In a paper published in Science in 1983, Stephen O’Brien, David Wildt, David Goldman, Carl Merril and Mitchell Bush showed that the cheetah (Acinonyx jubatus) had extremely low levels of genetic diversity, a pattern that they interpreted as resulting from a population bottleneck. This study was one of the first to apply genetic tools to a conservation problem. Thirty-three years after the paper was published, I spoke to Stephen O’Brien about his motivation to carry out this study, how this group of authors came together, and what we have learnt since about genetic diversity in cheetahs.
Citation: O’Brien, S. J., Wildt, D. E., Goldman, D., Merril, C. R., & Bush, M. (1983). The cheetah is depauperate in genetic variation. Science, 221(4609), 459-462.
Date of interview: 22nd December 2016 (via Skype)
Hari Sridhar: I wanted to start by asking you about your motivation for doing this piece of work. I looked up your publication profile, and I came to know that your work before this was on genetics, a lot on Drosophila genetics, and on genetics related to cancer. And then in 1980, you published a paper on the genome of the domestic cat. Did that in some sense lead to this piece of work on the cheetah itself?
Stephen O’Brien: Yes. Any scientist’s history is convoluted, and influenced by experience, but I have to say that I didn’t grow up being fascinated by cheetahs. I was a geneticist in the 1980s interested in lots of different things at the National Institute of Health here in the USA. Our emphasis was largely looking for genetic determinants that influence complex diseases, particularly infectious diseases. And although I was studying in humans, things like HIV AIDS, I was also interested in animal models. And the cats had a number of viruses that were interesting, like Feline leukemia virus and they also have a feline immunodeficiency virus, which is a first cousin of the AIDS virus. They have a coronavirus, which is related to the COVID-19 virus. And so, we began some studies on cats.
I had a young postdoctoral fellow, David Wildt, who had an avocation of looking at wildlife species. Wildt was a reproductive physiologist; he was very interested in understanding the patterns and the methodologies for developing better artificial or assisted reproduction in species that didn’t breed in captivity. David and his colleagues at the National Zoo were invited to investigate a problem that, shall I say, was inscrutable, a difficult problem, which was that cheetahs, as a species, were easy to capture and put in zoo collections, but they didn’t like to breed very well. While other animals bred fine – lions, foxes, and even elephants and hyenas – but the cheetahs were more difficult. So he began a discussion with his colleagues and the director of the National Zoo in Washington – Ted Reed – who had a meeting with Frank Brand, director of the Pretoria zoo in South Africa. Reed and Brand, both, recognized cheetahs were difficult to breed in captivity, and Brand had an off- site collection of 50-60 cheetahs that were having trouble breeding, just like cheetahs throughout the rest of the world. So Brand invited David and a medical team to come to South Africa to give them a medical exam. David was my postdoctoral fellow at the time, and I said to him, while you’re there, get blood samples from a handful of cheetahs and bring them back, and we’ll just test them to see what level of genetic variability they have. At that time, there had been maybe thousand studies with proteins and what we called allozymes, which are allelic variants of enzymes. Most species had something between10 and 50% of their markers were variable, and the heterozygosity levels was on the order of 15 to 25%. I thought cheetahs will just turn out to be normal, and then we’ll have to look for some other cause for their difficulties in breeding.
What David and his team discovered first was that cheetahs indeed had a series of reproductive characteristics that would provide a plausible explanation for the difficulty in breeding. It turned out that cheetah spermatozoa were markedly malformed. Most species have about 30% malformed sperm while cheetahs were closer to 70 or 75%; that is every Cheetah they looked at in the South African collection. Wildt figured that this might have an influence on cheetah reproduction.
I should mention that I was a little bit hesitant in 1982 to get into the population study in the first place because I had left population genetics as a principal discipline in the early 70s, mostly because I felt the field was stuck in a silly dispute. There were a lot of arguments about whether or not variation in natural populations of humans and other species were selectively “neutral” or whether they were adaptive. And these arguments kept coming up in the literature every month, every year, over and over, and I was getting kind of tired of the argument. I wanted to get into molecular biology, which was much more interesting. I remember very clearly going to a library, when the cheetah study was presented to me, to see if the field had changed much. When I read the latest issues of some of the journals of population genetics, I realized that it had not, so I got my confidence back about getting back into it.
