Science Friday - Ancient East Asian Genomes, COVID And Clotting, And Cassowary Plumage. May 22, 2020, Part 2

Episode Date: May 22, 2020

The cassowary, a large flightless bird native to Australia, New Guinea, and nearby islands, has a reputation for aggression and wickedly clawed feet that can cause serious injury. Indeed, they’ve been known to attack humans dozens of times, and even occasionally kill people. But they also have a beauty trick: Their glossy black body feathers have a structure for producing shine that’s never before been seen in birds. Where other black birds like crows are shiny because of structures in their feather barbules, the cassowary instead derives its shine from a smooth, wide rachis—the main “stem” of the feather. University of Texas paleontologist Julia Clarke explains how the cassowary’s color could help shed light on the feathers of extinct birds and dinosaurs—and how paleontologists are investigating the evolution of birds as we see them today. The novel coronavirus SARS-CoV-2 has primarily been considered a respiratory virus, causing acute problems in the lungs. But doctors around the world have recently been reporting unusual blood clotting in some COVID-19 patients. The exact cause of these blood clots isn’t yet known—there are several interacting biological pathways that all interact to create a blood clot. One theory is that the clotting is related to an overactive immune response, producing inflammation that damages the lining of small blood vessels. Other theories point to the complement system, part of the overall immune response.  Ira speaks with hematologists Jeffrey Laurence of Weill-Cornell Medicine, and Mary Cushman of the University of Vermont Medical Center about the unusual clotting, how it impacts medical treatment, and what research they’re doing now in order to better understand what’s going on in patients.  The history of a group of people can be reconstructed through what they’ve left behind, whether that’s artifacts like pottery, written texts, or even pieces of their genome — found in ancient bones or living descendents. Scientists are now collecting genetic samples to expand the database of ancient East Asian genomes. One group examined 26 ancient genomes that provide clues into how people spread across Asia 10,000 years ago, and their results were published this month in the journal Science. Biologist Melinda Yang, an author on the study, explains how two particular groups dominated East Asia during the Neolithic Age, and how farming may have influenced their dispersal over the continent. Subscribe to this podcast. Plus, to stay updated on all things science, sign up for Science Friday's newsletters.

This is Science Friday. I'm Ira Plato. Just a quick note before we get started, we miss you, we miss talking to you, and we want you to say hello. So please talk to us on the Science Friday Voxpop app, on Twitter, or even email us, SciFri at Science Friday.com. Later in the hour, we explore new insights into the genetic story of the early humans who populated East Asia. But first, in the bird world, you can be one of two branches of the evolutionary tree. Either you're one of the 10,000 flying songbirds, shore birds, and raptors, or you're one of just 70 species in the group of mostly flightless birds, like ostriches, emus, and the fierce giant cassowary, a native of Australia, New Guinea, and nearby islands. Casawaries with their strong legs and vicious toes have a well-earned reputation

as aggressive, dangerous birds than just a scary face. Producer Christy Taylor takes a closer look at new research on the evolutionary mysteries of cassoaries and their close relations. And she begins, of course, with their feathers. If you've ever looked at a cassowary, I hope you'll agree that they're not just weird-looking flightless murderers. They're also kind of gorgeous. They've got these bald, bright blue necks

and really glossy, fluffy-looking black feathers that drape their very powerful bodies. It's that black glossiness that caught the eye of Dr. Julia Clark, a paleontologist at the University of Texas in Austin. She joins me to explain how a close look at feather color can help scientists understand not just the evolution of cassowaries, but also their extinct cousins and the dinosaurs that gave rise to them. Welcome back to Science Friday, Dr. Clark. It's my pleasure to join you, Christy. Julia, when I look at a cassowary, my first question is really not why is it so shiny? Oh yeah, I guess that isn't most people's first question about cassowaries. Maybe their first question is, is it going to kill me? Shinniness is not unusual in many, many groups of birds, but in the group of birds to which casseroys belong, it is. So that's kind of what got us started on this. And I happened to be in a collection space in the Netherlands. And they had some cassowary specimens. And it was,

so striking. And these were even kind of a little bit dusty, you know? And I was struck by how shiny these feathers were. And I was like, how? Okay. So this feels like a question I would ask in a fable, but how did the cassowary get so shiny? You set out to investigate. What did you find out? Well, we at first thought there might be modifications of the structure on the outside most part of the feather so that the feather keratin could be particularly smooth and maybe more reflective. So we investigated that, and it didn't seem to be, you know, explanatory. It didn't seem to explain the phenomenon. And then my co-author, who did the sort of biophysics of this structure, found that it was actually some aspects of the dimensions of the rakeist or the center

