Speaker 0 00:00:00 <silence>
Speaker 1 00:00:05 ID the Future, a podcast about evolution and intelligent design.
Speaker 2 00:00:12 What is the simplest form of life today? Even the simplest single celled organism is an astonishingly sophisticated multi-part system consisting of a cell membrane, ribosomes enzymes, D N A R N A, repair mechanisms, and much more. But according to the naturalistic origins account proposed by many scientists and science organizations, life must have been much simpler in the distant past in order for a biogenesis to work. But how simple can a living cell actually be? Welcome to ID the Future. I'm Eric Anderson, and on today's show, we're joined by Dr. Robert Stadler to talk about the origin of life and the effort to determine the minimal viable cell. Stadler received a degree in biomedical engineering from Case Western Reserve University, a master's in electrical engineering from M I t and a PhD in medical engineering from the Harvard m i t Division of Health Sciences and Technology. He has worked in the medical device industry for more than 20 years, has over 140 patents, and is co-author of the book, the Stairway to Life and Origin of Life Reality Check. Great to have you back on the show, Rob.
Speaker 3 00:01:16 Hey, great to be here, Eric. It's always fun to talk about the origin of life.
Speaker 2 00:01:20 Absolutely. One of my favorite topics. So, Rob, I wanna step back a minute and kind of remind our listeners where we've been in our discussions, we've had a number of conversations about the origin of life and the challenges for a biogenesis. I encourage our listeners to go back and revisit those discussions while each of those conversations can stand on their own, there's an important connection that I just wanna take a minute to emphasize. Indeed, specifically a biogenesis research today is really proceeding from two separate angles. And I'm not talking about, you know, metabolism first, r n a, first membrane first. I'm talking about at a high level, from a standpoint of the theory, the first organism on earth must have been simpler, far, far simpler than what we see in life today. That's sort of a foundational requirement of the naturalistic origin story, because otherwise the theory can't be taken seriously.
Speaker 2 00:02:09 So there's a tremendous amount of effort to find this simplest living organism, or even we might say the simplest self replicator, which is the holy grail of a biogenesis research. And it's imagined that once that simple self replicator is discovered, then the magic of Darwinian evolution can step in and do the rest. Alright, so with that background, uh, there are two ways I would say that one can approach this question. We've talked several times, including last time, about what we might call the bottom up approach to the origin of life. So we start with bare molecules, r n a polymers, and try to come up with a simple self replicator. Today, what I'd like you to ha help us understand more about Rob is what we'll call the top down approach, taking an existing living cell and trying to simplify it down in the lab to the bare bones where it could still survive. Tell us a little bit about that approach.
Speaker 3 00:02:55 Yeah, it's fascinating, really, the last couple seen great progress here and finding the minimal viable living organism, um, and even human intervention to simplify things down, further knocking out genes that, that they're saying are not necessary. And, uh, you know, Craig Venter and his, his group at the Craig Ventor Institute are leading the way here. And, um, you know, they, they published a while ago what they called the simplest form of life, which was, um, they start with a mycoplasma myco, which is a very, very tiny bacteria that you find in the gut of a goat <laugh>. And they simplified it down from 901 genes all the way down to 473 genes. And they called that the J V C I Sin 3.0. And, uh, that was a nice accomplishment, really. But as we would predict, when you take something in, knock it down to to that kind of a minimal, um, life form, it becomes very fragile and delicate. And so they found, you know, that it, it was alive <laugh>, um, but it, it had irregular shapes, you know, it couldn't quite reproducibly form itself in the same shape, and it had vesicles forming in it, and it was called filament, which is when it kind of grows in a long, stringy way. And it doesn't, it doesn't divide, it just kind of keeps growing as a string. So it wasn't, wasn't great <laugh>
Speaker 2 00:04:26 Yeah. Not healthy for sure. Yeah.
