do nothave the complementary surface, they don't bindand the molecular machine does not form. Now,interestingly, remember Darwin's theory saysthat evolution has to proceed in small steps,tiny steps.Well, one way something like this mightform is by, you have to have mutations thatmight produce each of these interactions at atime. For example, I think there's a quotationfrom an article in Nature which kind of makethis point, and I'll explain it after I quoteit, it's from an article by a man named JohnMaynard Smith, who is a very prominentevolutionary biologist who died about a yearago I believe, and he wrote in a paper calledNatural Selection and the Concept of a ProteinSpace, which was published in Nature in 1970,"It follows that if evolution by naturalselection is to occur, functional proteins mustform a continuous network which can be traversedby unit mutational steps without passing through

nonfunctional intermediates," and by unitmutational steps, we mean each of those pluses,each of those H's, each of those OH's and so onthat I showed you in that little cartoon drawingon the previous slide.If for example a mutation came along thatchanged a positive into a negative charge anddisallowed an interaction that needed to occur,that would be a detrimental one. John MaynardSmith is saying that we need to proceed, youknow, one step at a time. So the point is thatthose little colored squares are enormouslycomplex in themselves, and further the abilityto get them to bind specifically to theircorrect partners also requires much moreadditional information. It is not a single stepphenomenon. You have to have the surfaces oftwo proteins to match.

Q. A difficulty of getting two changesat once?

A. Yes, that's exactly right. If you cando this one tiny, tiny step at a time, thenDarwinian evolution can work. If you need tomake several changes at once, two, three, four,there were multiple interactions that wererequired for those two proteins to bind. Ifyou need multiple interactions, the plausibilityof Darwinian evolution rapidly, rapidlydiminishes.

Q. And have other scientists made similarobservations?

A. Yes. On the next slide an evolutionarybiologist by the name of Allen Orr, who's at theUniversity of Rochester, published an article ina journal called Biology entitled A Minimum onthe Number of Steps Taken in Adaptive Walks inwhich he makes this similar point. He says,"Given realistically low mutation rates, doublemutants will be so rare that adaptation isessentially constrained to surveying andsubstituting one mutational step neighbors.Thus, if a double mutant sequence is favorable,but all single amino acid mutants aredeleterious, adaptation will generally notproceed," and translating that into morecolloquial English it means that you have tochange again those groups one at a time, andif you need to change two at a time in order toget a favorable interaction, then you arerunning into a big roadblock for Darwinianprocesses.

Q. Now, have you done any writing or research

that emphasizes this particular point?

A. Yes. On the next slide I believe is a copyof an article that I published with David Smokewhich was published last year in the journalProtein Science, which is entitled SimulatingEvolution by Gene Duplication of ProteinFeatures that Require Multiple Amino AcidResidues, and in this paper we were addressingexactly that problem. What happens if you needto change a couple of amino acids before you geta selective effect?And the gist of the conclusion is if youneed to change two at once or three at once,then again the expectation that that will happenat a probability becomes much smaller, thelength of time one would have to wait for sucha mutation to show up is much longer, thepopulation size of a species would have to bemuch, much longer to have an expectation of sucha mutation occurring.

Q. And this particular article, the oneyou wrote with David Smoke, you testified topreviously?

A. Yes, that's the same one.

Q. I believe we have a diagram to further makethis point?

A. Yes. Here again is a little simplifiedcartoon version of how proteins might interact,simply to point out the problem that is notapparent in the earlier drawings. Now I've madethe shapes of those colored proteins, I'vealtered the shapes. Now the A is a circle andwhat's that, a C, the C is a rectangle, and theother proteins have other shapes. How do we getthose to bind into a conglomerate molecularmachine?In order to get them to bind to each otherwe have to alter their surfaces to begeometrically and chemically complementary, andthat is a large and long, tall evolutionaryorder. As a matter of fact, it's so tall thatone can reasonably conclude that something likethis would not be expected to occur. So thepoint I want to make here is that even if onewas to have parts in the cell which if theycould develop binding sites to bind to eachother, and if that binding together wouldproduce a new selectable property, that stilldoes not help in Darwinian processes, becauseyou still have the problem of adjusting many,many different things before you get the finalresult.

Q. And this diagram is a figure from thechapter that you wrote in Debating Design,is that correct?

A. Yes. That's Figure 2.

Q. And that's the chapter that you've alreadytestified to previously?

A. Yes, that's correct.

Q. And I believe we have a slide with thefigure legend?

A. Yes, that's right. I make this pointexactly in my article in that book DebatingDesign. Let's just look at the bold andunderlined text. It's says, "Thus, the problemof irreducibility remains even if the separateparts originally had individual functions."So even if the parts can do something on theirown, that does not explain how one can get amultipart molecular machine in a cell.