part of the feather itself that was contributing to the shine. And to be clear, what we found was that cassowary shiny blackness is among the brightest known shiny blackness and living birds. So this wasn't just a moderate thing, but this is up in the zone of a shiny crow feathers, for example, but that shine in cassowaries is produced by having really fat, wide center parts of the feathers. It's actually the aspects of the feather geometry that are most important to determining that shine. Is being shiny a useful adaptation for either a bird or a dinosaur? Like, if you look at a cassowary, I feel like it has everything it needs just in those really powerful feet. Man, cassoiris are so fascinating. And if we think about what colors do more broadly, is that

they can be used in cryptis or camouflage, or they can be used in communication. and typically communication with other members of their own species. But it also could be since cassowaries live in these typically heavily forested environments, and we can't rule out the possibility that these black feathers could function in Cripsis. It could function in somehow making the cassowary blend better into a shadow-doppled forest environment. But I will say that most shiny feathers in birds that have been, been studied are related to communication. So they function in what we call the sexual selection system, which might be in things related to finding a mate. Because I feel like I don't have this

picture in my head quite yet. If we're looking at a feather, the part that the cassowary has that's shiny is like the trunk of a tree, right? Exactly. So how is a crow's feather, a black shiny crow feather? Where is that shine coming from if it's not like this tree trunk part of the feather? So if a feather is tree-like and it has this central trunk, that's the rakeas, then off of that come barbs. And then off those barbs come the twiglets, which are the barbie wolves. And in the crows and in many other birds, the shiny black color is conferred by changes in the structure of those twiglets. So in birds like a shiny pheasant or a shiny iridescent peacock, for example, you're going to have shine conferred by the arrangement of these melanin pigment-filled structures within the feathers themselves.

And there could be one layer of these or multiple layers. And the spacing of the layers could even determine whether they refract more of a reddish-tone shiny black or more of a blue-green tone, shiny black. So that's basically the mechanism that we've now found evidence for in non-Evian dinosaurs that have branched feathers. I'm really glad you mentioned dinosaurs because I know you're a paleontologist. And I really want to know why you're looking at living modern birds and their color right now. So I think sometimes kind of moving between being motivated by questions about things we see in deep time can bring us to ask new questions of animals in the present day. And conversely, we go the other direction.

Maybe we understand a mechanism now that we understand this mechanism of shine in the cassowary, we could bring that understanding to look back at the fossil record and say, could we find evidence of this form of shininess in the fossil record? What would those fossils look like? How would we maybe ask that question? So right now we have a dinosaur that's about 120 million years. that shows that those long, skinny melanin-containing structures that make shiny blacks in things like crows or things like chickens and ducks.

But we also have evidence from about 140 millionaires of another form of structural color. So that would have been potentially some shiny component. But what was really cool is that in dinosaurs that are even more distantly related to birds, We call these, you know, among friends, fuzzy dinosaurs. These are things, yeah, it was, you know. Adorable. Well, it's clear. They're not hair covered, but what they have are thin filaments, maybe several filaments connected together at the base.

Then maybe they have thicker filaments that would be with something we'd call a bristle. And those vary in different species of fuzzy dinosaurs, these dinosaurs that are more distantly related to birds. But we haven't found any evidence of these melanin pigment-based mechanisms for making shine in those filamentous structures. And so what's interesting about the casseroi, I think, is this is a mechanism of coloration that does not depend upon the shape of those pigment containing organelles that's really conferred by the shape of the bristle itself. And this might be a mechanism by which fuzzy dinosaurs got shiny. But now we can turn to the fossil record and maybe think how might this be preserved? Maybe there are feathers in amber, for example, maybe there are other,

you know, just exceptional cases. Because it really depends on what fossil records you look at, what kind of information you can get from them. I got to say, when I look at a cassowary, when I look at an ostrich, when I look at an emu, I feel like I'm looking at something that is a lot more closely related to non-avian dinosaurs than like a pigeon. You know, do we see that they're more primitive? So I think what we see when we look at them and are like, oh my gosh, big dinosaurs, is that we can recognize their affinities with these flightless, like all of the bipedal raptors

