Welcome to Baptist Board, a friendly forum to discuss the Baptist Faith in a friendly surrounding.
Your voice is missing! You will need to register to get access to all the features that our community has to offer.
We hope to see you as a part of our community soon and God Bless!
Thanks for the professional link, UTEOWE. It led me to this one.Originally posted by UTEOTW:
Thought some of you might enjoy reading the transcripts.
http://www.talkorigins.org/faqs/dover/kitzmiller_v_dover.html
I am currently reading the cross of Dr. Kenneth R. Miller. Interesting stuff.
http://www.grisda.org/origins/21091u.htmOriginally posted by Paul of Eugene:
I found interesting the new information about the genetic instructions for making hemoglobin - and how three primate species - one of them us - share a common defect for that gene. We have other copies of the gene that work, so its no big deal. We get our hemoblogin. But - sharing defects - how did that happen?
http://www.grisda.org/origins/21091u.htm </font>[/QUOTE]Well, this link seems to undermine itself completely.Originally posted by jcrawford:
</font><blockquote>quote:</font><hr />Originally posted by Paul of Eugene:
I found interesting the new information about the genetic instructions for making hemoglobin - and how three primate species - one of them us - share a common defect for that gene. We have other copies of the gene that work, so its no big deal. We get our hemoblogin. But - sharing defects - how did that happen?
It is interesting. Thanks for posting the link.Originally posted by UTEOTW:
Thought some of you might enjoy reading the transcripts.
http://www.talkorigins.org/faqs/dover/kitzmiller_v_dover.html
I am currently reading the cross of Dr. Kenneth R. Miller. Interesting stuff.
What does "Atillaed the hunt" mean?THE COURT: But as a signatory to the stipulation, I suppose you have Atillaed the hunt.
It is interesting. Thanks for posting the link.Originally posted by Daisy:
</font><blockquote>quote:</font><hr />Originally posted by UTEOTW:
Thought some of you might enjoy reading the transcripts.
So Behe takes something that is supposed to be IC and he claims, he himself is making this claim, that this IC system could evolve in a short period of time with none of the intermediate stages being useful and from a very small population and without most of the normal evolutionary mechanisms in play.Q. And let me just ask you a few questions, and you tell me if I'm fairly summarizing the results of your computer simulation. What you're asking is, how long will it take to get -- and please follow with me, I'm trying to do this slowly and methodically -- two or more specific mutations, in specific locations, in a specific gene, in a specific population, if the function is not able to be acted on by natural selection until all the mutations are in place, if the only form of mutation is point mutation, and the population of organisms is asexual?
A. I would have to look at that statement closely because there are so many different aspects to it that I don't trust myself to sit here and listen to you say that and form a correct judgment.
Q. Anything I said about that sound incorrect?
A. If you repeat it again, I'll try.
Q. I'd be happy to. Two or more specific mutations?
A. Actually, this dealt with one or more.
Q. One or more mutations?
A. Yes. If you notice, in figure -- if you notice in figure 3, you look at the x axis, you notice that there are data points there that start at one. So we considered models where there were one, two, and more mutations.
Q. Fair enough. In specific locations?
A. No, that's not correct. We assumed that there were several locations in the gene that could undergo these selectable mutations, but we did not designate where they were.
Q. In the specific gene?
A. We were considering one gene, yes.
Q. In a specific population?
A. Yes.
Q. Okay. If the function is not able to be acted on by natural selection until all mutations are in place?
A. Yes, that's what's meant by multiple amino acid residue, multi-residue feature, yes.
Q. If the only form of mutation is point mutation?
A. Yes, that's a very common type of mutation, which is probably half or more of the mutations that occur in an organism.
Q. And if the population of organisms is asexual?
A. Yes, we did not -- actually, we did not confine it just to asexuals, but we did not consider recombination.
Q. Are prokaryotes an example of the kind of organism that you were studying there?
A. Again, we weren't studying organisms, but, yeah, they're a good example of what such a model has in mind.
Q. And to say this very colloquially, you conclude that it will take a large population a long time to evolve a particular function at disulfide bond, right?
A. A multi-residue feature. That's correct, that's correct.
Q. And specifically --
A. I'm sorry.
Q. Go ahead.
A. Let me just finish. Depending on -- as we emphasize in the paper, it depends on the population size. And, of course, prokaryotes can oftentimes grow to very large population sizes.
Q. And here the conclusion, the calculations you concluded was that, if you had a population of 10 to the 9th power, that's a population of 1 billion?