Q. I just want to point out that that figurelegend in the figure is from pages 352 to 370in your chapter?

A. No, that's the whole chapter. The figurelegend is on one of those pages.

Q. As well as that previous diagram?

A. Yes, that's correct.

Q. Dr. Behe, if I understand you correctly, soeven if there are similar separate parts are inthe cell, that doesn't explain irreduciblecomplexity?

A. That's correct.

Q. Dr. Miller testified about somethingcalled the Type 3 secretory system, the TTSS,and he said that that showed that the flagellumwas not irreducibly complex, do you agreewith that assessment?

A. No, I disagree. That's amischaracterization.

Q. Why do you disagree?

A. Well, I think we have some slides fromProfessor Miller's presentation, and he saidthat, let us start with the bacteria flagellum,

and he has a drawing of the flagellum from arecent paper. Let me just make another similarpoint. You see these little three, four-letterabbreviations all over here? Each one of thoseis of the complexity of a hemoglobin moleculethat I showed on an earlier slide. Each one ofthose has all the sophistication, all the needsto have very complex features to bind togetherthat hemoglobin had.Can you press the slide again to advancethe figure on this same thing of ProfessorMiller's? Professor Miller says that well,okay, you start with the bacterial flagellum,and if you remove the pieces, then he says,press again, please, he says, "That leaves justten," and he says, his characterization, hismischaracterization of my argument is thatwhat's left behind should be non-functional.And if we go to the next slide of ProfessorMiller's, he says, "But it's not. Those tenparts are fully functional as a proteinsecretion system," but again I tried to be verycareful in my book to say that we are focusingon the function of the system, of the bacterialflagellum, and while a subset of the flagellummight be able to be used as something else, ifyou take away those parts it does not act as arotary motor. So it is irreducibly complex as Itried to carefully explain. I'm sorry.

Q. So is it fair to say that Dr. Miller makesa misrepresentation of what your claim is by hisrepresentation?

A. This is a mischaracterization, yes, that'scorrect, and I think I pointed that out on thenext slide. I pointed this out, as I saidearlier we've debated this back and forth fora while. I pointed it out recently in my bookchapter. I write, "Miller asserted that theflagellum is not irreducibly complex becausesome proteins of the flagellum could be missing,and the remainder could still transport proteinsperhaps independently."Again he was equivocating, switching thefocus from the function of the system to act asa rotary propulsion machine to the ability of asubset of the system to transport proteinsacross a membrane. However, taking away theparts of flagellum certainly destroys theability of the system to act as a rotarypropulsion machine as I have argued. "Thus,contra Miller, the flagellum is indeedirreducibly complex."

Q. Dr. Behe, even if that is true, doesn't theType 3 secretory system help us to explain the

flagellum, the development of the flagellum?

A. No, it does not help in the least. Andthat may be surprising to some people, so letme take a second to explain. Most people whenthey see an argument such as Professor Millerpresents will naturally assume that well,perhaps this part, this system that had fewerparts, the Type 3 secretory system, maybe thatwas a stepping stone, maybe that was anintermediate on the way to the more complexbacterial flagellum.But in fact a number of scientists havesaid that's not true, and perhaps we could seethe next slide. Yes, thank you. For example,in a paper published by Nguyen, et al. fiveyears ago they investigated the Type 3 proteinsecretion system, and they said the following,"We suggest that the flagellar apparatus was theevolutionary precursor of Type 3 proteinsecretion systems."In other words, they're saying that fromtheir investigation it looked like the morecomplex type or more complex flagellum camefirst, and then the system with fewer parts,the Type 3 secretory system came second andperhaps was derived from that. Exactly whatthe opposite of what one might first expect.

Q. Have scientists reached differentconclusions?

A. Yes, and it turns out that other groupshave reached different conclusions from thoseof Nguyen at all. For example, in a paperpublished by Gophna, et al. recently in 2003 inthe journal Gene they write, "The fact thatseveral of the Type 3 secretory system proteinsare closely related to flagellar export proteinhas led to the suggestion that the TTSS hasevolved from flagella. Here we reconstruct theevolutionary history of four conserved Type 3secretion proteins and their phylogeneticrelationships with flagellar paralog." Andthen they say, "The suggestion that Type 3secretory system genes have evolved from genesand coding flagellar proteins is effectivelyrefuted." In other words. They say thatthe conclusion of the first group was incorrect.Instead they suggest that the Type 3 secretorysystem and the flagellum developed independentlyof each other, perhaps from the same precursorgene. And I think on the --