Speaker 3 00:04:28 So then they added 19 genes back in there to make it more robust and more like a laboratory study, uh, specimen. So you can argue about whether the genes they put back in are now essential or maybe just nice to have, uh, but they made it more robust and that led to this paper that we're focused on today where they study, you know, how that new, this has 400, uh, 493 genes organism if that's able to actually evolve.
Speaker 2 00:04:59 Right, right. Okay. So we've got this, excuse me, we've got this, um, organism that's in the lab that's being sort of coddled. Tell, tell us a little bit about what it still has, at least in terms of its capabilities.
Speaker 3 00:05:13 Well, it, it has, um, all the things you mentioned. It has, uh, you know, the cell membrane, the ribosomes, R N A D N A repair mechanisms, even, you know, as required to have metabolic damage control. If the metabolism produces bad things, it's able to fix that and get rid of garbage, um, energy harnessing all those foundational features for life are in there in a minimal form
Speaker 2 00:05:40 <laugh>. Yeah. And that's how many, how many nucleotides? Do you know? Approximately how many we're talking about? Yeah,
Speaker 3 00:05:45 It's, it's down to 543,000 nucleotides. Okay. So a little over half a million nucleotides. And of course, we know that the nucleotides in the D N A are not the only information in a cell. There's information all over the place, but that's the easy one to quantify.
Speaker 2 00:06:02 Yeah. So there's still a lot here. We've got over 500,000, um, kilobase or 500,000, uh, base pairs of D N A. We've got all of these capabilities that the cell still has. So, so this wouldn't be Rob something that one would imagine on the early earth. Right. They're still trying to simplify it more and get something simpler.
Speaker 3 00:06:21 Yeah, it's very much so. I mean, this is interesting to us because it provides a kind of a threshold of mm-hmm. <affirmative> what natural processes would need to accomplish. You know, just having basic chemicals bumping into each other and reacting, what would they need to get to before you could say, oh, that's life.
Speaker 2 00:06:39 Yeah. Right. And, and the reason it's able to survive. Let me just emphasize this 0.1 more time, which we've discussed in the past. The reason it's able to survive in this minimal state, even as significant as that is, is because it's being coddled,
Speaker 3 00:06:55 Right? Yes. In order to keep it alive, they have to, it's almost a hedonistic lifestyle. <laugh> it gets, it gets fed everything, uh, on a platter, so to speak. I mean, all sort of pre-digested things. Um, all of the, the cellular building blocks are provided for it in simple form, and it's at the right temperature, 37 degrees Celsius, just like a goat gut would provide, and, and no light. Uh, so that's, that's what it needs to keep on going.
Speaker 2 00:07:26 And the, and the researchers are removing the waste products from the
Speaker 3 00:07:31 Yeah, that's a good point. So it's an obligate fermentor, so it can, it only survives by fermentation, which produces acidic waste, and if you don't clean up the waste, it's not gonna do very well. So every day they gave it a fresh new bath of, of the serum that it needs to survive on.
Speaker 2 00:07:50 Right. Okay. All right. So I just wanna point out that if we're talking about an organism surviving on the earlier earth, it's gotta do all this stuff itself. It can't rely on the researchers and the nice lab conditions to do that. But, uh, you know, fair enough, we're, we're gonna try within the lab conditions to see how we can minimize this cell and get to the point where we can find the, you know, the, the, the minimal viable cell within our lab conditions. At least that's fine. We can, we can, uh, you know, support that as a research effort for sure. So there's a recent paper that came out by, and I hope I'm pronouncing this right, if not, I apologize, Moger gait, Reiser Glass Etal, which is titled Evolution of a Minimal Cell. And this focuses on this top-down approach that we've been talking about and reports an exciting result. They say that this minimal cell, after being disturbed, was able to regain fitness during 2000 generations of evolution, which seems like a pretty big deal and pretty fast. Tell us a little bit about this paper.
Speaker 3 00:08:49 Yeah, so the, the paper is titled Evolution of a Minimal Cell, and it's in the, the journal nature in 2023. And it's, it's open access. So it's pretty easy to just Google what I just said and, and pop it up. You could read the whole thing yourself.