A. That's correct.
Q. To produce a novel protein feature through the kind of multiple point mutations you're talking about, it would take 10 to the 8th generations, that's what it says in the abstract, correct?
A. If, in fact, it was -- if, in fact, the intermediate states were not selectable.
Q. Okay.
A. And if this is by gene duplication as well.
Q. Okay. So 10 to the 8th generation, that's 100 million generations?
A. That's correct.
Q. And yesterday, you explained about bacteria, that 10,000 generations would take about two years in the laboratory, correct?
A. Yes.
Q. So 100 million generations, that would take about 20,000 years?
A. I'm sorry?
Q. 100 million generations, which is what you calculated here, that would take about 20,000 years?
A. Okay, yes.
Q. And those are numbers based on your probability calculations in this model, correct?
A. Yes.
Q. Now it would be true that, if you waited a little longer, say, instead of 10 to 9th generations, 10 to the 10th generations, then it would mean that you wouldn't need as big a population to get the function that you are studying?
A. That's right. The more chances you have, the more likely you are to develop a feature. And the chances are affected by the number of organisms. So if you have a smaller population time, and more generations, that could be essentially equal to a larger population size and fewer generations.
Q. So, as you said, so if we get more time, we need less population to get to the same point, and if we had more population, less time?
A. That's correct, yes.'
Q. Now would you agree that this model has some
limitations?
A. Sure.
Q. And you, in fact, were quite candid in indicating that in the paper?
A. That's correct.
Q. And if we could turn to, what I believe is, page 8 of the document. And if you look in the paragraph that's actually continued from the previous page that says, we strongly emphasize. And if you could --
A. I'm sorry. What page number is that?
Q. It's page 8 in the document. And it's up on the screen as well.
A. Yes, okay. I've got it.
Q. Could you read into the record the text to the end of the paragraph beginning with, we strongly emphasize?
A. We strongly emphasize that results bearing on the efficiency of this one pathway as a conduit for Darwinian evolution say little or nothing about the efficiency of other possible pathways. Thus, for example, the present study that examines the evolution of MR protein features by point mutation in duplicate genes does not indicate whether evolution of such features by other processes, such as recombination or insertion/deletion mutations, would be more or less efficient.
Q. So it doesn't include recombination, it doesn't include insertion/deletion of the mutations?
A. That's correct.
Q. And those are understood as pathways for Darwinian evolution?
A. They are potential pathways, yes.
Q. This study didn't involve transposition?
A. No, this focuses on a single gene.
Q. And transpositions are, they are a kind of mutation, is that right?
A. Yes. They can be, yes.
Q. And so that means, this simulation didn't examine a number of the mechanisms by which evolution actually operates?
A. That is correct, yes.
Q. And this paper, let's be clear here, doesn't say anything about intelligent design?
A. Yes, that's correct. It does imply irreducible complexity but not intelligent design.
Q. But it doesn't say it?
A. That's correct.
Q. And one last other question on your paper. You concluded, it would take a population size of 10 to the 9th, I think we said that was a billion, 10 to the 8th generations to evolve this new disulfide bond, that was your conclusion?
A. That was the calculation based on the assumptions in the paper, yes.
MR. ROTHSCHILD: May I approach the witness, Your Honor?
THE COURT: You may.
BY MR. ROTHSCHILD:
Q. What I've marked as Exhibit P-756 is an article in the journal Science called Exploring Micro--
A. Microbial.
Q. Thank you -- Diversity, A Vast Below by T.P. Curtis and W.T. Sloan?
A. Yes, that seems to be it.
Q. In that first paragraph, he says, There are more than 10 to the 16 prokaryotes in a ton of soil. Is that correct, in that first paragraph?
A. Yes, that's right.
Q. In one ton of soil?
A. That's correct.
Q. And we have a lot more than one ton of soil on Earth, correct?
A. Yes, we do.
Q. And have for some time, correct?
A. That's correct, yes.
Q. Could we have the bacterial flagellum power point?
A. So this is, in a way, a summary of Dr. Behe's argument. And one of the things that I think is important to make clear to the Court is that, it is absolutely true that there are many, many structures in the living cell, many biochemical pathways for which we don't have a detailed biochemical -- excuse me, a detailed evolutionary explanation. That is a point that all scientists will concede. Do Doctor --
Q. I'm sorry. Is that true just about evolutionary theory or is that true about any science?
A. That's true about anything. In cell biology, for example, I think most people and the court are aware that when a cell divides, the chromosomes that carry the genetic information of a cell are moved apart and separated into the two daughter cells. We have enormous arguments in the field of cell biology as to what the exact mechanism is by which that force is generated. We can all see it happen. Any high school student can watch the separation of chromosomes under a microscope in a high school laboratory. But we still don't know exactly what the motor or the mechanism is that moves these apart. There are many, many other unsolved problems in biology.
