Speaker 1 00:00:05 ID the future, a podcast about evolution and intelligent design.
Speaker 2 00:00:12 Hello, this is Tom Gilson with ID The Future. I have the privilege with a friend of mine, Kate, cover of leading an Apologetics fellowship group that meets in the Cincinnati and Dayton, Ohio area. A couple of meetings ago, we had a visitor by Zoom, Jonathan McClatchy, and a fellow with the Discovery Institute. We had question and answer time with him, but it was preceded by an actual podcast recording, which I led there. There were audio problems, you'll hear that, but I think you'll still enjoy the podcast and enjoy hearing from Jonathan McClachi, who I will introduce as we move into the actual event. For information on the Apologetics Fellowship, by the way, you can go to apologetics fellowship.org. That's apologetics fellowship.org.
Speaker 3 00:01:04 Today we're gonna hear from Dr. Jonathan McClatchy. Jonathan is a Christian writer, international speaker, debater, assistant professor at Satler College in Boston, fellow of the Discovery Institute with a bachelor's degree in honors in forensic biology, a master's in evolutionary biology, a second master's in Medical and molecular bioscience. And because he's quite the underachiever, he has a PhD in evolutionary biology. He's participated in dozens of moderated debates around the world with representatives of atheism, Islam and other worldview perspectives. He's spoken internationally and he is interested in promoting an, an intelligent, reflective, and evidence-based Christian faith. So my first question for you, Jonathan, is with your background in biology in a field where the intelligent design perspective is not, shall we say, terribly popular so far, how did you get interested in this study?
Speaker 4 00:02:05 Yeah, so as, as you mentioned, uh, I did my bachelor's degree in forensic biology at the University of Strath Law in Scotland between 2007 and 2011, and grew a fascination over those years, uh, in the wonders of the molecular world, uh, was often, uh, bewildered by how anyone could go through a four year university program in the natural sciences and come out an atheist at the other end. Because the evidence, uh, seems to me to be quite compelling for the truth of theism and span so many different disciplines, both in the life sciences as well as in the physical sciences. Uh, but during my, uh, undergraduate, I, I was fascinated by molecular machines in the cell and how they work and how they function, um, and how, uh, many of these systems, uh, require multiple sub-components that have to work together on unison and have to be very specifically crafted towards achieving some higher level objective.
Speaker 4 00:02:57 Um, and, uh, yes, I became fascinated with how you can develop, uh, um, robust, uh, inference to design and, uh, the, the epistemology of design detection. So that, that, and then, um, because I was so fascinated in this question of origins, I then, um, went on to do my ba, my master's degree in evolutionary biology. Uh, and I, I worked for a year, uh, between 2012 and 13 with the Discovery Institute. Uh, later on I came to become a fellow, um, of the Discovery Institute, uh, center for Science and College here. And, uh, then of course went on to also get another master's degree in molecular biology. And then I did my PhD in the, uh, the evolution of the tic cell cycle, which is a subject of fascination for me.
Speaker 3 00:03:39 Your fascination with molecular machines reminds me of why I didn't study biology among other reasons. <laugh>, I had, I had a very bad biology teacher, and, and I mean, very bad in the sense that he taught us Charles Darwin's life story six times. And I don't think he did it because we needed to hear it that many times. I think he forgot he had already done it, <laugh>. And, but the another thing about biology that bothered me when I was in high school back in the mid 1970s was they said that the cell wall lets sodium in and out and file and, and, and, and potassium in and out and calcium in and out. And I kept wondering, how does it know, and what the science has come to since then would suggest that we're starting to understand that. Is that right, Jonathan?
Speaker 4 00:04:32 Yeah. Um, we're, we're constantly growing in our understanding of <laugh> the wonders of the sale.
Speaker 3 00:04:37 So intelligent design proponents talk a lot about irreducible complexity. It's a topic that's been, uh, that's been in the field, has been in under discussion since Michael Behe published a book in 1995 called Darwin's Black Box. It's been very controversial. Could you just tell us what an irreducible complexity is, first of all?