and other dinosaurs that we more commonly encounter in the media, in museums. we can make that relationship more easily because they're big. They're bigger than other things. So what we know happens in the evolution of our living birds today is that they generally got smaller and they evolved flight. And then in these living guys like cassowaries and ostrich, they reverse that trend. So they lose flight and they get big. So it's not an ancestral bigness, but it does harken back. It helps us make that connection with non-avian dinosaurs. So is there any living bird that you would say probably has the most to tell us about how these birds arose from non-avian dinosaurs? Oh, man, I love them all, you know? I mean, you can't pick just one species as people used to do this. And actually, the most notable case was Scott's polar expedition, right? The thinking at the time was that penguins were one of the groups that were going to shed the most light on the origin. of birds because their feathers are highly, well now we know, modified and quote-unquote scale-like.

People thought that was a primitive trait, and they thought that if you could observe the ontogeny from the egg of a penguin, like an emperor penguin, you might know about the origin of birds. Well, all of those things are completely false. You would learn a lot about the development of penguins, which independently lost flight, but you wouldn't learn about bird origin. So there's no one species that's going to show you differentially more about that origin. But I will say that when you look at songbirds outside our windows, those are among the most heavily modified of living birds. They have a lot of

new traits that are absent in most other birds. And when we look at things like a chicken or a duck, those species have been you know, parts of groups that have been evolving independently for, I want to say, you know, more than 65 million years. So they have had their own separate history. Each one of those is, let's say, you know, if it's alive today, it's equidistant from the bird ancestor. So we got to look at them together to get that picture of what are traits that that ancestral bird might have, that we could bring down and look at a non-avian dinosaurs. We can't just single one out. Good luck to you in finding that. Thank you so much for joining me today. Julia Clark is a

professor of paleontology at the University of Texas at Austin. Thank you again so much. Thank you, Christy. That was a lot of fun. When we come back, we'll take a look at one of the lesser understood effects of COVID-19, mysterious blood clots. This is Science Friday. I'm Ira Plato. The COVID-19 epidemic has become known as a respiratory disease targeting the lungs of infected people. But doctors are also seeing strange responses to the virus in other parts of the body, including the blood. Doctors around the world are reporting unusual blood clotting and a large proportion of hospitalized coronavirus patients. Joining me now to talk about what they are seeing and how medical workers are responding to the clots are two hematologists. Dr. Jeffrey Lawrence,

Professor of Medicine in the Division of Hematology Oncology at Wild Cornell Medicine and attending physician at New York Presbyterian Hospital. And Dr. Mary Cushman, a hematologist at the University of Vermont Medical Center, Professor of Medicine and Pathology at the Larner College of Medicine at UVM in Burlington, Vermont. Welcome both of you to Science Friday. Thank you. Thanks. Thanks. It's great to be here. Thanks to have you. Let me begin with you, Dr. Lawrence. Early on, you noticed some unusual clotting in patients with the coronavirus. Please tell us about that. One of the very first patients that I saw was a young man, and this was early in March,

who had symptoms for about 10 days and then got very sick and came into the hospital and was put on a ventilator. And about three days into hospitalization, one of the nurses noted they had some very strange rashes on his bottom and called that dermatologist who did a biopsy. And they found out that it was a very unusual kind of lesion, one that they typically don't see, that had small blood vessels clotting. And there were so many clots and so many small vessels that on his backside, you could basically see the imprint of what a small macroscopal cells would look like right under the skin. And when they sent it to pathology, the pathologists recognized that it was something, some unusual kind of clotting that I had studied in some very unusual cases.

of rare disorders and wondered what was that doing in a patient with COVID, particularly a young man. And so we evaluated it for certain proteins that were associated with inflammation and associated with the immune system, complement, and found out that they were deposited there. And thought that was just very, very strange because it's not something that we're used to seeing in the intensive period setting, certainly not something we're used to seeing with other viruses. that was like in an afternoon, say on a Wednesday, and later that night I get a phone call from the autopsy room saying that they had a patient who had come in and just died and hit some unusual lesions on his skin.

And they biopsyed them and called me about them. And so basically we said, we have a pattern here. And in fact, over the next week, we found three more identical cases. And this was a clue to something funny was happening. And that kind of led us to start investigating what was happening to the same. the clotting system and what was happening to the immune system in these patients, and could they be intimately linked? How common is this?

