[00:00:04] Speaker A: Id the Future, a podcast about evolution and intelligent design.
[00:00:12] Speaker B: Welcome to id the future. Im your host, Andrew McDermott. Doctor Jonathan McClatchy is back with me today to discuss the engineering elegance and irreducible complexity of the process of bacterial cell division.
Doctor McClatchy is a fellow and resident biologist at the Discovery Institutes 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 bachelors degree in forensic biology, a masters degree in evolutionary biology, a second masters degree in medical and molecular bioscience, and a PhD in evolutionary biology. His research interests have included the scientific evidence of design and nature, arguments for the existence of God, and New Testament scholarship. He's also founder and director of Talkaboutdoubts.com. jonathan, welcome.
[00:01:06] Speaker C: Great to be here. Thanks so much for having me back.
[00:01:10] Speaker B: Now you're a resident biologist and a fellow at Discovery Institute center for Science and Culture. And as such, one of your duties is reporting
[email protected]. on on the evidence for intelligent design. And truly, it's been a pleasure to host you regularly here on the podcast so that we can unpack some of your articles. It's been a lot of fun. We've done episodes on the design and irreducible complexity of the bacterial flagellum. We did a three part series on sexual reproduction and how much of a headache it is to explain through evolutionary processes. We've also discussed the intelligent design of muscles and our system of hearing. And today youre here with me to discuss another design system in biology that exhibits evidence of irreducible the process of bacterial cell division.
Now, first, id like to start by defining irreducible complexity for those listeners who may not be as familiar with the term. It was coined by biochemist Michael Behe in his 1996 book Darwins Black Box. The idea stems from a criterion of failure that Charles Darwin himself offered up regarding his theory of evolution.
These are Darwins words. 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 well behe defining the term irreducibly complex as referring to a single system composed of several well matched interacting parts that contribute to the basic function wherein the removal of any of those parts causes the system to effectively cease functioning. And since natural selection can only choose systems that are already working, 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 on.
Behe also noted that as the complexity of an interacting system increases, the likelihood of natural selection producing it through an indirect, circuitous route drops precipitously. And of course, the more systems we can identify as irreducibly complex, the more we can say that Darwin's own criterion of failure has been met. Richard Dawkins has said that if evolution is not gradual, it ceases to have any explanatory power at all.
Jonathan, what would you add to that to help us better understand irreducible complexity?
[00:03:38] Speaker C: Yeah, so irreducible complexity is basically the argument that there are certain systems in the cell that require multiple different interacting components that have to be well matched one to the other in order to perform the basic task of that system. And if you are missing any part of the system, then the system ceases to work. And so this is a challenge for a blind, undirected process to account for irreducible complexity systems. Because how do you select for each step along that pathway without knowing where the target is and without having a selective benefit to select for at every step along that way, you have to pass through maladaptive intermediates to arrive at that complex endpoint. And irrespective of complexity, I think is not merely a challenge to evolutionary naturalism, but it's also a positive argument for intelligent design as well. Because intelligent agents uniquely the ability to visualize a distant complex endpoint and then bring everything together needed to realize or to actualize that endpoint or that goal, that objective, whereas unguided natural processes aren't able to do that, they don't have the capacity to visualize complexity or distant complex endpoints or higher level objectives. And so in light of the top heavy likelihood ratio where supposing design is involved, it's not particularly surprising that we'd find irreducibly complex systems. Whereas supposing that no design is involved, it's wildly surprising that we'd find irritable complex systems. It tends to confirm quite heavily the design thesis.
[00:05:25] Speaker B: Yeah, beautifully put. And I like your reminder that it's not just a negative argument showing the limits of a darwinian process, its also a positive argument showing an intelligent design process in action. Well, in order for a bacterial cell to divide, it must initiate a process of cell wall breakage and resynthesis to allow for the division. Now they say breaking up is hard to do. Well thats even true for, you know, little minute bacteria because if something goes wrong, it can result in cell death, as you note in your article. Lets start with the severing or breakage of the cell wall. Tell us how bacterial cells go through controlled breakage to facilitate that cell division.
