[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. I'm your host, Eric Anderson. And today I'm continuing our why It Matters series with the second half of my conversation with Dr. Scott Minik. Previously, Dr. Minik shared his personal journey to intelligent design and why it matters to him to continue sharing the evidence for design in the world. As we talk, Dr. Minick shares how he became involved in reviewing the results of the famous long term evolutionary experiment of Richard Lenski and how he and his colleagues conclusively demonstrated that the implications of this important experiment were not as the supporters of Darwinian evolution had claimed. We now join the conversation as I asked Dr. Minnick what advice he would give someone who is sitting on the fence about intelligent design.
What advice would you give to someone who maybe is sitting on the fence about intelligent design or has heard about it? Not sure what to make of this.
[00:00:58] Speaker A: Read both sides. You know, go deep. I think, you know, there's always a challenge and you have to keep an open mind. I remember an instance in 2004, you know, somebody slipped a Nature article under my door. I came into work in a lab about 10 o' clock and there's this paper on the floor of my office and it was from Lensky's lab, you know, where they had this program of IDA to show how information could be generated naturally. And you know, I read it, I read it carefully and I thought, okay, you know, maybe they've done it and. But then you could, you know, there are arguments against it that are good. But I started following that work and following his long term evolution experiments. And when he, when he got a mutant, it was growing on citrate.
I thought, no way, you know, I mean, I wasn't questioning that he got it, but it wasn't, you know, it wasn't some contingent mutation dependent upon all these neutral or mutations to begin with, you know, that couldn't be repeated, trained by the person that discovered that E. Coli could grow on citrate anaerobically. You know, there's Jacob Stokes that came out of Van Neal's group and in Stanford. And so I thought, okay, well, we'll repeat that work and see if we can come up with a better argument. And I think we did.
[00:02:25] Speaker B: Did you think when Linsky had reported that he had in fact shown a legitimate significant gain in function or were you kind of skeptical when you.
[00:02:34] Speaker A: No, no, I knew that E. Coli could grow on citrate anaerobically. It was just he somehow activated the transporter aerobically in fact, I bet James Foster in the biology department that was part of Lenski's beacon group, that when Lenski figures out what happened, you know, he's just got a promoter fusion with the anaerobic transporter. You know, what was more subtle was he had to have two mutations. He had to get the transporter activated. That's easy to do. Gene duplications are the most common mutations that occur.
But there was a defect from the very beginning in the E. Coli B that he chose to use. It can't grow on succinate, so it had acquired a mutation. Probably in the origins of its application to molecular biology by Lurie and Delbruck back in the 40s. It had a five base pair deletion and a gene required for succinate utilization. And so they had to get a suppressor of that for.
It's a sense that citrate, the transporter you transport in citrate, which is six carbons, but it's an antiporter, you shunt out a four carbon dicarboxylic acid, succinate or oxaloacetate. And to really efficiently grow and succinate, you've got to be able to capture those four carbons that you ship out when you break citrate. And you know, E. Coli B can't do that because of the mutation that it had had from the very beginning. When his experiments, once his experiments started, we did our experiments in E. Coli K12 which didn't have that defect. And we could repeat citrate utilizers very easily and show why you couldn't get them.
[00:04:17] Speaker B: Yeah, so I want to dive into this just a little bit because this is a very interesting, you know, of course the Lenski's experiment, the long term evolutionary experiment has been touted as one of the great evidences for what evolution can do. And in fact I would say Lenski's experiment is a really fascinating experiment. It's been, you know, hats off to them for doing this for so many years.
[00:04:37] Speaker A: Oh, I agree.
[00:04:38] Speaker B: Keeping at it. But when this came out that there was a strain that could metabolize citrate in the presence of oxygen, I think there was a lot of press that hit about how this was a new sort of gain of function. I don't know if they use that terminology, but a new feature, a new capability and there was even a hint that maybe we're seeing an incipient species was I think the term that was used at one point.
[00:05:01] Speaker A: Right, right, yeah.
[00:05:02] Speaker B: But back us up just a little minute. So E. Coli can metabolize citrate, generally, as a general.
Has that capability, right?
[00:05:10] Speaker A: Oh, yeah. It makes citrate. It has a citric acid cycle. You know, it's essential for.
[00:05:15] Speaker B: And so why is it not normally doing that? In the presence of oxygen, it can't
[00:05:20] Speaker A: transport citrate into the cell. All right, so if. If citrate were the only carbon source available, it wouldn't be able to use it because it just can't get it into the cell. It can make it in the cell. It can metabolize it inside the cell if it gets in. But that's the problem.
You got to get it inside the cell.