I know that we hear other cases in other hospitals. Is this something doctors are watching out for? Fast, vast majority of people, get infected with the coronavirus to get COVID-19, either don't have symptoms or very mild. Don't have to worry about this. But in the severe cases, the ones that filled up our adult emergency room and then filled up our pediatric emergency room with adults are unusual because of the level of clotting. So that typically when a patient comes into the intensive care unit, they're often put on

prophylactic blood thinners to prevent them from getting clots because they're going to be basically lying, isolated in intensive care unit. They may have an infection that will cause their blood to clot a bit more. So they're given prophylactic. Anti-clotting medicines. But we were seeing clotting on the prophylactic antich-a-clotting medicine. So we increased the doses in some of these patients and some of them were still clotting. And then we put them on full doses of in my clotting medications like Heprin that certainly ought to take care of the problem.

And we were seeing clotting anyway. In fact, one of the things that made me so cognizant of the problems that we were seeing at our hospital that was not specific to our hospital was when a kidney doctor was quoted on the front pages in the New York Times saying that, you know, we've gotten this disease all wrong. We're not going to run out of ventilators. we're going to run out of dialysis machines because we're clotting off the filters that are dialysis machines, and these are patients who are on full doses of antaclyculation. And then I knew we had a real issue, and this is something different from the kind of standard clotting that we were seeing. Dr. Cushman, what would be causing this kind of clotting in these patients?

The first sort of piece of news that I noticed in the medical literature with a paper out of Wuhan, China that suggested patients have high levels of biomarkers of clotting, namely a biomarker called D-Dimer, which is a marker of the generalized level of pro-clodability, if you will, within a person. And this is accompanied by high levels of inflammatory biomarkers as well. So there's really three key points that come out of this. that it seems that in some patients who have more severe disease requiring hospitalization, we have this thrombo-inflammatory process that is triggered.

And we don't fully understand the reason for the triggering of it. Some people believe that it's because the virus is affecting and disrupting the inner lining of blood vessels in small and large blood vessels and disrupting that protective barrier that, the interlining of the blood vessels and that releases substances that can allow the clotting system to be triggered. And this process is really fascinating because it's not been seen with the same pattern of these biomarker changes that we can measure in the lab. This has not been seen in other viral infections or bacterial infections. It's very different than what we're used to seeing. And so the second big finding that I noticed in the literature was that patients in the hospital who have this high level of D-Dimer tend to have worse outcomes.

They have a higher mortality compared to other patients and a higher likelihood of requiring a transfer to the ICU and a respiratory failure. And so it raises the possibility, as Dr. Lawrence alluded to, that thinning the blood to try to dampen down the pro-plotting effects could be beneficial to patients. And so the third point that came out pretty early in the literature out of China was that patients who had higher levels of D-Dimer, representing this thrombo-inflammatory drive, seemed to benefit the most from these low-jouge. doses of anticoagulation, of prophylaxis, if you will, that Dr. Lawrence referred to. And so it really raises the question of how we can preserve the outcomes of patients with biomarkers-based strategies that might provide, you know, escalated doses of blood centers and people who even don't have evidence of clot at the time. Very interesting and mysterious, Dr. Lawrence.

are you seeing any pattern to who develops these clots, any pattern with regard to age or blood type race, anything that might predict who's going to be throwing off these clots? Sure. So as Dr. Cushman said, you know, we all think that rising D. Dimers is a bad thing, but how high they should rise and what the trajectory of that rise is needs a control of critical trial. But we have kind of clinical points that can help you judge who might be more at risk for D-Dimers and more clotting. One of them is obesity.

So obesity, patients with diabetes, patients with hypertension, tend to have faster rises in D-Dimers. And women, apparently, women are much less prone to a severe outcome and have less serious diseases for the same ICU admission than men. And that's curious. So what's protecting women to some extent and what is harming people of older age people with obesity, people with diabetes, and people of hypertension. And in fact, the protective factor from women that occurs at all ages.

So there's one very large study, over 16,000 patients being conducted in hospitals in the United Kingdom, which showed that this protection of female sex occurred at every age range they look from 50 to over 90 years of age. and one of the characteristics that appears to protect women and may be harmful in terms of the setting of diabetes, obesity, and hypertension, is that patients with pre-existing diabetes, obesity, and hypertension have higher levels of this immune protein substance, a complement. They have higher levels at baseline without the COVID of these inflammatory components that Dr. Christian was talking about, and they have higher levels of D. Dumas. So they're kind of at a set point, if you're a male, older age, obesity, diabetes, hypertension to getting these occurrences.