Speaker 2 00:09:03 By the way, is this part of Vent's team or is this a separate group?
Speaker 3 00:09:06 Well, um, it is, it is associated with the j Craig Venter Institute. So he's, he's not an author, but it's part of his institute. Yeah,
Speaker 2 00:09:15 Sure. Okay. So this is continuing some of the research that's been done in the past that we talked about. Yep.
Speaker 3 00:09:20 Yeah, exactly. And so they took this, this very simplified cell and put it in this, this sort of hedonistic lifestyle, uh, for 2000 generations, like you mentioned. And they, they did some good science here by putting the, the wild type, the original mycoplasma, my, which is the one with 901 genes. And they also put that in, you know, in a separate experiment, but in the same kind of growth conditions as a control group to see, you know, what, what's growth like over here versus what it is for the minimal cell. And they define fitness as simply the rate of replication. So forget everything else, all that matters is who replicates the fastest under these specific hedonistic conditions.
Speaker 2 00:10:08 Yeah. And, and let me just, let me just, uh, this is a pet peeve of mine. So <laugh>, lemme just point out this self, um, serving sort of circular definition of fitness has started to receive a lot of criticism, even from some prominent evolutionists, because if you're trying to get an organism that's gonna actually function in the real world, you need to look at the function. And so this simplistic evolutionary view of just saying, well, whatever reproduces the fastest is the most fit is, is just preposterous. But anyway, carry on.
Speaker 3 00:10:40 Well, yeah, you would think that they would throw some challenges at it. Like, can you handle cold? Can you handle basic condition? You know, can you handle Yeah. Kind of toxin thrown in there that, that, that's fitness, I think, uh, part of fitness anyway, but they got that all out of the way and gave it these hedonistic situation and just looked at the rate of replication. So the, the minimal cell starting off at the beginning of this experiment, it took twice as long to reproduce as the wild type original one, and it was, uh, 30% smaller in size for each cell. And, and these are the smallest of cells. We're talking about 400 nanometers as the diameter of these cells. Really, really? That's really small.
Speaker 2 00:11:27 And, and just, just, sorry, sorry Rob. Just to clarify, um, for the minimal cell you're talking about the 493 gene version?
Speaker 3 00:11:33 Yeah, the 493 gene version, they call it J V C I, syn three B, that that's what they compared against the wild type. Yep. So after the 2000 generations, you know, drum roll please, these are the results. The, the minimal cell actually increased its ability to replicate, um, roughly back to where, where it began. So it approximately doubled its speed to replicate, uh, but the cell size didn't increase at all. And now looking at the wild type, the original mycoplasma myco, that one increased its rate of replication 30% more. So you could say it's 130% from where it was, versus it's still faster than the, the minimal type and the, the size of the wild type increased by 80%. So it increased its cell size and its replication speed, whereas the minimal cell only increased its replication speed.
Speaker 2 00:12:35 Okay. So I know you're gonna talk about the comparative here for a minute, but what, what's going on with the regular cell? Why is it, uh, do we know why it's increasing in size and replication speed under these conditions? Well, I
Speaker 3 00:12:46 Think if you put me on a hedonistic diet where I could just lay on a couch and you fed me all day, I'd probably
Speaker 2 00:12:52 <laugh> you might increase in size. Yeah. Maybe
Speaker 3 00:12:55 Replicate more often. Maybe
Speaker 2 00:12:57 <laugh>, that's, that's certainly, yeah. Yeah. <laugh>.
Speaker 3 00:13:02 So that's what happened. But the, one of their conclusions in the paper then is, is the big message is we conclude that adaptation was not constrained by genome minimization. So minimizing genes, throwing out all of that stuff they're saying did not constrain adaptation. It's interesting they use the word adaptation here, whereas evolution is the term they use almost always in the paper.