[00:06:06] Speaker C: Sure. The peptoglycan cell wall is a rigid structure that surrounds and protects the mercurial cell, and it confers upon the cell shape and structural integrity. As the bacterial cell prepares to divide.
The cell wall has to grow as the cell elongates in preparation for division. And in rod shaped bacteria like salmonella or escherichia coli, this takes place at different locations, different points along the cell. Whereas in caucus shaped bacteria like Staphylococcus, for example, the cell wall grows outward from the Fitz ring in opposite directions. The Fitz ring is what polymerizes around the division septum during cell division and cell wall growth requires the controlled cleavage of the existing peptoglycan layer. The cell has to grow, and that has to be accomplished by the controlled breakage of the cell wall. To facilitate that elongation.
The beta 14 glycosidic bonds that link the n acetylglycosamine and the n acetal muramic acid get hydrolyzed by enzymes that are known as autolysins. And these have to, of course, be very carefully controlled and regulated because otherwise it can result in programmed cell death or apoptosis, which, obviously you want to avoid. And so there are specific regulatory mechanisms that guide the localization of autolysins to the site of cell division. And these regulatory mechanisms ensure that the autolysins are only targeted to the appropriate region of the cell. These autolysins basically bind to the peptidoglycan at the site of division. They catalyze the hydrolysis of the peptide cross links within the cell wall. This cleavage weakens the peptaglycan at the division side, and this allows the cell wall to undergo controlled breakage. The gaps then get filled in with additional cell wall material.
[00:08:09] Speaker B: Okay, now, following that breakage process, bacterial cells have to resynthesize the cell wall to allow for the cell division process to complete. Tell us about that part of it.
[00:08:21] Speaker C: Sure.
The first stage when we're remaking the cell wall is the formation of the peptoglycan precursors.
A chain of five amino acids, a pentapeptide is added to n acetalmoramic acid, and n acetylglycosamine is subsequently attached to the end of the n acetal muramic acid, and the result is a peptidoglycan precursor.
There's a molecule called bactoprenyl, which is extremely hydrophobic, and it's embedded in the inner cytoplasmic membrane and its role is to shuttle the hydrophilic peptidoglycan precursors from the inner side of the membrane, where they're synthesized, to the outer side of the membrane, where they're needed for the assembly of the cell wall. And this protein back to pranil is essential. It's absolutely critical because the hydrophilic precursors cannot easily traverse the hydrophobic membrane on their own once this protein, bacterpranyl, arrives at the paraplasmic space.
In gram negative bacteria, it's a region between membranes or the cell exterior. In gram positive bacteria, it transfers the peptidoglycan precursors to the peptidoglycan assembly site and their glycosyl transferases. And penicillin binding proteins, which are also known as transpeptidases, utilize these precursors to build the glycans end chains and cross link them to provide the cell wall with stability and strength.
The penicillin binding proteins are responsible for catalyzing the cross linking of the peptide side chains between the diaminopimelic acid and d alanine on adjacent peptides.
In gram positive bacteria, cross links typically occur from an a lysine to a d alanine of adjacent peptides. At the end of the peptoglycan precursor, there exists initially 2d alanine residues, but one gets removed during the reaction, leaving one in the final molecule. In E. Coli, a specialized penicillin binding protein known as fits I is the key player in transpeptidation at the septum and localization of this protein. Fits I to the septum itself requires an intact n terminal membrane anchor in addition to the division proteins. Fits z, fits a, fits q, fits w, and fits lithe.
[00:10:48] Speaker B: Okay, so a very complicated process that is happening, and you can't really have the breakage without the resynthesis, can you? I mean, you have to have both at the same time.