Speaker 4 00:05:04 Absolutely. So, uh, irritable complexity as defined by behe in Darwin's Black box in 1996, basically, uh, refers to a system that is comprised of, uh, several well-matched interacting components, the removal of, one of which renders the system completely non-functional. And so the idea is that this presents a challenge to the, uh, to the new orian evolutionary scenario of stepwise evolution because, um, evolution has no end goal in mind. It has no t loss in view. It doesn't, it, it's not a goal directed process. Rather it's an unguided, mindless stochastic process of chance and physical necessity. There's a random component, namely, uh, genetic mutation, which are sifted by the mill of natural selection. Natural selection preserves those combinations of gene variants that, uh, that's, that promote the survival of the organism to reproductive age so that they can produce, uh, fertile offspring and pass on their genes.
Speaker 4 00:06:01 Uh, but it doesn't, uh, it, it is not able to visualize a complex endpoint to look into the future and, and realize that angle. That's a, a unique, uh, feature of, of intelligent causes. And so there's, there's a number of examples of complexity. Uh, perhaps the most famous one, or the kind of the flagship example that has become most famously associated with ible complexity would be the bacterial for jm, uh, which is a rotary motor that propels bacterial cells, uh, through liquid is, uh, been a subject of longtime fascination for me. Um, and, uh, behe champion that has an example, Ian Darwin's Black Box. Uh, another example would be, um, bacterial cell division machinery. And there's a number of different features of the bacterial cell division machinery that I think support, uh, um, the idea of Otis for complexity. So one example would be, um, the, so during material cell division, the cell has to elongate, uh, to, in the case of rod shape, bacterial cell double its original length.
Speaker 4 00:06:57 And then you have the, the formation of the, the, uh, fit what's called the Fit Z ring that, um, polymerizes or resembles around the division septum, and then the cell bifurcate into two daughter cells. And part of that process involves, uh, synthesize, uh, breaking the, the glycan, which is a cell wall in bacteria. Um, and the, uh, the pep the glycan has to be severed at various points. And, uh, you ha and there is, there's, uh, proteins on this auto lyin that, uh, perform that severing. And then you have to resynthesize the, the pap glycan cell wall. Um, and there is, um, various proteins involved there. You have ol, which shuttles the pap glycan precursors across the cell membrane. You have the penicillin binding proteins that perform the cross-linking of the, of the cell wall and so forth. And, uh, this is an example of it. Notice the complex system because you have to have a very careful, um, um, coordination between the severing of the pep and cell wall and the rebuilding of the cell wall. In fact, the penicillin binding proteins that perform the cross-linking, as their name implies, are the target for, uh, penicillin drugs, uh, because the penicillin interferes with that cross-linking process and results in the cell not being able to resize it cell while during cell division. And because of the automatic pressure, it basically bursts. So there, there's just a couple of examples of urgent complex systems.
Speaker 3 00:08:18 So the first one you mentioned was the, the, you you used the term rotary motor. And that's not just a metaphor, is it? The, the, the bacterial fle?
Speaker 4 00:08:29 Yeah. Um, exactly. The bacterial, uh, PHR motor is a rotary motor that propels bacterial cells are liquid, uh, in, uh, salmonella or coline, which are the model systems for studying, uh, fla. Uh, the spin at speeds of up to about 17 or 18,000 rotations per minute rpm in some organisms, like, uh, Vibrio species, uh, they spin at speeds of up to a hundred thousand rpm. They have a virtually 100% energy conversion efficiency, and they have, they're plugged into a single transduction circuit. So they get feedback from the environment and, uh, it's called chemotaxis. Uh, very, very elegant system. And unlike manmade motors, they actually have assembly instructions to build themselves from the inside out. And so they actually assemble themselves. Um, and it's, it's a fascinating process to study, but it's, uh, it requires very carefully, uh, choreographed gene regulation. And
Speaker 3 00:09:20 The second example you gave with a, a list of molecules that most of us are not using in our everyday vocabulary. The, uh, i, I think what you're saying there is that the, the sequence has to happen in a given order and it has to all happen, or else none of it happens. Is that a, a fair, uh, extreme condensation of what you were saying?