When Wildt brought the blood samples back to us, I put my technician on to running about 50 allozyme markers that we had developed in the laboratory for gene mapping and other kinds of studies So, when the cheetah data was finally examined, it was, shall I say, very interesting, because, as the technician said, these species are very boring because there’s no variation at all. But I didn’t find that boring; I found that interesting. And that’s the way it went, through the whole initial set of markers over and over, there was no variation. And then we looked at another method – 2d gels – which had 300 or 400 proteins, and they had a few variants, but not very many; much less than most species. This was the beginning of our thinking that the cheetah was unusual. It was unusual in that the entire species looked like a deliberately inbred mouse strain. It had very little variation.
As scientists, you don’t just stop there, because you know people are going to be skeptical and they’re going to be wondering if we looked at a statistical outlier, or whether we knew what you were doing, or whatever happened, even if we published in a big journal, which we did, in Science. So we expanded our studies, until we increased the markers to things like DNA variants and other variable marker genes. Perhaps the most remarkable demonstration of the cheetah’s genetic uniformity, and the one that caught everybody’s attention, was when we decided to take a look at what was thought to be the most variable complex of genetic markers or loci in any mammalian genome, the major histocompatibility complex- MHC – termed HLA in humans. The MHC comprises a group of about 220 genes of which half are active – the others are pseudo-genes – but in that group, about 60 of those active genes are involved in immune defenses. The principal MHC markers are involved in recognizing foreign bacteria, parasites or viruses and parsing them into small peptides, then presenting them to T cells, which made antibodies or cell-based immunity. Because of the constant history of infectious agents outbreaks in various species, over evolutionary time, it became adaptive to develop increased protein variability at those loci. Thus, individuals that retained increased variation in these functional MHC receptors, had more breadth to recognize things they’d seen before – bacteria, viruses – and also things they had never seen before. So, quickly, it became very clear that this group of genes was highly variable, much more so than others, evolving much more quickly than other genes that were not involved in immune recognition.
The way in which all of what I just described was discovered, was by work in mice, which were deliberately inbred for 20 or more generations and then by exchanging small skin grafts between them. Since every cell in the body has MHC markers on them which function as a recognition immune system to recognize foreign agents. So when you place a skin graft from an unrelated individual on a certain individual, it’s immediately recognized as non-self because of those MHC variants and rejected. So, we had the thought, well, what happens if we attempted skin grafts between unrelated cheetahs? And so this was a sort of a crazy idea that we had. But I had good relationships with the zoo director in South Africa by this time and also another facility in Oregon that had a collection of cheetahs. I persuaded both of them to allow us to ask their cheetahs to volunteer to have small skin grafts exchanged between unrelated animals. When we did that – we did six, in South Africa, and another eight in Oregon – and to make a long story short, all 14 were accepted as if they were identical twins– the grafts did not reject – while normally you’d expect the grafts rejected in about 14 days. We actually controlled for that, with a positive graft control, by putting a house cat skin on a couple of cheetah graft beds. So, when out-bred cheetahs with no known history of relatedness were able to accept skin grafts, they looked like immunological clones or identical twins in an immunological sense. And then the conservation community took notice. They realized, oh, my goodness, there’s something really interesting about the species and also about the interpretation. The interpretation turned out to be that, yeah, when some species lose diversity, or almost go extinct, there’s sometimes a hidden peril, which is the loss of overall genetic diversity, as a consequence of population historically dropping down to low numbers and then doing something that they actually are instinctively hardwired to avoid, which is to mate with close relatives. And the reason they do that is because there’s nobody else around; there’s only a few opportunities. So they mate with close relatives – brothers and sisters, mothers and their sons, fathers and their daughters. They do this over and over until the population gets bigger. But that process of mating with close relatives leads to a shedding of overall genetic diversity and the exposure of certain recessive genes that normally are covered by widespread heterozygosity, except when you breed with close relatives and you start to see it. The consequences of inbreeding can be adverse events in reproduction, survival and other things. The more we looked at cheetahs, the more we found them. So the cheetah soon became a poster child for conservation, and the beginning of considering, at least, diversity and other aspects of genetics in management of endangered species. So that’s the story.