[00:05:39] Speaker B: Okay, and so then take us through what happened in Linsky's experiment that you guys were able to later duplicate more quickly. What happened there.
[00:05:47] Speaker A: So he. At 32,000 generations, you know, he noticed a blip in one of the cultures in terms of its density of organisms present, small satellite. I think they might have missed it. They mentioned they might have missed it at first. But then at 30, I think 33,000 generations, you had a major increase in cell numbers. And these are growing on a very low level of glucose.
So citrate has always been used in traditional, what we call minimal defined media for E. Coli as a chelator for iron and other metals. But E. Coli couldn't grow on it.
[00:06:28] Speaker B: Okay, so for those of us who aren't. Aren't microbiologists, Scott. So in. In the. The medium in which the cells are growing, there is citrate and glucose. Right? Is that what's going on?
[00:06:38] Speaker A: Right, right, right. And that's by tradition.
[00:06:41] Speaker B: Yep.
[00:06:41] Speaker A: He had enough glucose present that they could go, you know, divide six or seven times and then stop. And so it's a very low level of glucose. Citrate was just probably in there, but for no reason other than that's the recipe for the medium. And then E. Coli figured out how to, as Lenski would say, access this lemony dessert.
Okay. But anaerobically, E. Coli does have a set of genes that are activated under anaerobic conditions to transport citrate into the cell.
So anytime you have a gene in the chromosome that's under differential regulation, you can get overrides pretty easily. And that's essentially what happened. It was, if you think of it, you have a single copy of the gene. Any gene is a little leaky, so you get a little bit of RNA transcribed, a little bit of protein made, you know, but it's pretty highly controlled. But if you duplicate that gene and then duplicate it again, and duplicate it again. So now you're increasing the number of copies, and these are pretty common mutations in bacteria. You're making your more and more leaky. And so if citrate's out there, it's going to be advantage for those few cells that are duplicated in that region.
Right. Now if you shift, you know, as he did every day, every 24 hours, you took that sample, that culture and put it back into glucose media. Well, now it's a fitness burden. You've got extra chromosomal, extra DNA, and that's a burden. So you're just going to recombine it out.
[00:08:14] Speaker B: Yeah.
[00:08:15] Speaker A: So it's a reversible mutation. You expand that region, you collapse it. Expand it, collapse it. But on the rare occasion that happened at 33,000 or 30,000 generations, that recombination out happened to hook the transporter up to a gene promoter that's normally expressed aerobically. Right. So now you've got, you've got your transporter being made all the time, and now it's just, you got to recover the succinate that you're using.
[00:08:43] Speaker B: So just again, for sort of a slave, folks, to restate. So E. Coli. A has the ability to utilize citrate. B has the ability to ingest or transport citrate across the membrane, but that is normally turned off in the presence of oxygen. Right?
[00:09:00] Speaker A: Right.
[00:09:01] Speaker B: Yeah. Okay.
[00:09:02] Speaker A: Right.
[00:09:02] Speaker B: So you've got a switch that says, yeah, bring in citrate, but don't do it. Now we're in the presence of oxygen, don't do it. But if we're in an anaerobic situation, go ahead and turn on that transport.
[00:09:13] Speaker A: Right, right.
[00:09:14] Speaker B: Okay, so, and then did the, did that switch get broken, so to speak, or was it just an extra copy that it got.
[00:09:21] Speaker A: It got fused to another gene during a recombinational reassortment process.
So it's just like you hook it up to a light switch that's on all the time instead of off when oxygen's present.
[00:09:36] Speaker B: Yeah. So this is like me, you know, I've got this light bulb out on my porch, Scott, that, you know, it's got a switch that says don't turn on in sunshine.
[00:09:46] Speaker A: Right.
[00:09:46] Speaker B: So this is like me coming out one day in the middle of a bright sunny day and seeing that the light is on and saying, wow, it's developed a new feature.
It stays on in the presence of sunshine. But what happens is the switch isn't working properly.
[00:10:00] Speaker A: Right, right. Yeah, you broke the switch. That's a good analogy.
[00:10:03] Speaker B: Broke the switch. Yeah, exactly. Okay, so then you're looking at this and you're like, no, this isn't a new species. This isn't particularly surprising. We can do this faster. Right. So how did you guys go about this experiment?
[00:10:15] Speaker A: Well, we did it in two ways. The first one was we just took E. Coli K12 and threw it in citrate as a sole carbon source and just put it on the shaker, aerated cultures. And sure enough, in 20 days you get a bloom and you analyze them, you sequence a genome and it's the same class of mutation that Lenski found.