Q. We have another study on this issue,correct?

A. Yes. I think that's right. In the year04 a man named Milton Sayer, who was the oneof the authors, the senior author actually onthe study by Nguyen, et al. that I referred to acouple of slides ago, wrote an article in ajournal called Transient Microbiology calledEvolution of Bacterial Type 3 Protein SecretionSystems, he says the following, "It is oftennot possible to prove directionality of anevolutionary process. At present, too littleinformation is available to distinguish betweenthese possibilities with certainty. As is oftentrue in evaluating evolutionary arguments, theinvestigator must rely on logical deduction andintuition."According to my own intuition and thearguments discussed above, I prefer pathwayfor the Type 3 system deriving from theflagellum. What's your opinion?" So I thinkyou can see from this the very tentative natureof the results regarding the Type 3 secretorysystem and the flagellum that in fact what isgoing on is very much up in the air.

Q. And again I believe we have another resultfrom --

A. Yes. Let me apologize that again this is acomplex subject, and so you really have to delveinto it to come to a firm conclusion. This is aquotation from a review article by a man namedRobert Macnab who was a professor of biology atYale University who died in the year 2003, andthis article was actually publishedposthumously. It's entitled Type 3 FlagellarProtein Export and Flagellar Assembly. It waspublished in journal Biochemica Biophysica Acta,and I underlined words that emphasized thetentativeness and the speculative nature ofdiscussions on this topic.Robert Macnab wrote, "It has been suggestedthat the Type 3 virulence factor secretionsystem evolved from the Type 3 flagellar proteinexport system since flagella are far moreancient, existing in very diverse genre thanthe organisms which are targets for Type 3virulence systems. However, it is possible thatthe original targets were other bacteria. Also,the possibility of lateral gene transfer cannotbe ruled out."Finally, one could argue that evolutionfrom a less complex structure, the needlecomplex, to a more complex one, the flagellum,is more probable than the other way around,"and he continues I think on the next slide, andI think I'll pass over much of this quotationand just go to the last line of his article, and

he says, "As the above discussion indicates,there is much about the evolution of Type 3systems that remains mysterious."So let me point out that in the past coupleof years we've had investigators suggest that infact the flagellum came first and the Type 3secretory system came after it. We've had otherinvestigators suggest that the Type 3 secretorysystem came first and the flagellum came afterit. We've had other investigators suggest thatthe Type 3 secretory system and the flagellumarose independently, perhaps from similar genes,so --

Q. Dr. Behe, so what do these widely differentopinions mean?

A. Well, maybe we could go to the next slide.To me it means this. We see the little cartoondrawing of the flagellum here, and this is acartoon drawing of the Type 3 secretory system.

Q. I'm sorry, this is one of Dr. Miller'sslides?

A. I'm sorry, yes. This is Dr. Miller'sslide. Science knows a lot of informationabout the structure of the Type 3 secretorysystem, a lot of information about the structureand function of the flagellum. It knows thesequences of proteins of the flagellum. Itknows the sequences of the proteins of the Typesecretory system. It sees many similaritiesbetween them, both in the amino acid sequenceand function, and it still can't tell how onearose or whether one arose first, the othersecond, or whether they arose independently.So this to me drives home the point thatsuch information simply does not come out ofDarwinian theory. Much like our discussion ofHaeckel's embryos earlier in the day, Darwiniantheory can live with any result thatexperimental science comes up with on thisquestion and then goes back and tries torationalize the results afterwards post hoc,and so to a person like myself this exemplifiesthe fact in fact these results have nothing todo with Darwinian theory. They are no supportat all for the claim that natural selectioncould have produced them. Quite the contrary.

Q. I just need to backtrack for one moment.If I may approach the witness, Your Honor?

THE COURT: You may.

Q. Dr. Behe, I handed you what's been marked

as Defendant's Exhibit, 238 correct?

A. Yes.

Q. Is that the study from Nguyen that youreferenced in your testimony on the sectionof the Type 3 secretory systems?

A. Yes, that's correct.

Q. It was inadvertently left out of your book,but I just wanted to make sure you identified itas an exhibit. You can just keep that with youand I'll retrieve it later.

A. Thank you.

Q. I want to see if I can get you correct,Dr. Behe. It's your opinion that this alsoshows that even knowledge of the structure andsequences of two systems doesn't necessarilygive a clue as to how these systems might havearisen, is that true?