Speaker 2 00:13:27 Hmm. Okay. So they're, they're kind of mixing their terminology here a little bit. First of all, they were talking about fitness, which is just the sheer replication speed. And then they've said, okay, because the replication speed was able to, did it match the, the wild type or get close to it, or,
Speaker 3 00:13:43 Well, in the end, the, the minimal cell got back to what it used to be, uh, and that's it. But the, the wild type went 30% beyond that as far as speed of replication.
Speaker 2 00:13:56 Okay. But they were impressed that the minimal cell was able to increase its replication speed, which they were referring to as fitness, and now they're referring to that as some kind of adaptation and saying, what, what was the quote again? We conclude that adaptation was not constrained by genome minimization. Yep.
Speaker 3 00:14:16 That's it.
Speaker 2 00:14:17 Okay. Well, that's, that's a little, we could pick that apart maybe, but, but, but go ahead,
Speaker 3 00:14:22 <laugh>. I think it's kind of a, I think it's a generous conclusion. I mean, adaptation, it was constrained in a lot of ways, I think, but it wasn't completely constrained. It's obvious that something changed and so you can give it credit for that, but the cell size didn't increase at all, whereas the wild type increased by 80%. And also this experiment just tested this one set of conditions, uh, it didn't test any kind of real challenge. And also, one last point is that there's no indication in the paper that this minimal cell evolved any of the genes that were stripped out of it. You know, it didn't evolve them back, so to speak.
Speaker 2 00:15:03 Yeah. Okay. That's what I was gonna ask. Whether, whether there was any real new function that was identified or any real new information that was identified, it sounds like they're just looking at the speed of replication. It didn't increase in size, it just got faster. And they're saying, okay, that's, that's a quote unquote adaptation, uh, you know, let's go publish.
Speaker 3 00:15:21 Yeah. And they didn't, I mean, they do give some details on what had changed within the cell, but there's no indication there that a new gene or any new information had entered the genome. It's more actually a devolution is what they have mostly specified in what they found.
Speaker 2 00:15:40 What do you mean by that?
Speaker 3 00:15:41 Well, by devolution I mean that it's genes that are breaking, actually, like there is this one particular gene called F T S Z. And that gene, I would say is non-essential because it wasn't in the original J V C I syn 3.0 that, that one that was barely hanging on. Uh, but it's one of 19 genes that they added back in there to make it a more laboratory studyable specimen. And that gene is useful for, um, uh, helping it to build the membrane as it's replicating. And that gene was, um, particularly hit by these mutations actually with a, either a, a nonsense mutation or a stop coon mutation. So that makes the protein half form instead of fully form in a ribosome. And that changed the f t s zine Z gene. Uh, they actually tested it by prospectively causing that to, uh, an organism to see what it did. And it actually gave it a 14% gain in fitness right off the bat. So much of the fitness gain that they speak of is actually a hit to this one gene ripping it in half, so to speak, and it somehow gave it a 14% fitness gain. Uh, they don't know exactly why, but that's what they found.
Speaker 2 00:17:03 Okay. Let, let me, let me restate just for our listeners, see if I've got this correct. So there's this, uh, this gene called F T SS Z gene, which we know is related to proper membrane formation because of the change from the 473 version to the 493 version of, of this organism. Okay. So we've got this gene that's related to membrane construction. Now in the new experiment, they know at least that this gene was being disrupted in some way, either by a stop code on it, location three 15 or some other change that was affecting this gene. And by disrupting this gene, by disrupting its normal operation, the speed of replication increased, which they're, they're calling fitness
Speaker 3 00:17:52 Yeah. By 14%. So, okay. You wanna call that evolution? I guess you can, but I'd call it devolution.
Speaker 2 00:17:58 Yeah. Yeah. So you're, you're breaking or disrupting this gene and the thing re reproduces faster. Okay. But yeah, I, I see what you're saying. So that's, that's a not a new function as far as we are able to determine, right. It seems to be a disruption, but it does result in faster replication.
