McLatchie: Why Cell Division Challenges Darwinism

Episode 2010 January 27, 2025 00:19:51
McLatchie: Why Cell Division Challenges Darwinism
Intelligent Design the Future
McLatchie: Why Cell Division Challenges Darwinism

Jan 27 2025 | 00:19:51

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Show Notes

One of the most incredible features of cellular life is the capability of self-replication. But can a Darwinian mechanism take the credit for the origin and design of the cell division process? On this episode of ID The Future, host Andrew McDiarmid concludes a four-part series with Dr. Jonathan McLatchie on the intelligent design and irreducible complexity of eukaryotic cell division. In his recent paper on eukaryotic cell division, Dr. McLatchie quotes a Latin expression Darwin uses in his famous book On The Origin of Species to describe natural selection: natura non facit saltus: nature does not make jumps. That’s Read More ›
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Episode Transcript

[00:00:04] Speaker A: ID the Future, a podcast about evolution and intelligent design. [00:00:12] Speaker B: One of the most incredible features of cellular life is the capability of self replication. But can a Darwinian mechanism take the credit for the origin and design of the cell division process? Welcome to I Do the Future. I I'm your host, Andrew McDermott. Well, today Dr. Jonathan McClatchy joins me as we conclude a four part series on the intelligent design and irreducible complexity of eukaryotic cell division. Dr. Jonathan McClatchy is a fellow and resident biologist at the Discovery Institute's center for Science and Culture. He was previously an assistant professor at Sadler College in Boston where he lectured biology for four years. McClatchy holds a bachelor's degree in forensic biology, a master's degree in evolutionary biology, a second master's in medical and molecular bioscience, and a PhD in evolutionary biology. His research interests include the scientific evidence of design in nature, arguments for the existence of God, and New Testament scholarship. Jonathan is also founder and director of talkaboutdoubts.com it's good to have you back, Jonathan. [00:01:17] Speaker A: Great to be here. Thanks for having me. [00:01:19] Speaker B: You're welcome. Well, in this episode we're capping off a series we've been doing on eukaryotic cell division. You've been studying this remarkable process for about a decade now, and you just published a paper in the free open access journal Bio Complexity titled Phylogenetic Challenges to the Evolutionary Origin of the Eukaryotic Cell Cycle. You've also written a number of articles on the [email protected] on the on the general subject and zooming into the specific components. Now, for those of you who may have missed the first three episodes we've done on this, let's do a quick review and then you can let us know what we're going to cover today. Now, in part one, we began by reviewing the basics, the differences between prokaryotes and eukaryotes, the phases of eukaryotic cell division, and the stages of mitosis. Then you discussed how the process exhibits irreducible complexity. Now, I want to make sure everybody's on the same page with that term. Can you remind us what we mean when we say a system exhibits irreducible complexity? Sure. [00:02:22] Speaker A: So in irreducibly complex system is where we have a complex biological system that is comprised of several well matched interacting components that work together in unison to bring about a higher level objective. And this is a significant challenge to evolutionary processes accounting for their origin because such systems appear to require foresight to bring about nitrous Election can only preserve those systems which already serve a selective benefit or utility. It cannot select for some future function. And so by an unguided search, without knowing what the target is, how would you assemble such a system while retaining a selective advantage at every step along the way without passing through any maladaptive intermediate stages? And so this is a significant challenge to evolutionary processes. And it's not only that, but it also supports intelligent design, because intelligent agents uniquely are able to visualize these complex higher level objectives and then bring everything together needed to realize those objectives. And so irredistically complex features are not particularly surprising. Supposing a mind is involved. We recognize that intelligent agents often produce systems comprised of several well matched interactive components that each contribute to the system's function. And if you were to remove any one of the parts, the system would cease to work, whereas unguided processes can't do that. And so in view of that top heavy likelihood ratio, it supports a design thesis over an unguided process. [00:04:03] Speaker B: Yeah. Great. And also in that opening episode, we mentioned the natural limitation of the natural selection mechanism. In your paper, you actually quote a Latin expression that Darwin used in his famous book on the Origin of Species. He used it to describe natural selection. Can you remind us of what that is and what it means? [00:04:22] Speaker A: Sure. So this is the idea that nature does not take sudden leaps, and, and evolution is a process that involves very gradual change over a long period of time through successive incremental stages. Whereas what we actually observe in the fossil record and also at the molecular level are these discontinuous jumps we see most notably in the fossil record in the cumulative explosion, but not limited to the humerun explosion. And then in biology there are examples of this as well. And the example that we're talking about here is the jump from the prokaryotic cell to the eukaryotic cell, and in particular the apparatus involved in cell division. In the eukaryotic cell. [00:05:12] Speaker B: Yeah, natura non facet saltus. Nature does not make jumps. And that's the built in limitation of Darwinian processes. By default, they're stepwise and gradual. And of course, what I like is that Darwin himself acknowledged this test of evolution himself in the Origin. He said if it could be demonstrated that any complex organ existed which could not possibly have been formed by numerous successive slight modifications, my theory would absolutely break down. And you know, we're taking them up on that challenge. That's exactly what we're doing here. We're showing evidence that these