A. That's exactly right.

Q. And could you explain that further? AndI believe we have some additional slides forthat.

A. Yes, I think some text with actuallyProfessor Padian wrote as part of his expertreport illustrates this problem, and I'd liketo quote you several sections from that report.On the next slide Professor Padian said thefollowing. He said that, "Darwin's mainconcern, however, was with the mechanism ofnatural selection, which cannot be observeddirectly in the fossil record."So to me this means you cannot see naturalselection. You see fossils, and how youclassify those fossils and what explanationsyou come up with them is not based directly onthe evidence. Rather, it's provided by yourtheory. And I think we have a further quotefrom Professor Padian. He said the following,and this is a long quote, so --

Q. If you could read it a little bit slowerfor our court reporter when you are readingthese quotes, please? Thank you.

A. Okay. "Molecular biology has producedtremendously powerful tools to compare the DNAsequence of all manner of living organisms, anda few extinct ones, and so help to derive theirevolutionary relationships. However, molecular

systematics can say nothing about therelationship or role of fossil organisms toeach other or to living lineages," and he givesan example."For example, several recent molecularanalyses agree that whales and hippos are eachother's closest relatives. From this conclusionsome authors have suggested that because bothkinds of animals spend time in the water, theircommon ancestors would have been aquatic. Onlythe fossil record could show that this inferenceis incorrect. Therefore, hippos and whales,even if they are each other's closest relativesamong living animals, did not have a commonancestor that lived in the water, but that wasterrestrial. Only paleontological research andmaterials could demonstrate this."And let me make a point about this.Professor Padian is saying that molecularstudies of DNA sequence of whales and hippossuggested or led to the suggestion that bothanimals had aquatic ancestors. But they didn't.They had terrestrial ancestors. That means thatthe molecular information is compatible witheither result, with the ancestors being aquaticor the ancestors being terrestrial.That means that the molecular informationcan't decide what the ancestors were andtherefore it can't tell what the selectivepressure was or other factors of what mighthave caused an ancestor of those organisms toproduce what we see in the modern world. Sothat means that does not speak to Darwin's claimthat natural selection drove evolution, okay?Well, molecular data can't decide the question.But nonetheless, Professor Padian told usthat paleontology did. Paleontology discoveredwhat seemed to be ancestor of both hippos andwhales, and saw that they are terrestrialorganisms. So can paleontology tell us whetherit was natural selection that drove theevolution of these organisms? Well, no. Onthe previous slide he said explicitly naturalselection is not shown directly in the fossilrecord.That means that there is nothing that canshow from the fossil record or from moleculardata that current organisms derive by a processof natural selection from organisms in the pastor how such a thing might have happened. Thatmeans that in fact the inference that such athing did is simply a theoretical construct inwhich we try to fit that data into our currenttheory. The current theory either predicts it,does not predict it, and may be consistent withsuch evidence, but a lot of theories might beconsistent with the same evidence.

And I think that, bring it back to theflagellum, I think that's illustrated in theflagellum and Type 3 secretory system 2. Weknow all the molecular data, we know lots ofstructural and functional studies, and yet westill can't tell how natural selection couldhave produced them.

Q. So are you saying then at best theevidence, and you were talking about sequencecomparisons and in particular the fossil record,at best they may be consistent with naturalselection but they also may be consistent withany number of mechanisms that might be derived?

A. That's exactly right. Perhaps intelligentdesign, perhaps complexity theory, perhapssomething else. But consistent does not, isnot the same thing as evidence for a theory.

Q. And the next slide we have is another quotefrom Dr. Padian that I'd like you to commentabout.

A. I think this also throws light on thistopic. Professor Padian said in his expertstatement, he said, "Darwin was not talkingabout how major new adaptive change took place.He was talking about how minor variations couldbe selected. He was really talking about thebaby steps of evolution. He made only the mostpassing references to how new major adaptivetypes might emerge," and I could comment thatno one disputes or certainly no one I'm aware ofdisputes that Darwinian processes, Darwinianmechanism, can explain some things in life. Andcertainly nobody disputes that baby steps couldbe explained by random mutation and naturalselection. It is exactly the new major adaptivetypes and new molecular systems for myself as abiochemist that is the focus of dispute.

Q. So again though when you say nobodyrefutes, is that saying that intelligent designdoes not refute this notion of baby steps thatDr. Padian is referring to?

A. That's right. It is very happy to say thatDarwinian processes are consistent with those.

Q. Here I believe is a continuation of thatparticular statement from his report.

A. Yes, this is Professor Padian continued,referring to Darwin, he said, "Though he wasconvinced that would happen in the course oftime," and let me just comment on that. Well,

that's interesting that he was convinced thatwould happen, but another way of saying that isthat Darwin assumed that these small changeswould add up to larger changes, or to major newadaptive features, but that is exactly the pointof contention. And for a point of contention anassumption is not evidence, let alone proof. SoI see this as very pertinent to the question ofthings like the flagellum Type 3 secretorysystem and other things as well.