[00:10:37] Speaker B: Okay, and how many generations would that be in 20 days?
[00:10:39] Speaker A: It was anyway from anywhere from nine to 100. And we did this 40 odd times, so.
[00:10:46] Speaker B: Oh, wow. Okay. So instead of 30,000 plus generations, this is 100 or less.
[00:10:51] Speaker A: Oh, yeah, yeah.
It's pretty easy to do. And what was interesting was, you know, this is a. It really addressed a fundamental question that Darwin had, was there's a strength of selection cause the frequency and the type of mutation that you generate. And he thought it would. And Lenski even published that this was his hypothesis that if you have a weak selection, organisms have time to figure out a solution around the problem that's going to be better than if you just put it like we did through the cells. And a strong selective. Either you're going to figure this out or die.
And E. Coli came up with the same solution both times.
[00:11:33] Speaker B: It's a pretty limited repertoire, and it's partly because it's a solution. I'm going to put that in air quotes even Scott, because we're breaking a regulator, right?
[00:11:42] Speaker A: Right. Yeah, yeah. There's one solution to the problem.
[00:11:46] Speaker B: Yeah. Okay, so you guys, that was one way you did it. And what was the other approach?
[00:11:50] Speaker A: The other approach was we repeated Lenski's experiments the same way and we use the same media and the same volume. But instead of transferring every 24 hours, we figured that there were gene duplications going on and that to allow these to be captured, to get a promoter capture, we transferred every week.
So we had glucose and citrate in the media. The organisms would grow on the glucose. And then we just gave time for those gene duplications to occur. But we would transfer once a week instead of every day.
And we got them after the second transfer, second week, boom, there they were.
So it just shows that you're dealing with a dynamic.
It's a reversible type of mutation that is kind of subtle until you really sit down and look at what's going on genetically.
[00:12:43] Speaker B: Right, okay. And it's taking advantage of capabilities the cell already had. It's not creating a new species or a new type of organism or anything like that.
[00:12:51] Speaker A: Right, right. Yeah.
[00:12:53] Speaker B: Okay. What was your. Did you reach out to Linsky? I know you guys published some stuff. Did you have any response on your work?
[00:13:00] Speaker A: Yeah, he wrote something on his blog that the work was good, but he questioned the motives of us.
[00:13:06] Speaker B: Questioned your motives?
[00:13:08] Speaker A: Yeah. Which was kind of bizarre.
[00:13:11] Speaker B: Your motive is to figure out what's going on and understand this system. Right?
[00:13:17] Speaker A: I mean.
Yeah, yeah. You know, and I think if you strip away citrate.
Lenski's experiments are great. You know, they've been going now for what, probably over 80,000 generations. That's approaching nearly 2 million years equivalent of human evolution.
But the bottom line is overall E. Coli hasn't generated anything new. And these are 12 parallel cultures. They've jettisoned anywhere from 2 to 4% of their chromosomes. So they're getting rid of stuff they don't need. That speeds up the generation time. It gives cells an advantage.
Six of the cultures develop mutations in the editing function, DNA polymerase. So they were making, you know, they have hyper mutational rates which can give you an advantage in terms of your mutating faster and. But in the long run it's not an advantage because you're just going to acquire too many mutations and that's the road to extinction.
[00:14:18] Speaker B: Yeah. Heading towards disaster. Yeah.
[00:14:20] Speaker A: Right. So.
[00:14:21] Speaker B: Well, and that's what I love about his experiment. I mean, it's, it's a, you know, one of the first real. I mean, there's been a lot with fruit flies, of course, but this is the first real long term, tens of thousands of generations to see what evolution can actually do. And pretty discouraging for their Darwinian story.
[00:14:39] Speaker A: Right. Except for the citrate. And Dawkins spent almost a whole chapter, you know, lauding the citrate results in his book Evolution the Greatest show on Earth. You know, this is the type of experiments that creationists would hate. You know, this is what Darwin predicted and I think that's just disingenuous. As you know, I love the experiment and I just disagreed in terms of the interpretation of.
Of citrate.
[00:15:05] Speaker B: Yeah, yeah.