Speaker 4 00:09:53 Yeah, exactly. So if, if you had the mechanisms for breaking the cell wall, for example, um, and the lyin proteins that are the enzyme, the lyin enzymes are involved in that, uh, are themselves under a careful control because it can result in programed cell death. But if you, if you evolve the, the process for breaking the cell wall without simultaneously having in hand a mechanism for rebuilding the cell wall, that would, uh, uh, be very problematic because as the cell divides, it's not able to rebuild the cell wall, and because of the osmotic pressure, the cell's going to burst. So, yeah, that, that's an ex an example, think a strong example of an istic complex system.
Speaker 3 00:10:27 And you've done some work in DNA replication. Can you give us a ground up view of what that's about, starting with maybe even what DNA is and why replication matters?
Speaker 4 00:10:42 Absolutely. So, uh, DNA is the, the information storage medium of the cell. Uh, it stores information in the form of, uh, four, uh, chemical subunits that we represent with the letters a act, T and G, uh, so adenine, thymine, guine, and, um, the sequential arrangement of those, those chemical subunits are those letters, if you will, uh, will, uh, determine among other things, the sequential arrangement of the amino acids that form proteins. So, um, in, in the case of, uh, the protein coating, um, sequences of genes, and so the DNA will undergo what's called transcription into, uh, an intermediary molecule called messenger rna. Um, and then, uh, it will be in the case of a UCA cell with, as a nucleus, it will be taken outside the nucleus into the cytoplasm. And at the cytoplasm, uh, it gets translated by two-part chemical factory called a ribosome, uh, into, uh, into, uh, a polypeptide sequence, which will then fold into a, into a, um, functional protein.
Speaker 4 00:11:46 So that, that's basically, uh, in a nutshell, uh, dna. There's a, there's a language system called the genetic code, uh, by which the, um, three letter words. So in DNA language words are comprised of three letters, and we call them codons. And these three letter words each specify particular amino acid. Um, and then there's three stop codons, and there's one start codon a u g, which codes for methymine. And methymine is always the first amino acid in any polypeptide. So in terms of DNA replication, the purpose of replicating DNA is to prepare for cell division. Um, and, uh, in Nucar cells, uh, this is known as, um, s phase of the cell cycle where the cells is undergoing, uh, cell division. And, um, the processes are very similar between ucar, um, and, uh, procars. So uars have a nucleus in the cell, Procars don't, so we are uars, whereas bacterial cells are procars.
Speaker 4 00:12:42 And then there's, there's another branch of procars and aia, uh, which, um, have some differences, um, from bacteria. Um, they're, they, they tend to inhabit, um, very, uh, extreme environments of temperature and pH, for example. Uh, what's interesting is that although the mechanisms between, uh, the three domains of life are very similar for DNA replication, the, uh, it, it's widely thought that the d replication machinery actually evolves twice, uh, because the proteins are not homologous between the bacterial branch of, of the evolutionary tree and the eukaryotic anar kale branch. So homo homology refers to similarity, uh, of, um, in this case protein structures, uh, that results from a common ancestor. Uh, they, they don't appear the protein components, even though the mechanisms are very similar, uh, or, or seem to be analogous, the protein components are not themselves homologous. And so it seems that, uh, the d replication machinery evolved convergently in these two branches of the tree, the L branch leading to carriers and akea, and the branch leading to bacteria.
Speaker 4 00:13:43 Now, um, so the, so Dina replication is preparing the sale for, um, for, um, its, its division. And so that's essentially the purpose of Dina replication. There's a number of different components that are involved in d replication machinery, and if any one of those components are missing, you wouldn't have Dina replication that worked half as well as it used to, or record as well as it used to, but it would be broken. And so this is a classic example of an irritably complex system. So what proteins do you need? Well, you need to initially, um, open up the, um, um, the DNA double helix prefer copying and perform the unwinding of the DNA double helix. And this is initially carried out by initiation proteins. And then you have, um, the protein called helicase, which is an enzyme that breaks the hydrogen bonds, um, along the DNA double helix repair for copying.