Q. So is it clear, I guess in summarizing youthink that the flagellum is in fact irreduciblycomplex, correct?

A. Yes, that's right.

Q. Does that affect necessarily the positiveargument for intelligent design?

A. Well, yes. Let's perhaps we can look atanother slide here that I just wrote out sometext to make this point clear. It's this. Forthe past number of, past hour or so we've beentalking about the argument against Darwinianprocesses, but I want to re-emphasize to saythat it is important to keep in mind that thepositive inductive argument for design is inthe purposeful arrangement of parts.Irreducible complexity, on the other hand,is an argument to show that Darwinism, thepresumptive alternative to design, is anunlikely explanation. However, one also hasto be careful to remember that Darwinism isn'tpositively demonstrated by attacks on theconcept of irreducible complexity. Darwinismcan only be positively supported by convincingdemonstrations that it is capable of buildingthe machinery of the degree of complexity foundin life. In the absence of such convincingdemonstration it is rationally justifiedto think that design is correct.

Q. So an argument against irreduciblecomplexity is not necessarily an argumentagainst design?

A. An argument against irreducibly complexityis not an argument against design, and moreimportantly it's not an argument in favor ofDarwinian evolution.

Q. Have other scientists agreed that Darwiniantheory has not yet explained complex biochemicalsystems?

A. Yes. I recall there on that slide that I

say Darwinism can only be positively supportedby convincing demonstrations, and almosteverybody agrees that such demonstrations havenot yet been forthcoming. For example, on thenext slide these are quotations taken from anumber of reviews of my book Darwin's Black Box,most of these are by scientists. The first oneJames Shreeve, a science writer, but all of themmaking the point that we do not yet haveDarwinian explanations for such complexstructures.For example, James Shreeve, the sciencewriter, writing the New York Times said,"Mr. Behe may be right that given our currentstate of knowledge, good old Darwinian evolutioncannot explain the origin of blood clotting orcellular transport," and James Shapiro, who is aprofessor of microbiology at the University ofChicago, wrote in a review that, "There are nodetailed Darwinian accounts for the evolution ofany fundamental biochemical or cellular system,only a variety of wishful speculations."Jerry Coyne, who's a professor ofevolutionary biology at the University ofChicago wrote in a review of the book in thejournal Nature, "There is no doubt that thepathways described by Behe are dauntinglycomplex, and their evolution will be hard tounravel. We may forever be unable to envisagethe first protopathways."And Andrew Pomiankowski, who is anevolutionary biologist I believe at theUniversity College London, wrote in a reviewin New Scientist, "Pick up any biochemistrytextbook and you will find perhaps two or threereferences to evolution. Turn to one of theseand you will be lucky to find anything betterthan 'evolution selects the fittest moleculesfor their biological function.'"So this is a sampling of writings byscientists agreeing with the point that no,we do not have these demonstrations yet thatDarwinian processes can produce complexbiological systems.

Q. And these were scientists, and in one casea science writer, who are commenting on yourparticular book, correct?

A. Yes.

Q. And have scientists in other contexts madesimilar claims?

A. Yes, another good comment on this was byFranklin Harold, who I mentioned before, he'san emeritus professor of biochemistry at

Colorado State University, and in his book TheWay of the Cell published by Oxford UniversityPress in 2001 he kind of echos James Shapiro.He says, "We must concede that there arepresently no detailed Darwinian accounts of theevolution of any biochemical system, only avariety of wishful speculations," and perhapsI might add that besides these people one canadd also complexity theorists, who also likeStuart Kauffman who also deny that such thingshave been explained in Darwinian theory.

Q. Sir, have some scientists argued thatthere is experimental evidence that complexbiochemical systems can arise by Darwinianprocesses?

A. Yes, there have been a total of two sucharguments which I regard to be very important,because these were claims that there had beenexperimental demonstrations, not justspeculations, not just stories, but experimentaldemonstrations that either irreduciblecomplexity was incorrect or that complexsystems could be built by Darwinian processes.

Q. And one of those claims was raised byDr. Miller, is that correct?

A. That's correct. I think on the next slidewe see that he wrote in his book FindingDarwin's God ,which was published in 1998, hesaid, "A true acid test used the tools ofmolecular genetics to wipe out an existingmultipart system and then see if evolution cancome to the rescue with a system to replace it."So here he was making the point well, hereone test of this claim of irreducible complexityand the ability of Darwinian processes to makecomplex systems, well, is to find a complexsystem in a cell, destroy it, and then see ifrandom mutation and natural selection can comeback and replace it. And I have to say I agreethat's an excellent test of that claim. However,I disagree with Professor Miller's furthercomments and conclusions.