Another thing that's peculiar and it's come out of a large study from New York City of 5,700 patients, New York City and its surrounding, and the 16,000 United Kingdom study, is that why is it that people with HIV for their numbers tend to be getting less severe disease? And why is it with patients with cancer? if you make a list of the 10 risk factors for getting disease, cancer is the very lowest risk factor. It's barely statistically significant with a relative risk of 1.1. So what's so special about cancer patients and what's so special about HIV? You know, our hospital would like to say is we just take great care of cancer patients

and we're very good at social distancing. We use television and so forth. But I think it's something more than that. And I think it's telling us something about what's bad at having high levels of preexisting complement and what's good about having some level of immune suppression. Perhaps that's what's driving cancer as less of a risk factor. Perhaps that's what's driving patients with HIV, even when they're on their HIV medicine, because they still have defects in their immune system, and particularly they have defects in the immune system involving their innate immune system, which complement is part of.

So long-winded explanation say that we don't know what the driving forces, as Dr. Cushman said, to set all this clotting stuff off. We know that there are three pathways that are involved. There's a clotting pathway, there's the inflammation pathway, and there's a complement pathway. And all of them can turn on each other. So you have this insidious positive feedback loop between clotting and the immune system with inflammation

and the immune system with complement. And if you can't shut it off, and you may need to intervene more than one pathway, then you're in a lot of trouble. And in terms of, is it the virus that sets it off, at the very first. And what's so special about COVID? Well, one of the things that we and others have shown in early papers is that the virus itself has a protein on its surface, little spikes if you see seeing pictures in the newspapers, which can directly bind to a component, can start causing

platelets, can start initiating clodding factors. So the virus itself may set this off, and if you can't control it for whatever reason, you're kind of stuck. in this insidious loop. And so that's why clinical trials are so important, why we need to try multiple interventions, not just antivirus drugs, not just bloodthening drugs, but also, you know, I complement drugs and anti-inflammation drugs. What do people need to know about the clotting? You know, they tell us when you're a certain age, you should take a little mini aspirin to

prevent the clotting, possibly preventing strokes. Anything like that to be doing here? Yeah, I would say for this disease, the type of clotting that's going to be most common, apart from the clotting that seems to be tightly linked to the disease itself, like these microclots that might form in the lungs or kidneys or on the skin, the most common type of abnormal clotting that's going to occur in patients with this infection is deep vein thrombosis and pulmonary embolism. We also call that venous thrombosis. And these are clots in the larger veins of the legs. that are returning blood back to the heart. And the danger of those clots is that pieces can break off and travel to the lungs, which is pulmonary embolism, and that's a life-threatening type of abnormal clot. This is the third leading vascular disease after heart attack and stroke.

So it's very important, but the public awareness is pretty low on it. So only about 50% of people, even know what it is. And any infection, any acute infection or any hospitalization can raise the risk of venous thrombosis. And COVID seems to be more strongly triggering of these venous thrombosis events. The jury is a little bit out in terms of what the exact incidence is, but it's felt that it's higher. So prevention is really important. So the average person should just be aware of this. And, you know, we don't yet know if this is also affecting people who are sick at home with COVID. You know, most people with this infection don't

get hospitalized. And so if you're sick at home with it, for example, being aware that venous fibrosis could occur is important, and that means knowing the symptoms, which are leg pain and swelling, sometimes discoloration at the legs, chest pain and shortness of breath, and also being sure that if you have symptoms like this, that you don't ignore it and that you seek medical care. We're finding that a lot of people are afraid to come to hospitals with acute illnesses, because they're afraid they'll catch the infection in the hospital. But really being aware that this disease exists and being aware that it can cause death at the worst, it's important to recognize.