Speaker 4 00:14:33 Um, and of course, you don't want the DNA double helix re kneeing during copying. And so you have proteins called single stranded binding proteins, the bind to the single strands of DNA to prevent them from re kneeling. During copying, you have, um, the, um, the DNA polymerases that actually performs the DNA replication. You have the, um, topa isomerase that, uh, alleviates suying ahead of the replication for it because of the, uh, torso stress that is induced by the unwinding. This can result in, uh, these supr cos forming. And we think about an old telephone cord forming a, a super coil. And so this is, uh, alleviated by, uh, a class of enzymes called tosome, which basically, uh, cut one strand. They pass the other strand through the break, and then they reseal the break. And so that's, that's very important. Otherwise, the DNA could break During copying, you have to have, um, uh, a, a protein called primase, which is basically a, um, it's a form of RNA polymerase because DNA polymerase is not able to commence, uh, dino replication itself without a free chemical group known as a three prime hydroxyl group.
Speaker 4 00:15:43 And so that has to be synthesized for it by, um, uh, uh, an polymerase is called a primase because the primase, unlike the, unlike the DNA polymerase, uh, can synthesize, um, um, uh, um, the gra nucleotide without the need for an initial three prime hydroxyl group. You also, um, have, with respect to the, um, the lagging strand, which, so you have two strands of dna, right? You have a, what's called the leading strand and the lagging strand. The leading strand is in a, a five prime to three prime direction, and that's a direction that DNA replication takes place. Um, but the, the other strand is anti-parallel, meaning that it's running the opposite direction. And so that strand has to be synthesized backwards. And so that's done in a discontinuous fashion, uh, by looping this other strand around. And then, um, synthesizing these short r n a sequences called primers, uh, by the primers enzyme, and then extending from those discontinuously dis extending from those in, uh, separately or individually forming what are known as, um, zaki fragments, which are just these short DNA fragments, which then later have to get glued together.
Speaker 4 00:16:55 And there's an enzyme for doing that called liga. And the, uh, primers have to get removed, uh, by RNA excision, enzymes are replaced by, uh, DNA and, uh, and so forth. Um, so if, if any of those, um, components were missing and that's just, um, the peak of the iceberg, then you wouldn't have a system that worked half as well as it used to record as well as it used to, but it would be broken. Um, so for example, um, you, you also have, um, so without the dna, the DNA polymerase, for example, there no replication could take place at all, right? Uh, the RNA primers would be laid down at the organ replication, but there would be no further extension from those primers. Um, if the DNA liga, um, which links the DNA fragments that are produced in the Lani strand, if it were missing, then the newly replicated DNA n strands would just remain as fragments.
Speaker 4 00:17:41 Uh, there's also a sliding clamp, by the way, that clamps the DNA polymerase onto the strand of DNA n to prevent it from falling off during copying. So without the sliding clamp, the, the DNA polymerases will frequently fall off the DNA template, and that would make it too inefficient for replication. Uh, in the absence of the RNA excision enzymes, the RNA fragments would remain covalently attached to the newly replicated RNA fragments. Uh, without the DNA kease, uh, the DNA polymerase would stall because it cannot separate the strands of the template DNA n a ahead of it. And so little or no new DNA n would be synthesized. Uh, if you didn't have the primase, then the RNA primers cannot begin on either the, the leading or the lany strand. And so DNA replication would, uh, not be able to begin, uh, if you didn't have the single stranded binding proteins, uh, then the DNA strands would rene, uh, before they could be copied.
Speaker 4 00:18:33 And so that would also not work. And you also have another enzyme called telomerase, which resizes the end, um, of the, uh, of the chromosome because, uh, because of the, uh, the RNA primer, which, uh, which has to get removed, the, uh, sequences of de the, the chromosomes would, would shorten with each round of replication. And so you have a, a, a rib of protein known as a telomerase, which resizes, uh, the end of the chromosome to prevent shortening with each round of replication. So again, if any of those components were missing, then you wouldn't have a system that worked half as well as it used to record as well as it used to, but it would be broken. And so, um, how are you supposed to buy a step-wise Darwinian pathway put together, um, this sort of, um, system with this higher level objective without knowing where the target is? So that's really the, the, the novel of the issue when it comes to IAL complexity.
Speaker 3 00:19:22 So the, to, just to put this in context, uh, let's, let's talk size for just a second. How large is a typical DNA n uh, molecule in, in nanometers or whatever?