Q. What was the particular system that he waslooking at?

A. Well, he was referring to what is shown ina little cartoon version on the next slide.This is a figure again taken from thatbiochemistry textbook by Voet and Voetdiscussing a system called the lac operon.Now, an operon is a little segment of DNA ina bacteria which codes for a couple of genes,

and genes code for proteins, and the proteinsusually have related functions or function as agroup, and one of them is called the lac operonwhich is used to, the proteins of which arenecessary for the bacterium Escherichia coli tometabolize a sugar called lactose, which is amilk sugar.And it consists of a number of parts. No,let's go back one slide, please, I'm sorry. Allthese little squares here, this little greenthing represents a very complex protein calleda repressor, which will bind to the DNA, andwhen it binds there it stops another proteincalled an RNA prelimerase from binding to thesame spot, and therefore the information carriedby these genes is not expressed, and that'simportant because the sugar lactose is usuallynot present in the bacteria's environment, andmaking proteins that metabolize lactose in theabsence of that sugar would be wasting energy.So the bacterium wants to keep that turnedoff until lactose is around. So the repressorturns off the operon, and that means that thegenes for these three proteins here are notturned on, not expressed. This first one, whichis labeled Z, codes, is the gene for a proteincalled a beta galactosidase, okay? That'sactually the enzyme which chops up lactose.We don't have to go into the detail of howthat happens.This little thing marked Y codes forsomething called a permease. Now, a permeaseit turns out is a protein who is job it is toallow the lactose to enter the bacterial cell.The bacterial cell is surrounded by a membranewhich generally acts as a barrier to largishmolecules, and there's this specialized protein,this specialized machine called a permeasewhich, when lactose is around, grabs the lactosefrom outside the cell, turns it around, andallows it to enter to the inside of the cell.In the absence of that permease the lactosemight be present in abundance in the bacteria'senvironment, but it can't get inside the cell.And so the bacterium can't use it. One otherdetail of this before I go on is that thisrepressor kind of sticks to the beginning ofthe gene and turns it off, but when lactose ispresent in the environment a small moleculewhich is a derivative of lactose can bind to therepressor, and that, and again start thinking interms of the complex shape and structure ofhemoglobin, when that happens it interacts inspecific ways in order and causes the shape ofthe repressor to change, and that changed shapemakes it now no longer geometrically andchemically complementary to the site that it

bound on the lac operon, and it falls off.So in the presence of the inducer the repressorfalls off, this prelimerase can come along andthose proteins get made in the cell.

Q. Would you like the next slide?

A. Yes, thank you. Now I'm going to simplify,after that discussion I'm going to try tosimplify nonetheless. So let me just listsome parts of the lac operon. There's thegalactosidase, the repressor, the permease, allthree of which are proteins, and something thatI've written IPTG/allolactose. That is thesmall molecule which can bind to the repressorand cause to it fall off of the operon,allolactose is something, is a metaboliteof lactose itself, and that's the substancewhich usually binds to the repressor in thecell, but there's also an artificial chemicalcalled IPTG, which stands for isopropylthiogalactoside, which is sold by chemicalsupply companies, which mimics the action of theallolactose, and when a scientist comes anddumps some IPTG into the beaker, that binds tothe repressor and causes those genes to beexpressed, to be turned on.Okay, those are the parts of the lacoperon. Now, for purposes of furtherillustration let me just mention that inE. coli there are thousands of genes, and manyof them are grouped into operons. Unbeknownstto the experimenter, whose name is Barry Hall,there also existed in the E. coli another operoncalled the EBG operon, which he called it thatbecause it stands for evolved betagalactosidase. He thought this protein evolvedin response to the selective pressure that heput on it, and it turns out that that operonalso codes for a galactosidase, anothergalactosidase and another repressor as well.