Q. I'm sorry. Please continue.
A. Sure. So it's important to note that Dr. Behe's argument does not say simply, well, there are complex structures within the cell for whom we do not understand the detailed evolutionary origin of, that's absolutely true. But his argument really rises to a different level. What I've shown on this slide is a diagram of the bacterial flagellum.
Now bacteria, of course, are very, very simple cells. They're found everywhere in nature. They're found, for example, in our digestive systems. They're found in the skin. They're found on the surface of the table. Some bacteria have little whip like structures called flagellum. You might almost considers them to be outboard motors. And these things whip around at very high rates of speed, and they propel the bacteria through water, or sometimes they pull the bacteria in sort of a screw like motion through the water.
So it's marvelous machines. They are acid powdered reversible rotary engines. These are marvelous little machines, and they are made of a whole series of protein parts, some of which are shown in this little diagram here. Now if we can animate this slide a little bit. Next point.
Now what I wrote here is that, Dr. Behe has made very clear in what I think is fairly called his biochemical argument from design, that that argument depends upon a much bolder claim than simply saying, scientists have not completely explained how this structure evolved. And that bolder claim is shown in the next animated section of this slide.
And that is that, the evolution of complex biochemical structures cannot even or ever be explained in principle. And, of course, what he means by that is, there is some aspect of this complexity, which means we can say not just, we haven't figured it out yet, but we will never figure it out, and that's where the evidence for design lies.
Now if I may advance to the next slide. I'll try to use Dr. Behe's words to explain why he holds this point of view. The reason that evolution cannot explain, he says, the origin of such structures is because they have a property, which he calls irreducible complexity, or they are irreducibly complex. I thought it best for the Court to read the description of irreducible complexity in Dr. Behe's own words.
So in the lower part of the the slide, I have a quotation from page 39 of his book, Darwin's Black Block. And I will read that to the Court. Quote, By irreducibly complex, I mean a single system composed of several well-matched, interacting parts that contribute to the basic function, wherein the removal of any one of the parts causes the system to effectively cease functioning.
And now, from my point of view, the key part of the argument, and I'll continue to read. An irreducibly complex system cannot be produced directly by slight, successive modifications of a pre-cursor system -- and that's how evolution would have to produce it -- because any pre-cursor to an irreducibly complex system that is missing a part is by definition non-functional.
So his argument is that, if you have a multi-part system, and all the parts are necessary to function, you can't produce that system five parts at a time, six, seven, and gradually build up the complex system, because there is no function possible until the last part is snapped into place. And that's why evolution cannot produce that system.
Now the next slide is another quote of Dr. Behe's that tries to make this point absolutely explicit as to why you need the system to be working. He points out, another quote, Darwin's Black Box, page 39, quote, Since natural selection can only choose systems that are already working -- and if you remember, his contention is, if you're missing a part, you're not working -- then if a biological system cannot be produced gradually, it would have to arise as an integrated unit, in one fell swoop, for natural selection to have anything to act upon, closed quote.
And Dr. Behe rightly points out that, to imagine such complex systems arising spontaneously in one fell swoop is something that no serious biologist would argue could happen, and I will not argue either. So his point is, as long as irreducible complexity holds, then any system we can identify as irreducibly complex couldn't have been produced by evolution. It's a very, very coherent argument.
Q. Does he identify some organisms that he calls irreducibly complex?
A. Well, counselor, not so much organisms, but he certainly identifies some machines and some structures that he regards as irreducibly complex, one of which, of course, is the bacterial flagellum. And I pointed out, this slide contains a diagram of the flagellum. And to the right is actually sort of what we call a false color, but an electron micrograph showing a bacterium with several flagellum protruding from one end.
So that is one of the principal systems to which he points. Now the next slide, please. And I should also point out, to be a little more responsive than I have been to your question, that Dr. Behe also says, the blood clotting cascade that we talked about earlier as an example of an irreducibly complex system, the eukaryotic cilium, similar system to the flagellum, that's irreducibly complex, the vesicle targeting system that parcels out things in living cells, and also the immune system are all examples of irreducibly complex systems.
Now what I did in this slide was to prepare a graphic to make this point as clear as possible to those of us in court today. And that is to emphasize that complex biochemical machines composed of multiple interacting parts, if they work, they can have a function that's favored by natural selection. The essence of the biochemical argument from irreducible complexity, however, is that the individual parts of that machine have no function of their own.