The other risk factors we've talked about, like obesity and older age, are also risk factors for venous rombosis. So if you have those conditions, you want to be especially cautious about it. Okay, so you just joined us. I'm Ira Flato, and you're listening to Science Friday from WNYC, studios. You know, this has been called the novel coronavirus, and it seems like there's still so much we don't know about it, isn't there? Oh, absolutely. It's almost endless the questions that could be posed. And I think that in hematology research, the research community is super

charged right now to try to do our part to help answer some of these really critical questions, getting back to this idea of anticoagulation and hospitalized patients. If we were, to just start anticoagulating every patient who comes in the hospital, we would cause a lot of bleeding complications. And we don't know really whether that's the right intervention. You know, maybe an intervention towards the complement system is better or an anti-inflammatory approach is better. So we don't really know the answer. Yet we're seeing these kinds of protocols arise in hospitals. And it's good because people are doing what they think is best. but doing what you think is best, you know, best for your patient isn't always the right thing.

And so that's where the role of research comes in and really trying to, in a supercharged way, proceed to launch, you know, major research efforts to answer this question. So that's kind of what's driving us in our clinical trial to say, okay, let's pause here for a moment and figure out really get the evidence that we need to understand if this is the best of or not, you know, trying to solve these questions of racial disparities. Is it all due to socioeconomic factors, or is there a biological difference in the chagulopathy in these patients that is contributing to the worst outcome? You know, we really don't know. And we can't get these answers without research. So for your listeners who are, you know, science, ekey people,

you know, this is the scientific process is laid out right here for you to see. And I think it's for really exciting time for answering new questions. And maybe we'll find out answers to questions that relate to other diseases as well. We have run out of time. I'd like to thank both of you. Dr. Mary Cushman, haematologist at the University of Vermont Medical Center, Professor of Medicine and Pathology at the Larner College of Medicine at UVM in Burlington, Vermont. Dr. Jeffrey Lawrence, Professor of Medicine in the Division of Hematology, Oncology at Wilde-Cornell Medicine, and attending physician at New York Presbyterian Hospital. Thank you both for taking time to join us today.

You're very welcome. You're welcome. We're going to take a break. And when we come back, tracking through the history of China via genetics, this is Science Friday. I'm Ira Flato. The human family tree is complicated, like most families. The roadmap of how our ancient ancestors journeyed out of Africa and across the globe

is filled with twists and turns, dead ends, and missing pieces. One of those missing pieces is how early humans populated East Asia. Scientists are using ancient genomes to fill in that story, and producer Alexa Lim has more. The history of a group of people can be reconstructed through what they've left behind. That can be artifacts like pottery, written text, or even pieces of their own DNA, found in ancient bones and in their living descendants. A group of scientists examined 26 ancient genomes from East Asia that give clues to how people spread through that continent 10,000 years ago.

Their results were published this month in the journal Science. Melinda Yang is one of the authors on that study. She's a professor of biology at the University of Richmond and Virginia. Welcome to Science Friday. Hi, thanks for having me. So you looked at the genomes of East Asians who lived during the Neolithic age, which is around 10,000 years ago. Can you describe that era?

humans were living in communities then? What were they like? I would say that the Neolithic age started around 10,000 years ago. That was like the early Neolithic. And then that lasted until about 4,000 to 3,000 years ago when you start transitioning into the Bronze Age. And so this period is largely defined by the development of farming and associated with farming very settled communities that start across this time period changing in complexity. So at the very beginning 10,000 years ago, there's so a lot of questions about, oh, there's a little bit of evidence of farming, but there's a lot of things that show it's not their major mode of economy. And then by the late Neolithic, you start getting very established complicated settlements that sometimes show levels

of hierarchy. There may be walls that are around these settlements. There may be sort of things that look like prestige items that sort of suggests that there's perhaps some inequalities, you know, amongst the people that live within that community. So like I mentioned, you collected these samples of ancient genomes. What was the main question you were trying to answer in your study? So we had populations, well, we had individuals, sorry, from northern China, sort of along the lower edges of the Yellow River, sort of the main river in northern China. And then we had individuals from southern China who were along the southern coast near the Taiwan Strait. So basically with these two, we sort of have samples from the two major regions of China.

But because we have these samples, we could start asking, okay, what are the differences between these two groups? There's not really a clear difference between these two groups today, if you look at their genomes of present-day populations. And so what was it like at this point? In the early Neolithic, are there changes that we can observe that are tied to this time period? But I think the first thing is we just had no samples from this area, and it's a major archaeological region. There's major transitions that are happening during this time period. So we wanted to be like, what is it that's happening in mainland China? Right. Whenever we talk about like genetic splits in populations, it gets like complicated of keeping track.