biological systems and processes could not have arisen by numerous successive slight modifications. Well, in the second and third episodes of our series, we began to take a closer look at the intricate mechanics of eukaryotic cell division. Part two focused on the mitotic spindle, the structure and function of microtubules, and the roles of various motor proteins in the division cycle. And then in part three, we dove into the checkpoints that are built into eukaryotic cell division. In a nutshell, remind us what the checkpoints do. [00:06:20] Speaker A: Yeah. So the checkpoints that are involved in eukaryotic cell cycle control ensure that the cell is ready to move into the next phase of the cell cycle. So there is the restriction checkpoint, which determines whether the cell is able to commit to another round of cell division. It's also known as the G1S checkpoint. There's also the DNA damage checkpoint that ensures that the cell is able to progress, that there's into S phase, that there's no damage to the DNA. There is also the spindle assembly checkpoint, which determines that the cells are ready to progress from metaphase into anaphase. And in particular, the microtubules or spindle fibers have to be correctly associated with the kinetochores. Otherwise it can result in aneuploidy, which is where you have the misegregation of chromosomes, resulting in the daughter cells having the wrong number of chromosomes. And so the spindle assembly checkpoint is very important for that purpose. [00:07:23] Speaker B: Okay, and today we're going to compare the disparity between prokaryotic cell division and the cell division process in eukaryotes. The Darwinian paradigm would have us believe that the one came from the other. But when you take a close look, there's essentially nothing in common between the two systems. They exhibit different parts and different design logic. Your paper features a two page table presenting an overview of the differences in cell division mechanisms in prokaryotes and eukaryotes. I found that to be quite helpful. Can you briefly lay out just a few of the key differences that make these two types of cell division so different? [00:08:01] Speaker A: Sure. So, in eukaryotes, cell division occurs by a process known as mitosis. At least in the case of somatic cells. Sex cells use a related process known as meiosis. But there are a number of different phases in mitotic cell division. So these are prophase, prometaphase, metaphase, anaphase, telophase. So during prophase, the chromatin condenses into the familiar chromosome structures in which the chromatin becomes visible under the microscope. During prometaphase the nuclear membrane disintegrates and breaks into membrane vesicles. The kinetic ores form also during this stage and become attached to the microtubules that radiate from the centrosomes, also known as the microtubule organizing centers at the spindle poles. Then, during metaphase, the condensed chromosomes line up in the middle of the cell, driven by motor proteins that we've discussed previously, kinesin and dynein, associated with the microtubules. And during anaphase, the chromosomes break up and cystochromatids are pulled to the opposite poles of the cell. And then finally, during telophase, which occurs at the same time as cytokinesis, two daughter nuclei are formed and the chromosomes unravel back into their original expanded chromatin formation. So that's the process of cell division in eukaryotes. Now, the process of cell division in eukaryotes is a universe apart from, from that mechanism employed in prokaryotic cells. That is, in bacterial cells or archaeal cells, they're a universe apart. There's essentially nothing in common, either in terms of the protein components involved or the underlying logic. So bacterial cell division occurs by a process that's known as binary fission. So rod shaped bacteria, such as E. Coli or Salmonella elongate to twice their original length. And this is followed by invagination of the cell membrane and the formation of a septal ring in the middle, and the elongated bacterial cell splits down the middle, forming two daughter cells. And of course, there are variations on this mechanism. So, for example, in Colobacter, no septum is formed and the division is asymmetrical. But as I said, the underlying logic, as well as the protein components, are completely different between those two systems. [00:10:28] Speaker B: Okay. And in your paper, you sought to determine the extent to which one can identify remote homologues of the eukaryotic cell cycle components among prokaryotes. First, what are homologs? And can you explain in simple terms what you found about the homologues between the two processes? [00:10:48] Speaker A: Sure. So homologues are proteins that are believed to share a common ancestor with another protein and are often similar in structure or in amino acid sequence. And what I determined in my paper is that the vast majority of the components involved in eukaryotic cell division, that is in mitosis, do not have homologues among prokaryotes, in particular among the archaea. The archaea, of course, are believed to be closer related to eukaryotes than bacteria. And in Particular among the Asgard archaea, which is a superphylum of archaea, which is believed to be the closest living archaeal relatives of eukaryotes. For the vast majority of the components that were involved in eukaryotic cell division, there are no homologues among prokaryotes. And that's surprising, I think, given an evolutionary perspective, because components that are involved in eukaryotic cell division appear to be eukaryotic de novo innovations that arose after the split between the archaeal and eukaryotic lineages. [00:12:09] Speaker B: Okay, now your paper presents a clear challenge to a Darwinian evolutionary pathway for these two self replication systems. And I want to take a few minutes to unpack that carefully. First, do you find any evidence that these two systems are related through descent with modification? You're saying that there's no homologues or homologues. So is there any other evidence that might connect them? [00:12:32] Speaker A: No, I actually think that this is pretty strong argument against the ancestor dependent relationship of eukaryotes and prokaryotes. I mean, as I've argued in detail elsewhere, the mechanism of cell division in prokaryotes appears to be irreducibly complex. And as I argued in particular in my recent paper and in some recent blog posts on evolution news, the