HS: That’s a really interesting story. You mentioned inbreeding and the bottleneck. In the paper you say that the bottleneck could have been recent or ancient. Subsequent to this study, have you been able to put a date on this bottleneck?
SO: Well, the answer to that is we have. And we did that by looking at other markers, other genetic variants, in the genome that are known to evolve a little bit faster than the coding genes. And these are, traditionally, the mitochondrial DNA, which evolves about 100 times faster than coding genes, and the stutter sequences known as microsatellites or short tandem repeats-STRs. STRs are short, repetitive sequences of two or three bases that expand because of mistakes in replication. And there are a few 1,00,000 of them in the genome of every species, including cheetahs. And so we knew the approximate mutation rate of microsatellites, and also mitochondria, and when we looked at these markers in cheetahs, we were surprised to see that the variation there was higher than we had expected, given the studies of the coding genes. We did back calculation of how long it might have taken to come up with the level of variation we’re seeing in cheetahs; the number came out to be about 12,000 years ago. When we looked at fossil record history, the bottleneck coincided with a major event that was very important, that happened across the world, at the end of the geological period called the Pleistocene. Around time, the glaciers were retreating for the last time in North America and also in Europe. Cheetahs occurred in Europe, Asia and North America before the time, but they disappeared from North America completely afterwards
The fossil record also tells us that cheetahs grew up in North America. They actually are closely related to an American cat species called puma. About 4 million years ago, a split occurred from the ancestor that led the pumas on one lineage and cheetahs out the other. This all happened in North America. In North America, the cheetah grew to be the world’s fastest animal and the world’s second fastest animal, the American pronghorn, also evolved running away from it! The pronghorn is still in North America, but not cheetahs. Ten thousand years ago, what happened was there was a great extinction of mammals, one of the largest in the history of the mammalian radiation, which spans some 100 million years. During the Pleistocene extinction, about 40 or so species of large vertebrates disappeared from North America. These were the mastodons, the mammoths, the American Lion, the sabretooths, a number of large flesh-eating birds, eagles, vultures, condors and teratorns. You find them all in the Rancho La Brea Tar Pits outside of Los Angeles in California, which is a fossil bed of these extinct species. And so, abruptly, the cheetah went extinct. Interestingly, it was the same time as the bottleneck, which we imputed from the genetic structure of modern Africa cheetahs. So the next thing we suggested was, well, probably that bottleneck 10,000 years ago had something to do with the genetic impoverishment that we’re seeing today. Now, because cheetahs went extinct from North America, and we just happened to discover this with our pipettes and our syringes and our genetic technologies in Africa in the 1980s.
We now believe that cheetahs went extinct in North America, and they, plus all those other species that went extinct in North America, never came back. There are no elephants, lions, giant ground sloths and sabretooths. Pumas went extinct in North America too, but they came back from South America, and their modern genetic structure looks an awful lot like cheetahs, which is low. We are guessing that, before the late Pleistocene extinctions, perhaps at least 100,000 years earlier, or maybe even a million years earlier, sometime in the past, that cheetahs from North America made it across the Bering Straits into Asia. And then they basically set up housekeeping over there. And then when the Pleistocene extinction took place, it probably affected them as well, and that bottleneck caused a founder effect as they migrated across into Africa more recently, and led to the genetic impoverishment we see today. I wasn’t there at the time! It’s not 100% certain exactly the timetable to the migrations and the genetic reductions. But what I just said is the simplest explanation that we could come up with.