Speaker 3 00:18:15 And unfortunately, that's the only gene they really went into depth in, did give some more generic results. And they said that they found that 16 genes in the wild type organism and 14 genes in the minimal organism were also impacted. And they weren't the same, they were different sets of genes, uh, but they didn't go into detail of what had changed and why that mattered, uh, except they threw in a little hint that it had something to do with lipid synthesis. Um, that's about it. So I think there's more work to be done and maybe some assumptions made as to what these changes might, you know, calling it evolution is, I think an assumption here. Mm-hmm. <affirmative>,
Speaker 2 00:18:56 Well, so go back just a second here. When these organisms are in this situation, what, what's their replication rate or the error rate of, uh, replication here?
Speaker 3 00:19:06 Yeah, that's interesting. 'cause this, uh, mycoplasma ides, uh, the original wild type, um, I, I guess you could say it's the, the Guinness Book of Records holder for the, the sloppiest, D n a replicator of, of known living things. It, it replicates d n a and it makes one mistake. So one bad nucleotide out of 33 million that it replicates. And that sounds like incredibly accurate replication to me, but in the world of living things, replicating d n a, that's as bad as it gets. One out of 33 million are mis misplaced.
Speaker 2 00:19:44 Okay. So in, in human terms, if I'm typing a page, uh, what do I have to type out to hit 33 million pages <laugh>, or three, 3 million letter? If
Speaker 3 00:19:53 You, if you took something like more than a hundred novels and you just had to take your, your keyboard and retype a hun over a hundred novels and you made one typo, uh, that would be roughly one out of 33 million characters missed. So that's pretty darn accurate.
Speaker 2 00:20:11 <laugh>. Yeah. Yeah. Sounds pretty good to me too, based on my typing. But, but okay. So you're saying that this is the worst with <laugh>. It's the worst organism we've got.
Speaker 3 00:20:20 And I think it's fascinating to compare this to the bottoms up approach that you mentioned in the beginning where some people think that just chemicals bumping into each other coming together can make r n A and can make self replicating ribosomes or enzymes. And I, we recently had a conversation about a paper from Gerald Joyce's group, and it was, you know, a very impressive R R n A molecule that could replicate other RNAs. And, uh, that thing, just for comparison purpose is that that rib zyme a piece of r n a that's used to replicate other RNAs, it made a mistake in one out of 12 nucleotides. Yeah.
Speaker 2 00:21:02 Well, that's worse than my typing Rob. Well,
Speaker 3 00:21:04 That's why out of 12 is pretty bad typing <laugh>. Yeah. And, uh, you know, they admitted in that paper, this is a quote from the paper, they said the fidelity of R n a polymerization should be considered a major impediment to the construction of a self-sustained r n a based evolving system. Yeah. So this shows where we're at from bottoms up is we have one mistake out of 12 versus the top down approach looking at this minimal cell, it makes one mistake out of 33 million. Mm-hmm. Mm-hmm. <affirmative>. So you see the, the, the gap here between
Speaker 2 00:21:39 Yeah. Between
Speaker 3 00:21:40 What can be done by simple chemicals and what life needs to do.
Speaker 2 00:21:45 Yeah. Yeah. That's, that's a huge gap there. That's an important point, this brick wall that they've hit on the bottom up approach. Okay. So even with this, um, one out of 33 million, which sounds pretty good to us, the authors are suggesting that given the number of generations, I think about 2000 generations you said, and the number of organisms in the culture, that it would be able to sample every position numerous times, right?
Speaker 3 00:22:11 Yeah. They, they claim in the paper that each and every one of the 54, uh, 540,000 nucleotides in the genome would've been mistakenly changed at least 200 times during the course of the experiment.
Speaker 2 00:22:25 Yeah. And then they have this quote that says, neither cell type, I guess referring to the wild in the minimal cell, would be limited by the availability of genetic variation to fuel adaptation. Which if they're just talking, I guess in the very narrow sense of, Hey, in this experiment, all of these nucleotide positions could have been sampled and therefore this, uh, they could have all contributed in some way to this increase in replication speed. Okay, that's fine if that's what they're saying. But if they're, if they're making a broader statement, Rob, that this gives rise to the ability to this organism to go on and adapt and become better and improve, what's your view on that?