Q. So this was the system that Dr. Miller wastalking about in --

A. Yes, I'm afraid this is the background forthe system that he started to discuss in hisbook.

Q. Which he sees it as experimental evidenceto refute the irreducible complexity claim?

A. Yes, that's right, and if you look on thenext slide you'll see the part of his book wherehe discusses that. He says of the system, hesays, "Think for a moment. If we were to happenupon the interlocking biochemical complexity of

the re-evolved lactose system, wouldn't we beimpressed by the intelligence of its design.Lactose triggers a regulatory sequence thatswitches on the synthesis of an enzyme that thenmetabolizes lactose itself."The products of that successful lactosemetabolism then activate the gene for the lacpermease, which ensures a steady supply oflactose entering the cell. Irreduciblecomplexity, what good would the permease bewithout the galactosidase? No good of course."And he continues that same discussion on thenext slide, he continues, "By the very samelogic applied by Michael Behe to other systems,therefore, we can conclude that this system hadbeen designed, except we know that it was notdesigned. "We know it evolved, because wewatched it happen right in the laboratory. Nodoubt about it, the evolution of biochemicalsystems, even complex multipart ones, isexplicable in terms of evolution. Behe iswrong."

Q. Is Dr. Miller right?

A. No. Dr. Miller is wrong. Now, ProfessorMiller is always enthusiastic and he alwayswrites and speaks with great excitement, but Isay that when you examine his arguments closely,under close inspection they simply don't hold upand this is enormously exaggerated, and theresults of researcher Barry Hall that he isdescribing here I would happily have includedas an example of irreducible complexity inDarwin's Black Box.So let me please try to explain why I saythat. Reading Professor Miller's prose onewould get, and I certainly did get when I firstread it, the impression that this system wascompletely knocked out in that it completelycame back under the experiments that Barry Hallconducted. But it turns out of this multipartsystem, only one part, the protein betagalactosidase, was knocked out by experimentalmethod.Everything else, the repressor, thepermease, and we'll see later IPTG, andimportantly as well other proteins which didvery, very similar jobs in the cell, were leftbehind. And the worker Barry Hall himself wasalways very careful to say that he was onlyknocking out that one protein.

Q. The galactosidase?

A. Yes, that's correct. I think on the nextslide he makes that point. This is a quotation

from a paper by Professor Hall recalling hisexperiments that he did earlier on the lacoperon. He says the following, "All of theother functions for lactose metabolism,including lactose permease and the pathwaysfor metabolism of glucose and lactose, theproducts of lactose hydrolysis, remain intact.Thus, reacquisition of lactose utilizationrequires only the evolution of a new," and thisshould be a beta, "beta galactosidase function."So let me point out that what he did in hislaboratory was to take an E. coli bacterium andusing molecular biological methods to knock outor destroy the gene for that one part of the locoperon, the beta galactosidase. He left thepermease intact, he left the repressor intact,everything else was intact. He just had to getone more component of the system.And what he saw was that he did getbacteria that were again able to use lactose.And when he did the experiments in the 1970's,that's all he saw. He saw he had bacteria thatcould grow when they were fed lactose. Butyears later after methods had developed andafter he had the ability to do so, he askedhimself what protein was it that took over therole of the beta galactosidase, and he named itEBG, evolved beta galactosidase.But when he looked at it further he foundit to be a very similar protein to the one thathe had knocked out. Essentially it was almosta spare copy of the protein that had beendestroyed. So this slide makes a couple ofpoints. Let me just point to a couple. TheEBG protein that took the place of the betagalactosidase is homologous to lac proteins.That's a technical term, that means they'revery similar. Their protein structures, theirsequences are pretty similar, and odds aregood that they have the same sort of activity.What's more, after further investigationProfessor Hall showed that even the unmutated,even the EBG galactosidase before he did hisexperiment, the unmutated galactosidase couldalready hydrolyze, although it was inefficient.So again this was almost a spare copy of theprotein, and I think on the next slide, I'llskip that last point on the next slide to drivehome the point I want to show you what are theamino acid sequences of the area around what'scalled the active site of the protein, which iskind of the business end where the lactose bindsand where the chemical groups reside which willcause it to be hydrolyzed into two componentparts.Notice this. Look at these sequence ofletters. Now, I know that they don't mean much

to most people in here, but notice the sequenceof letters, these are the amino acid sequences,abbreviations for the amino acid sequence ofvarious beta galactosidase enzymes found inE. coli and a related species. Notice here,let's start in here, there's an R here,HEHEMYEHW. Look up top, there's RHEHEMYEHW, thesame thing on the lower one, too. They'reactive sites, their business ends are almostidentical. Like I said, these are essentiallyspare copies of each other.

Q. So in fact it wasn't a new evolved elementto this system. It was a spare part that wasalready existing?

A. Well, it was there and it did undergo smallchanges. But nobody, nobody denies thatDarwinian evolution can make small changes inpreexisting systems. Professor Miller wasclaiming that a whole new lactose utilizingsystem had been evolved in Barry Hall'slaboratory, and that's, you know, that's very,very greatly exaggerated.