HS: Have you redone this study with newer techniques and a larger sample size, from the wild and other captive populations? If yes, does the pattern remain more-or -less the same?
SO: Well, yes to all those questions. We’ve certainly sampled bigger populations. The original studies were done in South African cheetahs, from either South Africa or Namibia. Extended studies later included samples from populations in East Africa. We did an expedition there in the late 1980s and we sampled them. And we’ve collected several thousand individuals across the years. One of my original collaborators was a young woman named Laurie Marker who is, today, the chief executive officer of the Cheetah Conservation Fund. Laurie is a California native who moved to Namibia and set up a Cheetah conservation program in 1990. She’s probably one of the most important conservation advocates, at least in mammals, of our generation. She has gone on and continued to collect samples, set up a genetics lab, set up a reproduction lab and continued many conservation and research programs. So it’s really blossomed into a conservation success story.
I will mention one thing, which is that when we originally made the discovery in the 1980s, there was a lot of discussion and a lot of comments. Popular media would tell the story very dramatically, sort of the way I just did now. Maybe it was my fault, but it gave the impression that the cheetahs were doomed. I’ve had some push-back because of that, from the ecologists particularly. The truth is, I agree with ecologists that the cheetahs are not doomed because of their genetics. And the reason that I say that is because their bottleneck took place 12,000 years ago. If they were doomed, they would have gone extinct long ago. But in fact, they continued to grow until they numbered some hundreds of thousands in Africa. This means the genetic problems and the correlates associated with it, although they’re real, are not limiting. They don’t stop them from breeding in the wild. Today habitat protection and the loss of areas to live in is probably the biggest threat that they have right now. So, in many ways, cheetahs are a success story. So that’s something I’ve said more and more recently, because I want to, at least, not be the source of an unfounded horror story. I am the source of the data, or we are – my students and I – but the truth is that my interpretation is that they can be saved. This is, of course, what Laurie Marker thinks, and that’s why she’s continuing to run the programs the way she is.
So yeah, there’s been a lot of follow up on it. In fact, just about every kind of genetic marker that I could think of across the last three decades, we’ve tried on the cheetahs, and they all come up with pretty much the same answer. My final point is the most recent analysis, which just came out last year, in which we’ve sequenced the entire genome of one of the cheetahs from the Cheetah Conservation Fund – Chewbacca – who was an ambassador, and seven other cheetahs from the original collections, and they show pretty much the same thing: Around 90 and 99% of the cheetahs’ overall previous genetic diversity is gone.
HS: Soon after this study, did you become interested in other species of conservation concern?
SO: Well, yes I became interested in it because once the cheetah story came out, particularly the Science paper in 1985 – both the 1983 and 1985 papers had cute cheetahs on the cover. And they caught everybody’s attention in the conservation community. I think it was the beginning of a serious consideration of genetics at management tables. And my phone didn’t stop ringing. I wrote a book in 2003 called Tears of the Cheetah, which tells stories of many of these species. Tears is sort of a familiar popular description of the studies we pulled off on lions, orangutans, humpback whales, koalas, mice…lots of things, Florida panthers, all the other conservation icons; many of the others. And I’m happy to say now, that 30 years later, conservation genetics is alive and well, and it’s a thriving discipline. There are a lot of conservation genetics textbooks, people teach courses on it. I direct an international conservation genetics course, a two week workshop, every year or so, where we bring youngsters in and expose them to the leaders of conservation genetics research.
HS: Before you did this study, was there no suspicion of the genetic homogeneity of the cheetah?
SO: No, there wasn’t. Not before we reported the data. At least, I never heard about it.
HS: Was this the first study using genetics in a conservation context?