Speaker 3 00:23:04 Yeah, well, what, what they're talking about here is in individual independent changes in single nucleotides. And there's plenty of that, plenty of that if you call that variation. But to build up a new gene or a new function, of course, you don't just need independent nucleotides. You need a cohesive information containing structure that has a specific sequence of nucleotides. And that is super hard to achieve by just random, you know, uh, lottery. So I think they might be overstating this here where, um, to make, to make new genes, you gotta have something more than just a lottery.
Speaker 2 00:23:43 Yeah. And again, according to what we're seeing here, there's no evidence that there were any new genes or any new functions in fact created, but just a disruption of this F T SS Z gene, not, not a real impressive, and as you say, maybe even call it devolution, but there's another issue here, you know, even with this disruption of the F T S Z gene, you and I were talking earlier, is that random? Do we know that that's a random change in what was going on there? Yeah.
Speaker 3 00:24:07 When speak people speak of evolution, they speak of random changes and natural selection, but are they really random or is, or is the organism, does it have a built in, um, ability to change the genome to its own benefit, which I would call more adaptation, um, and in preferential ways that can handle stresses mm-hmm. <affirmative> and, and they don't really call that out. It's difficult of course, to show that it was truly random or more of a preferential, uh, change to a genome, but a little bit of evidence that it may have been a preferential change at a certain spot is that that F T SS Z gene often was hit in that location three 15 there. Uh, maybe it was random, but maybe the organism purposely changed things there for its own benefit, which I would call adaptation, not evolution.
Speaker 2 00:25:00 Right. Yeah. Okay. So it sounds like there might still be some additional work needed to pin down whether this change, particularly at three 15, uh, which suspiciously looks like it might be a little bit more than, than non-random, but it sounds like there's more work still to pin that down. For
Speaker 3 00:25:16 Sure. Yeah. Yeah. It's difficult.
Speaker 2 00:25:18 Okay. Well, thank you, uh, Rob, for walking us through this. What's your takeaway from this experiment?
Speaker 3 00:25:23 Well, it's clear that this, this, uh, minimal organism can change. And, and it did. You can't argue that <laugh>. Mm-hmm. Uh, but it seemed to me that a lot of the change came from this F T S Z gene, which I would call non-essential. 'cause it was added back into the already living organism. Other changes were detected, but they didn't really characterize that we kind of discussed this, that what we're seeing here, it's called evolution in the paper. But I, I think that's a stretch. I, it may be better to call it devolution or adaptation than evolution. 'cause there's really no evidence of innovation. There's no new genes or certainly not restoring the genes that were stripped out of this, this poor bug. And, and I would love to see additional experiments where they, they tried different kind of stressful conditions, you know, maybe change the pH or change the temperature or put in some kind of toxin and see, see if it can survive compared to the wild type. So in the end, I'm not too thrilled with their conclusion that when they say that the adaptation was not constrained by genome minimization, yeah.
Speaker 2 00:26:29 It's a very narrow, it's, it's a very narrow, if we were to rewrite that statement, we might say under these very specific lab conditions, the cell was able to, uh, increase its replication rate. I mean, that's, that's the conclusion, right? <laugh>
Speaker 3 00:26:45 Yeah. That's a sober judgment of what they actually found. So back to the big picture then of how this study provides a kind of boundary of, uh, or a threshold, I guess, of where simple chemicals would need to get to in order to call it alive <laugh>. There's certainly more work to be done here, but I feel like over time we're inching closer to defining this threshold. And we're now at 493 genes and 540,000 base pairs of d n a, quite a complex organism. And I would say, you know, this goes along with my belief that a biogenesis is not scientifically tenable, that you just could never have natural processes just physics and chemistry on their own that could get to that level of complexity.