[00:10:59] Speaker C: That's exactly right. And this is why this is such a significant challenge to an evolutionary account of how such a complex system could have come to be. Because absolutely critical to cell division and virtually all bacteria is the ability to resynthesize peptoglycan. And the mechanism of action of the beta lactam antibiotics, which include penicillin, cephalosporins and monobactams, is to interfere with the peptoglycan cross linking. And as their name implies, penicillin binding proteins are the target of penicillin drugs, which results in them losing their enzymatic activity. And the activity of the autolysons weakens the at the cell wall to such an extent that the cell lies or bursts open, and because they're not able to rebuild that cell wall in a coordinated fashion, because the penicillin binding proteins which perform the cross linking have been interfered with.
Some other non beta lactam antibiotics, such as lactavisins, have a similar mechanism of action, and antibiotics may also target cell wall precursors. For example, the antibiotic neeson associates with the cell wall precursor lipid two and lockshellen in a stable complex, and thereby effectively inhibits the peptidoglycan synthesis cycle. But all this is to show that how crucial it is that the bacterial cell can resynthesize the cell wall in a coordinated way after its severing by these very tightly regulated autolysin enzymes. So, I mean, consider the following two observations. So firstly, critical to the elongation process is the severing of the peptoglycan cell wall by the autolysons. And critical secondly to cell viability is the resynthesis of the peptic glycogen cell wall. So these processes have to be very highly coordinated. So if you have the mechanism for severing the cell wall coming to be without simultaneously having a mechanism in hand to rebuild the cell wall, then the cell would not survive the division process. So both mechanisms have to arise together. And this is in fact an example of what I would call irreducible complexity on steroids, because cell division is absolutely crucial for differential survival, which of course is a requisite for natural selection. And so you can't really get off the ground without assuming the existence of the right thing you're trying to explain, namely a self replicating cell.
[00:13:38] Speaker B: Yeah, that makes sense. Well, some have claimed that the breakage process may have been co opted into the cell division process over time. What's wrong with that idea?
[00:13:49] Speaker C: Yeah. So on this objection, you might have a situation where the mechanism for repairing the brakes in the cell wall rose first and then that became co opted into the cell division machinery.
But this really doesn't work, because without being able to sever the cell wall, there could be no division. As I said before, there would be no differential survival and by extension there would be no natural selection. So you don't even get evolution off the ground until you have a self replicating molecule or a self replicating cell.
[00:14:17] Speaker B: Yeah, yeah. So co option, not an option here. Well, virtually all bacteria conduct these processes as part of cell division, but there's one notable exception that you note in your article, and that's mycoplasma. Tell us about that and whether it's relevant to the argument that these processes exhibit irreducible complexity.
[00:14:37] Speaker C: Yeah. So the process of severing and rebuilding the cell wall is critical to cell division. In almost all bacteria, there are a small handful of exceptions. So mycoplasma doesn't have a cell wall. But this has little relevance to accounting for the origins of the mechanism of severing and rebuilding the peptidoglycan in those species that do possess a cell wall. And as, as soon as the cell wall, which is a rigid outer layer that provides structural support to the cell rows, there would need to be a mechanism for remodeling and splitting it to allow the bacterial cell to divide into two daughter cells. And moreover, mycoplasma species are obligate parasites, so they dwell in osmotically protected habitats.
And furthermore, in place of a cell wall, they typically have sterols in their cytoplasmic membrane, which imparts to them greater rigidity and strengthen.
[00:15:32] Speaker B: Okay, now you write that these processes, the severing and the resynthesis of cell wall during bacterial cell division, require foresight. And I want to dwell on that word, foresight, for a few minutes before we close here today. Give us your definition of foresight and tell us, are evolutionary processes capable of foresight?
[00:15:51] Speaker C: Yeah. So, foresight is the ability to visualize a distant, complex endpoint and natural processes. Evolutionary type mechanisms don't have the ability to look into the future and retain particular components or functions or systems in view of some future utility. It's going to work now, and if it doesn't work now, is not going to be retained by natural selection. Whereas intelligent agents have the capability, the unique capability, of visualizing distant, complex endpoints and bringing together all that is needed to actualize or to arrive at that complex, higher level objective.