SO: It was the second. The first study was the northern elephant seal. This was just a few years earlier. The northern elephant seal is this big 4000-pound giant seal, with their big Jimmy Durante noses and they dive hundreds of feet. And it’s well known for its interesting harem structure, where you have one male servicing all the females, while the bachelors watch by, sort of with envy. These animals virtually disappeared off the Pacific Coast of the US and South America in the early 19th century. And then there were a couple discovered in Guadalupe Island, and they sent a Smithsonian expedition down to see if they could find it. They saw six, they shot five of them, believe it or not, and they came home and they reported the story. They regaled how successful they were. Well, they missed a couple, because the seals started to come back, and due to protection off the coast of the Pacific, the northern elephant seal grew up to over 100,000, maybe 200,000. And then in the 70s, a scientist from University of Rochester named Robert Selander, decided to sample them, using the same allozyme techniques we had done in the cheetah, a few years earlier. Selander looked at 24 markers, a small number, but he didn’t find any variation. He published that study in Science and he said this is something we ought to be looking for. So I would say he was the first, but we were the ones that really pulled the rug out, because the data were much more comprehensive for the cheetah.
HS: I wanted to find out a little bit about the other authors on the paper. David Wildt, you, mentioned, was your post-doc. Could you tell us a little bit about the other three authors: David Goldman, Carl Merril and Mitchell Bush?
SO:, Mitch Bush was a clinical veterinarian at the National Zoo. And he, at the time, was an incredibly accomplished veterinary clinician, whose anesthesiology with dangerous species was legend. He trained virtually all of the major zoo veterinarians in the United States in the 1960s, 70s, 80s and 90s. He published hundreds of papers, which most veterinarians don’t do. And he’s one of my heroes, to tell you the truth. He’s retired now and he lives in Arizona, with his family. And he just made this amazing counterpart.
David Goldman was a post-doc, a young scientist at NIH, who I got to know. He was interested in proteomics, two-dimensional gels stuff, and he provided us with the technology that allowed us to validate cheetah variation using that technique. I also talked him into doing the first paternity of a giant panda in a captive situation at the National Zoo. He helped us with that a few years later, when the female was inseminated by the male in surprise copulation, but also artificially inseminated using sperm from by a London male. Today, David grew to become one of the leaders in neuroscience genetics, having contributed to understanding the genetic determinants of depression, schizophrenia, and many other chronic mental illnesses. He’s still active, a laboratory director of the NIH-national institute of alcoholism and alcohol abuse
Carl Merril is an entrepreneur who left NIH and founded several companies. I kind of have lost track, because he made so much money, that I didn’t look any further at what he was doing. I run into him occasionally, once in a while, as we all do with our old colleagues. We’re all kind of getting up there now.
HS: And did all the authors ever meet during the study?
SO: Oh, sure. We all met during the study. Carl was David Goldman’s supervisor when David was a post-doc.
HS: If you don’t mind, I want to quickly run through the names of the people you have acknowledged to get a sense of how you knew these people and how they helped.
SO: Janice Simonson and Mary Eichelberger were laboratory technicians who were working with me. Janice ran the gels. Dirk van Dam was a zoo director in Netherlands who helped encourage the study. Brand was the Zoo director in Pretoria, who was the one who helped organize the first steps along with Ted Reed. Anne Van Dyk was the curator of the cheetah breeding facility in South Africa. Dave Meltzer was the veterinarian who worked with Mitch Bush to exchange skin grafts in south Africa. Ebedes and Frankenhuis were other veterinarians who consulted on some of the studies. Bleijenberg and der Boer were also veterinarians. Lee Simmons was the head of the Omaha zoo, who provided us with some cheetah samples and allowed us to sample his animals. Boever was the veterinarian at the St. Louis zoo. Lindsey Phillips was a deputy veterinarian with Mitch who helped us interpret a lot of the clinical data. JoGayle Howard was a young post-doc who grew up to be a major veterinarian scientist who led conservation genetics in black footed ferrets, clouded leopards and other species. And then the other people – Ross MacIntyre, Wayne Johnson, and Jeff Powell – were colleagues of mine, who read the draft of the paper and gave me insight. MacIntyre was my major professor, as a graduate student in the1960sat Cornell.