Speaker 2 00:27:32 Yeah. So let me, let me just on that, on that sort of point, big picture here. One of the quotes from the paper that jumped out at me is they said, if we assume that our findings are somewhat general, it appears that cellular functions are robust to streamlining over time, which is desirable when using minimized cells for biotechnology and bioproduction, uh, uh, unpack what they mean by that, and then what's your take on that?
Speaker 3 00:27:58 Well, it's been shown, it's been proven that, um, simple bacteria, they like to actually streamline their own genome. If they don't need a gene, they'll just get rid of it. They'll jettison it because it makes them simpler and easier to replicate, faster to replicate. So out there in the wild bacteria are trying to be as simple as they can be. And so human efforts to try to further simplify that life, I don't think are gonna go very far because the world is already producing minimal things on its own, and they're, and they're doing okay as long as they can survive, they'll keep on doing it. <laugh>.
Speaker 2 00:28:37 Yeah. And, but they're talking about if, if I'm understanding what they're trying to argue here, they're saying that cellular functions are robust to streamlining. I mean, they, they, it seems like they've jumped from faster reproduction to calling that fitness to calling that adaptation. And now they're even saying cellular function is robust. Uh, and, and they, they've kind of done a, I don't wanna call it a bait and switch. I don't know that it was necessarily intentional, but I think their sort of, uh, maybe their viewpoint of how evolution must be working is coloring their view that they're saying, well, we've now got cellular function when in fact the only thing we've seen so far is a disruption of this F T S Z gene. And kind of saying that, Hey, since cellular functions are robust to streamlining of the genome, then hey, you know, <laugh>, you know, this is, this is great. This is amazing.
Speaker 3 00:29:36 Yeah. I think as you'd said before, you, you, you should put a little asterisk on that statement they made and say, under very limited specific hedonistic conditions, we think that streamlining is, is maintaining function, but maybe not when conditions change.
Speaker 2 00:29:53 Yeah. And maybe not even maintaining function. I mean, something's going on to disrupt this F T S Z gene. Okay, it's going faster, it's reproducing faster, but that's probably 'cause they broke something. Um, so anyway, I just, I I found this quote to be a little bit Yeah. You know, you, you, you mentioned when we were talking earlier, sort of junk d n a, you know, the idea that, hey, if, if we're losing genes and reproducing faster that we're evolving <laugh>.
Speaker 3 00:30:18 Right? Right. That's not, not a robust way to get things done. Right. <laugh>,
Speaker 2 00:30:23 <laugh> not, not a recipe for progress. Okay. Any, any final thoughts, Rob?
Speaker 3 00:30:29 No, I'm just, uh, very excited to see more work like this come out because it really does help to define this boundary of, of minimal life. And I think it helps to clarify the great challenge that a biogenesis has to face.
Speaker 2 00:30:42 Yeah. And I, and again, I, you know, for our listeners, um, I wanna emphasize we're not, you know, I, I'm laughing a little bit at the conclusions here, but I wanna emphasize that this is good work that's been done. We're not criticizing necessarily the, the, the fact that they're working on this. This is exciting research. We wanna see more of it. But the conclusions and the way that this is spun as some kind of, you know, great triumph for evolution and a biogenesis is, is really, I, I think not supported by the facts.
Speaker 3 00:31:11 Agreed. Yep.
Speaker 2 00:31:12 Well, thanks Rob for being with us today to help us understand more about the minimal cell. This was fascinating. Thank
Speaker 3 00:31:17 You. My pleasure.
Speaker 2 00:31:18 Thank you for listening to this episode of ID The Future. To learn more about the Origin of Live, visit
[email protected] or on your favorite podcast app. And as always, consider sharing a link with a friend. For ID the Future, I'm Eric Anderson. Thanks for listening.
Speaker 1 00:31:37 Visit
[email protected] and intelligent design.org. This program is Copyright Discovery Institute and recorded by its Center for Science and Culture.