Q. Again do you have additional slides toemphasize the point?

A. Yes. This might be hard to explain, butProfessor Hall says in one of his papers that,"The evidence indicates that either AS-92 andsys trip 977," these are the same of some aminoacids, "are the only acceptable amino acids atthose positions, or that all of the single basedsubstitutions that might be on the pathway toother amino acid replacements at those sites,are so deleterious that they constitute a deepselective valley that have not been transversedin the two billion years since those proteinsemerged from a common ancestor." Now, translatedinto --

Q. Yes, please into English.

A. -- more common language, that means thatthat very similar protein could only work ifit became even more similar to the betagalactosidase that it replaced, and if youthen also knock out that EBG galactosidase, noother protein in Professor hall's experience wasable to substitute for the beta galactosidase.So the bottom line, the bottom line is that theonly thing demonstrated was that you can gettiny changes in preexisting systems, tinychanges in preexisting systems, which of courseeverybody already had admitted.Another interesting point, another

interesting point is shown on that figurefrom Voet and Voet, the inducer, this littlered dot, this little red dot actually standsfor this chemical that binds to the repressorwhich changes its shape which causes it to falloff of the operon and allow the prelimerase tocome in and transcribe that information. Well,it turns out that the EBG operon, this place inthe DNA and E. coli that had that spare betagalactosidase, did not have a spare permease.So the system was stuck, because it didn'thave its own permease. When the repressor bindsto this operon, the normal lac operon, if thereweren't any lactose around then the repressorwould be essentially stuck there indefinitely.And even if lactose were present outside thecell, it had no way to get inside the cell. Sowhat Barry Hall did to allow his experiment tocontinue was that he added the inducer. Headded that artificial chemical IPTG that he canbuy from a chemical supply house, and he tooksome and sprinkled it in the beaker for thespecific purpose of allowing the bacteria tosurvive so that it could take these small littlesteps to produce a new beta galactosidase.

Q. You have a slide to demonstrate that?

A. Yes. And Barry Hall was always verycareful to explain exactly how these experimentswere performed, and he brought it directly tothe attention of readers when he described hissystem. For example he writes, "At this pointit is important to discuss the use of IPTG inthese studies. Unless otherwise indicated, IPTGis always included in media containing lactose,"and that italics is Barry Hall's emphasis. Hewanted to make sure his reader understoodexactly what he was doing."The sole function of the IPTG is to inducesynthesis of the lactose permease and thus todeliver lactose to the inside of the cell.Neither constitutive nor the inducible of allstrains grew on lactose in the absence of IPTG."In other words, if this intelligent agent, BarryHall, had not gone to the store and gotten someIPTG to help the bacteria survive, they wouldnot have lived. This would not have occurred inthe wild. This tells us virtually nothing abouthow Darwinian evolution could produce complexmolecular systems.

Q. So again this system would not have workedin nature but for Barry Hall interjecting theIPTG to make this system work?

A. Yes. I should point out that Professor

Miller does not mention this aspect of BarryHall's experiments in his discussion, in hisbook Finding Darwin's God.

Q. Is that a significant oversight?

A. Well, I certainly would have included it.

MR. MUISE: Your Honor, we're about to moveinto the blood clotting system, which is reallycomplex.THE COURT: Really? We've certainlyabsorbed a lot, haven't we?MR. MUISE: We certainly have, Your Honor.This is Biology 2. It's a quarter past, and ifwe're going to go until 4:30, it's probably notworthwhile to start up on the blood clottingbecause it's fairly complex and heavy and a lotof it is going to be --THE COURT: Well, we don't have an issue asto his availability through the day tomorrow Iassume?MR. MUISE: He's available, Your Honor, foras long as we need him.THE COURT: Any objection if we --MR. ROTHSCHILD: No. He started it.THE COURT: I was just waiting to see whatyou'd say.MR. MUISE: We've gone from Biology 101 toadvanced biology. So this is where we get.THE COURT: We will recess then for today,and we'll reconvene at 9:00 tomorrow andwe will pick up with Mr. Muise's directexamination at that time. So have a pleasantgood evening, and we'll see you tomorrow.(Court was adjourned at 4:15 p.m.)Tammy Kitzmiller, et al. vs. Dover Schools4:04-CV-02688Trial Day 10, Afternoon SessionOctober 2005I hereby certify that the proceedingsand evidence are contained fully and accuratelyin the notes taken by me on the trial of theabove cause, and that this copy is a correcttranscript of the same.s/ Wesley J. Armstrong________________________Wesley J. ArmstrongRegistered Merit ReporterThe foregoing certification of thistranscript does not apply to any reproductionby any means unless under the direct controland/or supervision of the certifying reporter.