Let me say one other thing. Yeah. In today’s attribution ethics, probably three quarters of the people in those acknowledgements would have been co-authors, if the paper were written today, because we tend to include more co-authors now, than we did then. In those days, the authors were the people who were the leaders, and if they had a technician or two, or a colleague who they had lunch with and talked about their work, they didn’t include them as co-authors; they were acknowledged.
HS: When you were doing this study, did you make a trip to South Africa and see the cheetahs? When is the first time you saw a cheetah?
SO: Well, it was after we published this paper, but it wasn’t much afterwards. I think the first time we saw the cheetahs was when we went on the east Africa trip to collect them, in1985 or 1986. I’ve, of course, since then, been to South Africa several times. I’ve met Ann Van Dyk, Frank Brand and Woody Meltzer and all these people.
HS: Do you remember, roughly, how long it took you to write up this paper?
SO: I would say, it was about three weeks, once data collection and analyses were complete.
HS: Did you do most of the writing? Did the other authors also contribute to the writing?
SO: Certainly, everybody read the paper and commented on it. Were there a lot of people contributing in the beginning? Sure. I mean, I had to get the information right to make sure, from David and Mitch who collected the samples. Table 1 was a series of polymorphism studies. This was something our group was doing, so I knew all this stuff pretty well. The 2D gel came from David Goldman. That’s the Figure 1. So there was only a 2D gel and the table in there, and the rest of it was largely just narrative like I’ve just given you.
HS: Where was all the lab work done? Was it done in your lab back in the US?
SO: Yes, it was all done in the laboratory in Frederick, Maryland – the National Cancer Institute.
HS: How did you pick the zoos from which to collect samples? Did you know people at these zoos?
SO: Our original samples, the big samples from this paper, came from the first South African collection trip. Van Dyk had maybe about 60 or 70 cheetahs but Mitch and David brought back 50 blood samples from them, a good sample for an endangered species. But remember, this was the time before they had all these rules about carrying endangered species across country lines. It was before they had all of these constraints, regulations and permit processes which interfered with research samples getting in and out. So, that’s the reason we were able to do it. After that, we started collecting samples, David, Mitch and I, in a methodical way. Every time we went anywhere, we collected every cat we could find for 15-20 years. We got a big grant from the American Zoo Association to look at the cats in South America. So I delegated Warren Johnson to lead that. Laurie Marker was over in Namibia ,and the San Diego Zoo began their frozen Zoo collection. Soon the number of samples in freezers was getting to be pretty good, big, and it allowed us to work not only on cheetahs, but on lions ,tigers , elephants , clouded leopards, , Pumas, and on Florida panther and other species.
HS: Was Science the first place you submitted this paper to? Did it have a relatively easy ride through peer review?
SO: I think Science was the first one we sent it to. No, I don’t think it was that easy. I think they tried to make sure that it was robust, through a rigorous peer review. I had to deal with the Science editor, Eleanor Butz, who was very tough; she looked at every sentence. I can’t remember if the reviewers were hostile or not.
HS: What kind of attention did this paper receive when it came out?
SO: I think it was widely seen, particularly among the zoo community and the conservation community. When the 1985 paper came out, that described the skin grafts and it also talked also about the cost of inbreeding with respect to homogenization of immune defenses. As an example, there was an outbreak of a deadly disease that killed a lot of cheetahs in Oregon. People began to say, oh, we got to pay attention this now. In the beginning, what it did was it opened up the gates to more samples. Zoos were very happy to help us, particularly because we had partners like Lee Simmons and Ted Reed, who were directors of zoos and major players in Zoo Directors Association. And they would pick up the phone to the guy in Philadelphia or Boston or Texas and say, look, these guys are good; we’ve never had this kind of scientific enquiry before; we need to help them. So they did.
And we had the best veterinary input as well. There was no question about safety because we had Mitch Bush and his fellows, who had reputations as big as there was in zoo veterinary medicine.
HS: After doing this work and getting into the genetics of conservation, have you become involved and interested in other aspects related to conservation? Or is the focus still largely on genetics?