process of cell division in eukaryotes appears to be irreducibly complex. And so how do you go from one irreducibly complex system to another irreducibly complex system without passing through any maladaptive intermediate stages, particularly when all of the or most of the components have to be replaced? And so that's problematic from an evolutionary perspective. Going from one irreducibly complex system to another, keeping everything up and running. And cell division, of course, is absolutely fundamental to differential survival. If you don't have self replicatability, then you have no differential survival and therefore natural selection. So this is absolutely crucial. And given the disparity between those two systems, coupled with the fact that both appear to be irredistibly complex, it seems to be quite problematic for an evolutionary view. [00:13:53] Speaker B: Yeah, yeah. I mean, if they were related and one came from the other, not only would each of the prokaryotic cell division components need to be replaced, but most of the proteins with which they are replaced would need to arise de novo. Now, I want to explain to our listeners what that term means, because it's important here, tell us what de novo means and why. This is a bridge too far for a natural process, meaning that they arose. [00:14:19] Speaker A: Without ancestors that we can identify. So they seem to have arisen from scratch, essentially after the split between the prokaryotic and eukaryotic lineages. There are no, as I've said before, there are no homologues for the vast majority of, of the protein components that are found in mitosis, as I discussed in my paper. And so you not only have to account for going from one irispocomblic system to another without passing through any maladaptive intermediate stages, but you also have to account for the components being completely replaced as well, which is just, in my opinion, it strains credulity. [00:15:02] Speaker B: Yeah, yeah. So you're saying that the available evidence suggests that the proteins associated with eukaryotic cell division arose after the split between prokaryotes and eukaryotes. Why is this important in challenging the claim that both are related? [00:15:18] Speaker A: Well, as I've said, it's difficult, it is extremely difficult to envision going from one system to the other without passing through any maladaptive intermediate stages, and in particular accounting for where all of these new components arose from by an unguided process, an unguided search. And so you not only need to create an entirely new mechanism from scratch, and there's essentially no parallel to the mechanism found in prokaryotic cells, but you also have to replace virtually all the components, and the few that for which you do have homologs in prokaryotes, they have to be repurposed as well. So it just, in my opinion, strains credulity that an evolutionary process could account for that translation transition. [00:16:08] Speaker B: Yeah. Well, if undirected processes are incapable of producing the complex machinery associated with mitotic division, is there any other cause that can? [00:16:18] Speaker A: Well, I think intelligent design can account for this because can account much better for this evidence than an evolutionary process, because intelligent agents can. They have the capacity for foresight, for planning and so forth. And we habitually associate irresistibly complex systems with intelligent agents, with rational, conscious deliberation. And so when we find these sorts of systems in biology, then it's not unreasonable, I think, to infer that a mind is involved in, particularly in the case of such finely engineered and elegant systems such as cell division. [00:17:04] Speaker B: Yeah. Now, here's a question. Are you going to continue to study this in detail or do you think you've reached a level of thoroughness where you're ready to move on to other things? [00:17:15] Speaker A: Oh, absolutely. It's still a topic of particular fascination for me, and I hope to give some presentations, talks, and maybe even write a book at some point relating to the Subject. [00:17:27] Speaker B: Yeah, well, we'll definitely look for that. So where can listeners go to read your coverage of this in detail? I know you've got your paper. [00:17:36] Speaker A: Yeah, so there's the paper, which is open access in the journal Bio Complexity. There's also my blog post, evolutionnews.org and of course this podcast series as well. [00:17:46] Speaker B: Okay. And if by chance listeners have a question about something you've said in this series or they'd like to unpack something with your follow up with something, can they reach you? Are you reachable? [00:17:59] Speaker A: Sure. My email address is jmcclachyiscovery.org okay. [00:18:03] Speaker B: Yeah. So there you have it, listeners. If you want to follow up or you're totally confused and need Dr. McClatchy to rescue you, we are here. That's what we're doing. We're putting this information out and we want you to understand it and be able to share it. So whatever we can do to help with that, we will. And of course, beyond this series, Jonathan, you and I have had quite a few conversations unpacking numerous biological systems that exhibit evidence of intelligent design. I mean, we've done episodes on muscles, on hearing our digits, no, not our phone number, but the origin of our fingers and toes. We did one on the blood clotting cascade, backing up and defending Michael Behe's work. We did a three part series on sexual reproduction and why it's such a spicy problem for Darwinian evolution. That was fun. And we've looked at the life friendly properties of water and sunlight and that doesn't even count our chats about Bayesian reasoning, Bayesian logic and how we can apply it to the cumulative case for intelligent design. So lots of conversations to listen to. You'll find all those episodes and many [email protected] or by subscribing and looking back at the list of episodes on your favorite podcast platform. Well, Jonathan, until next time, I know you're going to be back soon. We've got lots to talk about. You're always putting new ideas out there and new insights. So I'm looking forward to our next chance. Thank you for ID the Future. I'm Andrew McDermott. Thanks for listening. [00:19:36] Speaker A: Visit [email protected] and intelligent design.org this program is copyright Discovery Institute and recorded by its center for Science and Culture.

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