And because they have no function on their own, they cannot be produced by natural selection and, therefore, the impediment, the reason you can't get to here from there, you can't go from individual parts to the machine, is because the individual parts have no functions of their own.
Now evolutionary biology has grappled with this problem before. And the next slide shows how evolutionary biologists generally explain the evolution of complex machines. And that is, they agree, yes, there are such machines. You need all these parts for a particular function. But where these machines come from is, they come from pre-existing machines which have functions of their own, and that the individual parts of these machines originate in components that have different functions.
So the way in which evolutionary biology picks up Dr. Behe's challenge is to basically say, you're wrong, that the individual parts of these machines cannot have a function that is favored by natural selection. Now that, of course, in this slide, this is not evidence, of course, in the scientific sense. This is merely an argument.
But the reason I like the way that Dr. Behe has put his argument, and I like sort of describing it this way, is because it actually is amenable to a scientific test. Something that most arguments for intelligent design are not. And the next slide.
Q. I'm sorry. This is -- is Dr. Behe's argument for irreducible complexity, is that an argument directly for design?
A. That's a good point. The answer is, no, it's not. It really is an argument that says why such systems are not produceable by evolution. So it's a negative argument against evolution. It is in itself not evidence. Even if the argument were correct, it's not evidence of a designer, it's not argument for design, it simply is an argument that the evolutionary mechanism wouldn't work in this case.
Q. So that's why this argument is testable?
A. That is correct. As I mentioned earlier, one of the problems with intelligent design is that it doesn't make any testable predictions. This actually isn't a testable prediction of design either. This is simply an argument as to why evolution wouldn't work. And that can be subjected to a test.
Q. Please continue.
A. Thank you. Next slide, please. So what I have done in this slide is to place the graphic summaries of the argument from irreducible complexity that I just made in the upper left-hand corner of the slide, and in the upper right-hand corner, I have basically put the evolutionary explanation using the same graphic convention. And the nature of the test that I or any other scientist would propose is pretty simple.
If you animate the slide, you'll see that Dr. Behe's prediction is that the parts of any irreducibly complex system should have no useful function. Therefore, we ought to be able to take the bacterial flagellum, for example, break its parts down, and discover that none of the parts are good for anything except when we're all assembled in a flagellum.
If evolutionary theory holds, however, and we can animate again, and we'll show that in the right-hand side, evolution makes an extremely straight forward prediction. And that is, when we look at these irreducibly complex structures, we ought to be able to find parts of those systems that actually do have useful functions within them.
So we can do a very straight forward either/or test to distinguish between these two alternatives. So what I'd like to show in the next slide is how such a test can be conducted. This is a -- in the upper right-hand corner of the slide is a graphic representation from a review article showing some of the proteins involved in the construction of the bacterial flagellum.
Now the individual names of the gene products need not concern us. They often begin with FL for flagellum. But as you can see, just as Dr. Behe says, this is a complex multi-part biochemical machine. Now the test that I would propose, we can animate the slide, please, to start with this flagellum. And if Dr. Behe is correct, if we take away even one part, there should be no function.
But I'm going to propose that we take away not one, not two, I'm going to propose we take away 30 parts. And what I'm going to propose to do is, take 30 of these proteins away and see what is left. And the slide that I set up is animated, and what we have done is -- actually, could you go back for the animation and then do it again?
And let's watch the Court do it, and we'll do the animation now. Thank you. And you can see the parts that I have removed are on the outside and the inside, and what are left are 10 proteins that span the inner and outer membrane. These bacteria, many of them are surrounded by two membranes.
These 10 remaining parts are shown in the next diagram, which will come up on the slide. And this is a diagram showing where these 10 parts are. They exist at the very base of the flagellum near one of the cellular membranes.
Now the prediction that is made by Dr. Behe in his book is extremely straight forward, which is, since this was an irreducibly complex machine, and we've taken away most of its parts, what's left behind should be non-functional because, you remember, he wrote, any pre-cursor to an irreducibly complex machine that is missing a part is, by definition, non-functional. This guy is missing 30 parts.
Next slide. Well, it turns out that what is actually left behind when we take those parts away is a little structure with those 10 parts, which is known to microbiologists as the type III secretory system. And I can see, Mr. Walczak, you're saying, why, of course, it's the type III secretory system.
THE COURT: That certainly was on my mind.