SO: Yes, I’ve become interested in conservation policy and in how it works. But my salary didn’t come from working in conservation, or at least it didn’t when I was in the National Cancer Institute; it came from studying genetics of human diseases and animal models. I was able to defend the work in the conservation because a lot of it was supported by the outside money, like from the World Wildlife Fund or National Geographic who supported these expeditions. So we were taking technology that had already been developed for human genetics and for medical type of applications and allowing the students to use it on the animals. Yet, whenever they used it on the animals they discovered something amazing and it would wind up in the cover of Science or Nature. Good science was good science; I never apologized for it, but while it was going on, it was kind of walking a tightrope in terms of defending what resources I was managing. I’ve never given up being passionate about conservation. I think, you know, as I look back on it, one of the things I enjoy the most is the people you meet. They’re all pulling in the same direction, which is towards saving the species. That doesn’t mean they don’t fight or disagree or argue; they do. Still, they’re the people that want to change the world and make a difference. Being associated with these people is something that makes us all better.
HS: Have you ever gone back to reading the paper again in these 33 years?
SO: Well, of course, I read it when I wrote the cheetah chapter in Tears of the Cheetah. That was only12 years ago. I read it along with some of the others because I wanted to remember exactly what I had said and the logic that was there, but in the context of historical resurrection.
HS: This is such a nice easy paper to read.
SO: In those days I really strove very hard to be readable. Shortly thereafter, Scientific American asked me to write an article; that was a real training experience, learning how to write for them. Since then I’ve written four other articles for Scientific American, articles for National Geographic and a popular book . Now, when I teach, I try to explain to my students how important it is to explain to non-specialists ,what it is you’re trying to say and why it’s important and why you believe it. I mean, I like to kid people when they ask, who’d you write the book for? And I say, well, I wrote for my sister; my sister’s a folk singer.
HS: In the very last line of the paper, you say, “It is tempting to speculate that similar circumstances that have produced precipitous monomorphism followed by niche perturbation might explain extinction of successful species in the past.” Of course, it’s difficult to figure out what the genetics of extinct species were, but I wanted to know if there’s any evidence for monomorphism being linked to population declines for other species?
SO: There have been a lot of ancient DNA studies done in many different species that have disappeared. I was involved in the Florida panther studies that show genetic impoverishment even before the modern times. Some of the other ones that have been looked at that have gone extinct as well.
HS: Would you count this paper as one of your favorites among all the papers you have published?
SO: I think this paper was the beginning of one of my most important contributions to science. I wouldn’t call this my favorite paper,but it certainly was the first of several, which was part of one of the things I’m most proud of. I guess that I was a little bit in denial about it, as I worked for a medical institute for so long. But truth is that sometimes your avocations are better than your vocations. I’m very proud of what has happened in the conservation field, because before this paper and before the applications of hard science to conservation, decisions were made based upon the chutzpah or the personality of the managers. They would make decisions based on guesswork. I tell my students now, you don’t have to do that anymore. You just put the data down on the table. You let the data speak for itself, and that will make a difference. And, of course, what happened, because of the cheetah story. I had the luxury of having some outstanding young people insist on coming to my laboratory to learn how to do this. I mean, there’s a group of them that have gone on to be major conservation biologists ,scientists and geneticists, and I’m very proud of all of them.
HS: What would you say to a student who is about to read this paper today? Would you guide their reading in any way? Would you point them to other papers they should read along with this? Would you would you add any caveats to their reading?
SO: You know, you really have thought about these questions. These are good. I think that this 1983 paper does tell a story as it happened in a good historical context. It came out at a time that was really exciting. We published a more extensive follow-up cheetah study in Science in 1985(227:1424) which is complementary. Interesting to me was that in the same 1985 issue of Science, right next to our cheetah study was the first description of the BLAST algorithm, written by David Lipman, soon to become the founding director of the National Center for Biological information – NCBI – which hosts the GenBank database. Lippman’s BLAST algorithm was like back to back with our study. We laugh about that whenever we get together, about how young we were and how important those two papers were. Time passes.
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