[00:15:06] Speaker A: I think there's one thing that, you know, when you talk about the authority of science that I've seen time and time again in my career that, you know, when the authority makes a decision, it's not always necessarily correct. In 2003, I don't know if, you know, I was contacted by the Defense Intelligence Agency asking if, you know, I had any graduate students that had military experience. And I said, no, and why? And who are you and why are you asking? And they were trying to get groups together to go into Iraq to look for biological weapons. And I ended up volunteering, and I thought for the right reason, because Colin Powell said they captured these mobile weapons laboratories, that Saddam was brewing this stuff. He'd reactivated his biological weapons program. And so I got over there, and they asked me to inspect these weapons trailers, right? And I was one of two civilians in our group, and our detachment commander was a Marine colonel. And I said, well, you know, Colonel Bohannon, why do you want to send me out there to look at these things? I mean, you've already made the call. Colin Powell went before the UN this is a smoking gun. He said, well, we just want a couple more eyes on them, so why don't you go out and look at it? I was out there for 15 minutes on both these trailers, and I had no buy. I mean, I was biased to think that they were weapons trailers. I mean, they were fermenters, because I knew some of the people that had been on the first call. And I started looking at these and saying, wait a minute. This isn't a fermenter.
There's no spargers, there's no system to aerate. There's no sample ports. There's no harvesting equipment. You know, this is nuts. And the back of these trailers had these, you know, racks for cylinders, gas cylinders. And I wrote up a report that night when I got back to my quarters and put it through the zipper net, the high security thing to the CIA and. And just listed all the reasons why I didn't think these were fermenters. And all chaos broke loose. Bohannon was in my. Pounding on my door at 6am the next morning, saying, swearing at me as only Marines can do, what have you done? You've got everybody wrapped around an axle, you know. I said, well, you asked me to go look at these trailers. I've done fermentation at this level. These aren't fermenters. But it turned out that, you know, the Brits had been saying that all along. And we went out and figured out that they were hydrogen generators for weather balloons that Iraqi forward observer would use to measure wind drift. And what's even more ironic is that's what the Iraqis said they were in the first place. So here you had all the authorities, academia, colleagues, PhDs that had inspected these things, the CIA, upper level intelligence analysts. And you have somebody from northern Idaho says, wait a minute, you know, that's not what these are. And then you figure out what their real purpose is. And so that's the point that I love to get across, is that all the experts are saying, this is how life arose, this is how life diverged.
But there's another explanation, you know, and we know it, we know it, but boy, you take a lot of flack.
[00:18:40] Speaker B: A guy from northern Idaho says otherwise,
[00:18:44] Speaker A: and he finally said, you have so screwed up this whole situation. I said, well, what are you going to do? Send me home? I'll go.
[00:18:51] Speaker B: You can't fire me. I quit.
So how long were you over there?
[00:18:57] Speaker A: The whole thing was for training, and then deployment was about six months.
[00:19:02] Speaker B: And that's outside of Baghdad or where were you at?
[00:19:05] Speaker A: Yeah, right outside of Baghdad. We were right near the airport. The whole. Across from Camp Victory, where they were holding Saddam, although we didn't know it.
[00:19:14] Speaker B: Interesting, interesting. Well, Scott, last of all, if you had to pick one aspect of the natural world that kind of calls out to you as evidence for design, what would that be?
[00:19:23] Speaker A: I think it's DNA. You know, as Crick said, it's a frozen accident. It's the same code in E. Coli and tulips in your garden in, you know, your own cells. You know, it's not evolving. How did we get there in the first place? And how did we get the best code, you know, that can translate nucleic acid chemistry to protein chemistry? You know, it's a, it's a mind blower. And it functions on the same properties that we write code. You know, if you look at E. Coli, I think Jim Shapiro in one of his papers wrote E Coli can grow on milk sugar, lactose. How does it do that? It goes if lactose is present and if glucose is absent. And if you have laczy A, then transcribe beta galactosides and permeates.
That's a simple logic statement. If, if, if, then.
And that's how we write code. And E. Coli is doing it. The simplest organisms are. Are following that same logic.
[00:20:20] Speaker B: That's beautiful.
[00:20:21] Speaker A: Generated by the blind forces, you know.
[00:20:26] Speaker B: Exactly.
Yeah, that's beautiful. Well, hey, Scott, thanks so much for being with us today to share a little bit about your story and why the evidence for design matters to you as you keep pressing forward and following the evidence, where it leads. I've enjoyed chatting with you today and hearing about your experiences.
[00:20:42] Speaker A: Okay, likewise.
Thanks for having me.
[00:20:45] Speaker B: Thank you for joining us for this episode of I Do the Future. To hear more inspirational stories from those involved in putting forward the remarkable evidence for design in nature, join us again here at ID the Future or on our sister YouTube channel, Discovery Science. And as you listen to these important stories, please consider sharing a link with a friend for ID the Future, I'm Eric Anderson. Thanks for listening.
[00:21:08] Speaker A: Visit
[email protected] and intelligentdesign.org this program is copyright Discovery Institute and recorded by its center for Science and Culture.