So, that is what we mean by foresight. And foresight is indistinguishable from intelligence. And so, as soon as you have a process, such as irreducibly complex systems in biology or embryogenesis, where you require foresight to visualize going from a zygote fertilized egg to the final form of the organism, obviously, you have a process of cell division and differentiation specification, and that requires that you have a goal in mind that you're headed towards. Obviously, if you only get halfway across embryogenesis, then you're not going to have a viable organism. So that's another example of something that requires foresight. Another example would be apoptosis, which is a mechanism during embryo development where our digits form by programmed cell death between our digits and that's how our fingers and toes emerge during embryogenesis. And of course, that has to be very carefully controlled and regulated and requires a process of foresight. How would natural selection select for a process involving cell death without knowing what the purpose is or knowing what the target is? So, foresight, I think, is when we see complex systems that require foresight to bring about. I think that's a very powerful evidence of design and a very strong challenge to naturalistic evolutionary accounts.
[00:18:03] Speaker B: Yeah, indeed. Well, and at this point, I want to remind listeners that one of our colleagues has written a whole book on how the chemistry of life reveals planning and purpose. It's called foresight, by brazilian chemist and professor doctor Marcos Eberlinda. In a chapter on bacteria, bugs and carnivorous plants, Doctor Aberlin reminds us that bacteria are often seen as rudimentary forms of life, but one look at their molecular structure is enough to convince us otherwise. Bacteria are extremely sophisticated, fully equipped with many exquisite molecular machines.
So if you're ever tempted to think, why are we talking about bacteria? I mean, who cares about tiny bacteria? Whats that got to do with me? Well, the idea is that even if the simplest forms of life exhibits stunning complexity and engineering prowess, all the more so do we. And that complexity in design demands an adequate explanation. We can tell an evolutionary just soul story, or we can acknowledge the limits of darwinian processes and study living things as products of engineering and foresight. And in his book, Eberlein encourages us to dip a toe in the ocean of ingenuity, ingenuity that in our universal experience is wedded to a powerful, unique. Sorry, let me resay that last sentence there.
In his book, Eberlin encourages us to dip a toe in the ocean of ingenuity. Ingenuity that in our universal experience is wedded to a power unique to intelligent agents. And that is foresight. Jonathan, closing words on this topic today.
[00:19:38] Speaker C: Yeah, this is just one example of many hundreds or thousands of systems that we could discuss, which exhibit irredistic complexity and point to the necessity of foresight to explain their origin, which of course, is going to be indistinguishable from a mind an intelligent agency. And so, yeah, I totally second your recommendation for Marcus Eberlin's book on foresight. I'd also, of course, recommend all of Behe's and books. Darwin's black Box is a great introduction to the subject of iridespa complexity, and there are many other great resources. Secrets of the cell. The video series with Michael Beakey is also an excellent good place to start.
[00:20:20] Speaker B: Yeah, yeah. And I'm looking forward to unpacking more of the irreducible complexity of various biological systems with you in the future. Thanks for stopping by today, Jonathan.
[00:20:30] Speaker C: Thank you.
[00:20:32] Speaker B: Well, we'll include links to Jonathan's article on bacterial cell division, as well as Doctor Aberland's book foresight in the show notes for this episode. And I'll even throw in the secrets in the Cell series that Jonathan just mentioned. Great video series, unpacking Doctor Behe's central arguments, so all that's
[email protected]. and of course, you can find more of Doctor McClatchy's writing and his
[email protected]. and that's spelled Jonathan McClatchy McLhouse atchie.com well, for ID the future, I'm Andrew McDermott. Thanks for listening.
[00:21:12] Speaker A: Visit
[email protected] and intelligentdesign.org dot this program is copyright Discovery Institute and recorded by its center for Science and Culture.