Speaker 4 00:19:33 So it, it, it depends on the species. So for example, for humans, our DNA is about 3 billion base pairs, um, of dna, um, 3.4 billion base pairs of dna. Um, there are other organisms that have bigger sequences. There are other organisms that have shorter sequences, but cur tend to have far smaller, um, sequences of DNA than, than we do
Speaker 3 00:19:57 Into, uh, uh, you know, the, the end of an race or, uh, on aest or something like that. They're very,
Speaker 4 00:20:04 Yeah, I, I, I haven't calculated that, but they're, they're very small. Uh, if you were to take all of the DNA out of your cells and stretch it end to end at you would certainly die.
Speaker 3 00:20:13 <laugh>, <laugh>, pardon me. How many different parts and steps have you counted out? How many were involved in that list of, uh, different proteins, different peptides, et cetera, that you counted out? How many members of that list are there, would you say? Have you counted it or can you guess?
Speaker 4 00:20:38 Of the ones I listed? Yeah. So yeah, I mentioned, uh, polymerases, liga sliding climb. You also have a clamp loader that loads on the sliding climb incidentally. Uh, you have the RNA excision enzymes, you have the DNA helicase, the primase, the single strain binding proteins, uh, um, of which there are multiple, you have the tase enzyme, uh, and so forth. So yeah, there, there's, there's a significant number of these proteins, um mm-hmm. <affirmative>,
Speaker 3 00:21:05 One less is is not just one less, one less is death. So how does, how did this happen evolutionarily? How, how did, how did evolution bring this about?
Speaker 4 00:21:18 Well, this is a big question because, um, DNA replication is of course necessary for self replica ability without rep, without being able to replicate your genome. You, uh, you can't replicate, you can't divide, um, and segregate your genetic material. And so you can't really appeal to natural selection to explain the origins of DNA replication without, uh, pres presupposing the existence of the very thing you're trying to explain. Because DN replication is necessary for self replication, and self replication is necessary for differential survival, which is itself a prerequisite for natural selection. So you can't invoke natural selection to explain the origins of d replication machinery without assuming the existence of the right thing you're trying to explain. Um, and, uh, there's, there's also, um, causal circularity problems. So DNA n um, as, you know, codes for proteins, but proteins are needed to replicate the DNA N and to transcribe it into, uh, messenger RNA and so forth.
Speaker 4 00:22:16 And so there's this chicken and egg paradox, or causal circularity problem. And of course, origins of life theorists often, uh, re respond to this by posit postulating, what's known as an RNA world scenario, which is to say that RNA was the first, uh, information storage medium prior to, uh, the, the DNA protein world. You had an RNA world, and RNA can not only serve as an information storage meeting, but also, um, RNA can fold into three-dimensional, into three-dimensional structure. It can form, um, uh, complementary base pairs with itself, and, uh, and so it can perform some le some, uh, catalytic activity, but the catalytic activity can be performed by r by by ribozymes, is very limited relative to that that can be, uh, performed by protein enzymes. And, uh, the rib engineering experiments have not shown that, uh, ribozymes can completely self replicate. And so that's also a significant challenge to the evolutionary paradigm for accounting for these sorts of systems. So, um, I don't think that the RNA worlds in, and also RNA, of course, is very unstable relative to dna. Um, so it is got an extra two pri hydroxyl grip, which makes it more, um, unstable and also it's single stranded and not double stranded and so forth. And so, yeah, I don't think the RNA world really, um, explains the cause of circularity problem either.
Speaker 3 00:23:38 So I think what you're saying, the question was how did evolution cause this to have that? I, I don't hear you saying that there's an answer to that question
Speaker 4 00:23:48 Exactly. Uh, I I think that, uh, these observations are wildly surprising on the hypothesis that, um, of naturalism of naturalistic evolution, but they're not particularly surprising if we suppose that a mind was involved. Uh, and this is how I would argue that we should conceive of evidence, and this is a classic vision, conception of evidence, that evidence is that what renders a prob a hypothesis more probable probably true than it was previously. So evidence is measured in terms of a likelihood ratio or the probability of the evidence existing, given the hypothesis that's true, um, on the numerator versus on the denominator, the probability of that same evidence existing, given that the hypothesis is false. And to the extent that that's top heavy, that's the extent to which you have evidence for your hypothesis. And when it, and it, it doesn't need to be the case that the evidence is highly predicted on the hypothesis.