THE WITNESS: Exactly. Now I was expecting a question of, how do you know it's not type II or type IV? The type III secretory system is a little molecular syringe that some of the nastiest bacteria in all of nature have. Yrsinia pestis, for example, which is the organism that causes bubonic plague, is a type III secretor. And what it does is, it gets inside our body, crawls up alongside, and uses this syringe to inject poisons into a human cell.
And in the lower left-hand corner of the slide, I have some diagrams showing the operation of a type III secretory system. Now the connection between this and the flagellum is that the type III -- the 10 proteins in the type III system are almost a precise match for the corresponding 10 proteins in the base of the bacterial flagellum.
So it's very clear that a subset of those proteins has an entirely different function, a beneficial function, not for us, but for the bacterium, and a function that can and is favored by natural selection. Can I have the next slide, please? So the summary of this example is really very straight forward.
When we take this complex multi-part system, which is the bacterial flagellum, the prediction made by Dr. Behe from irreducible complexity is when we break the parts apart, we should have no useful functions. Anyone missing a part is, by definition, non-functional. We follow that up. We do break it apart. And lo and behold, we find -- actually, we find a variety of useful functions, one of which I have just pointed out, which is type III secretion.
What that means, in ordinary scientific terms is that, the argument that Dr. Behe is made is falsified, it's wrong, it's time to go back to the drawing board.
I'm not sure what the point of your long quote was or what you are trying to prove with it. What do you mean by IC, anyway - Intelligent Creation?Originally posted by UTEOTW:
So Behe takes something that is supposed to be IC and he claims, he himself is making this claim, that this IC system could evolve in a short period of time with none of the intermediate stages being useful and from a very small population and without most of the normal evolutionary mechanisms in play.
Miller just reveals himself to be another neo-Darwinist racist and facist demi-god when it it comes to molecular and genetic theories of human evolution from African monkey and ape ancestors. Witness his following remarks:Originally posted by UTEOTW:
[QB] You might also be interested in Miller's testimony on IC since he destroys Behe.
Maybe monkeys were created by God for the sole purpose of making monkeys and apes out of people like you and I, Bunyon.Originally posted by Bunyon:
"I found interesting the new information about the genetic instructions for making hemoglobin - and how three primate species - one of them us - share a common defect for that gene. We have other copies of the gene that work, so its no big deal. We get our hemoblogin. But - sharing defects - how did that happen? Evolution points to an answer, it originally occurred in a shared ancestor."-----------------------------------------------------------------------------------------
Maybe we did not come from the monkeys, maybe they came form us.
Miller just reveals himself to be another neo-Darwinist racist and facist demi-god when it it comes to molecular and genetic theories of human evolution from African monkey and ape ancestors. Witness his following remarks:Originally posted by jcrawford:
</font><blockquote>quote:</font><hr />Originally posted by UTEOTW:
[QB] You might also be interested in Miller's testimony on IC since he destroys Behe.
Irreducible complexity (IC) equals Intelligent creation (IC), no?Originally posted by UTEOTW:
"I'm not sure what the point of your long quote was or what you are trying to prove with it. What do you mean by IC, anyway - Intelligent Creation?"
You post on Behe but do not even know what IC is?
That is classic. No wonder you don't get the point of the Behe cross examination quote. He shows himself to be wrong.
Nonsense. You dare argue with Professor Michael Behe? What "peer-reviewed" articles and books have you published recently?Let's try to explain it. Behe says that certain systems must be fully assembled before they will work. He says that these systems will not work if all of the parts are not already there. He says that this means that any intermediate stages would not be useful and therefore would not be able to be acted upon by selective pressures to build said system. They must be made all at once to be useful and are therefore IC.
The response is too show that said IC system can actually function with fewer parts. One way this has been done is to show that some flagellum use fewer parts than in Behe's example. So that means that his example is not really IC if it can still function with some parts missing.
The second and more important flaw is to show that various combination of the parts can havea useful function without the others. This allows for selection to choose these parts even before they are all together to make the part he calls IC. In the case of the flagellum, the TTSS has many fewer parts but still is useful. This shows us that often times in evolution, selection acts upon other uses before finally putting together the parts for a new use. [/QB]
Darwin was an author of confusion. Who do you believe in anyway? God, Charles Darwin or yourself?Originally posted by UTEOTW:
"Maybe monkeys were created by God for the sole purpose of making monkeys and apes out of people like you and I, Bunyon.
Knowing God, I wouldn't put it past Him, would you?"
What god do you believe in that is the author of confusion?
The God that most of us here believe in is not the author of confusion.