Speaker 4 00:24:40 It just has to be better predicted on the hypothesis than it would've been otherwise. And so, in the case of, uh, in order be complex system, like what we see with D NR replication, uh, the, the hypothesis that a mind was involved in the origins of d r replication renders the evidence that we observe not particularly surprising, but that evidence is wildly surprising if we don't suppose that amine is involved. And so you have this, um, overwhelmingly top heavy likelihood ratio that confirms the hypothesis of design as being, uh, very strongly supported by this evidence. And
Speaker 3 00:25:12 This is not the case that we don't know enough, and therefore we must think God did it. We can't, we don't know how it had happened, therefore, we're gonna conclude there was some supernatural agency involved. This is the, this has been an increasingly strong case as we have grown in our knowledge, rather than a decreasingly strong pace.
Speaker 4 00:25:38 Exactly. The more that we've learned, uh, the more, the stronger the design inference has become. And, um, in fact, uh, uh, theism was widely taken for granted throughout most of human history. Uh, in fact, prior to Darwin, the majority of the critics of, uh, Christianity would actually be deists rather than atheists, right? You have the, the deist controversy. Um, and, um, and, um, Darwin came along and he provided a mechanism by which he could allegedly explain away this appearance or illusion of design without, of course, to an actual designer. Now, if Darwin got it wrong, as I contend that he did, then we're back to where we were before, Darwin is Darwin where the, the evidence of design and nature in particular from living organisms is just overwhelming. And in fact, the challenge to naturalism in the case for design has become far more exacerbated or enhanced since the times of Darwin in view of our modern advances in both the life and physical sciences.
Speaker 4 00:26:38 Uh, so we now, um, understand the information basis of life and which was unknown to Darwin. I he didn't even know about genetics at the time, uh, even though, uh, Gregory Mendel was a contemporary, and apparently, uh, he had, uh, Gregory Mendel's work, although he hadn't, uh, read it at the time of his death. And, uh, now we understand the information basis of life. We understand that molecular machines run the show in biology, uh, and so forth. And that world was completely hidden to Darwin. And I think that, uh, it really makes the case for design a thousand times stronger than it was, uh, prior to, to Darwin's, uh, Darwin and, and his origin of species.
Speaker 3 00:27:13 We're, we're close to the end of what we have to discuss here, but I'm wondering if you have anything else you wanna add before we close our conversation?
Speaker 4 00:27:22 No, I, I think, uh, we covered, uh, quite a bit. Um, one, one, uh, additional nuance I'd add to IAL complexity, uh, which I think if, uh, circumvents a lot of the criticisms that are sometimes leveled against the concept. So, uh, if you read the likes of Ken Miller or Nick Mansky or some of the other critics of IDIs complexity, one of the most common criticisms is, and this is true for example, in Nick, Nick Mansky, mark Powell's 2006 nature or paper where they criticize aeros complexity of the material for genome is that some species lack this particular protein component, therefore it's dispensable. And it's not, it, it doesn't contribute to an, a complex system. And the way that I conceive of aerosol complexity is not so much in terms of structural components, but in terms of functions that need to be performed. You can change the identity of the structural components, replacing them with other, either other proteins that perform the same job or by different ways of achieving the same functions. Um, and so it's the, it is the functions rather than the structural components. That's the crucial part of I, you can, you can even have, um, one function being performed by multiple proteins, uh, or you can have, uh, one protein that performs multiple functions, but really the, the, the functional components or the, the, the, or the, the, the functions that need to be performed to achieve this high level objective is more important than the identity of the component itself. That's something, something to bear in mind.
Speaker 3 00:28:42 Good. Well, thank you Jonathan. It's been a treat. Pleasure to talk with you about this, learn some more, uh, your addable complexity, the DNA aspect of it. We appreciate your being here with us on ID the Future.
Speaker 4 00:28:56 Absolutely. Thanks for having me.
Speaker 3 00:28:59 For ID the future. This is Tom d thank you for listening.
Speaker 1 00:29:04 Visit
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