It's like trying to keep track of all the characters and Game of Thrones, right? Yeah. So then what you're saying is, you know, there were these two genetically distinct northern and southern groups. And then they kind of mixed. Is that what happened? That's one of the first big findings that we saw is that when we looked at these past populations, perhaps really starting from the early Neolithic. So that's about 9,500 to 8,000 years ago are the samples that we have from then, and then we have it from both sides. And when we looked at them and we compared them to each other, we found that they were much more, they were very genetically distinct from each other in a way

that present-day populations from those two areas were not. So that was our first big thing of like, oh, here we can find this differentiation from each other that is very hard to discern if you just use modern human genomes from the same regions today. Then after that, like the very fact that we see that difference between back then and today sort of was this marker of like, hey, ad mixture is likely the big thing or some intermixing between these populations is likely the big thing that is made it so that today's populations don't have this level of differentiation. And when you say admixture, that means they're having kids with each other, right?

Yeah, so ad mixture is a technical term, sorry. So basically when they're having kids with each other, if they're from two very distinct groups of people genetically, then you can sort of see that mixing in the genome because you get one from your mom, one from your dad in terms of like your chromosomes, each of your chromosomes. And so therefore, if there's really different patterns, say your mom comes from a population that has a mutation A and then your dad comes from a population and has mutation B, you're going to have a mix of those, right? And then if you're looking at it in a population level, you're looking at sort of like frequencies of these mutations. And if you have ones that show up that you don't

typically find, it's more likely that it came from an outside population than that it was its new and separate mutation that happened at the exact same spot. That's really statistically unlikely. Right. And so then why did the northern population start moving down or why did it start becoming more dominant? So here, I'm going to say it's a bit more speculation, but what we need is, is I think more samples from these areas, but because of the fact that we see this occurring in, like in the early Neolithic, you don't really see this mixing, but then you do see it by the late Neolithic within those southern populations. And then you do see most of that northern ancestry today. The combination of that and previous archaeological studies that have shown that there's this expansion of farming that sort of comes out from the Yellow River region, which became like a major. farming area by the late Neolithic. And so this area, these people were likely moving southward and carrying some of their farming technology with them, right? And so therefore, you see a later spread of farming technology in certain areas of the south. And so therefore, you sort of have this

overall story of a north-to-south wave that's occurring across many different regions. And when we're studying this, we're seeing it over and over again in different places. So that's really neat. So then where did the Southern group go? One of our other major findings here is, big thing here is we don't have samples from more inland southern China. So who knows what, you know, on that other side and like what types of ancestries are there. But at least these people that we do have from coastal mainland China, what we found is that they show a really close relationship to present-day Austronesians.

And so Austronesian refers to sort of a language family that's found in Taiwan, in islands of Southeast Asia and islands of the Southwest Pacific. But what's really cool is that these ancient southern East Asians, they show a really close relationship to these Austronesians. What I mentioned is that the southern ancestry sort of still exists a little bit in humans today. So they clearly mixed with the northern populations that were coming down. And so they still persist in mainland China. But then in these peoples also moved into Taiwan and then into, you know, the rest of Southeast Asia and the

Pacific Southwest, I guess in a way to say they have like the living remnants. And so that's where they still exist sort of in the most clear genetic ancestry of them. Right. Okay. So I want to take a step even further back. One of the earliest modern human scientists found in East Asia dates back to 40,000 years ago. Who was that person? Yeah. So that was the Tandrian Man. He is an individual that was found at a really important site for paleoanthropology. That's right. in Western Beijing, but he's 40,000 years old. And so he's very clearly, mostly related to modern humans, very clearly a homo sapiens. The big finding that we had with him was that this is essentially an early Asian. So it's not very closely related to East Asians, but it's closest to them

relative to Europeans, for instance. And so we have sort of something that's, you could call Asian-like in terms of their genetics, 40,000 years ago. in this area. But it's also the ancestor to, you know, all the Southeast Asians. It's also ancestor to Native Americans before they cross the varying strait. So you have like a very old Asian ancestry is what I'd call it. There's more recent stuff from other studies that show that there's other ancestries that are also super old and diverged and separate from present-day East Asians that we find more recently that are in Southeast Asia. There's something that exists in Japan, that's also a fairly old ancestry, and none of these look like present baby

stations today. We know that the Tandrian individual, their ancestry, had to have persisted in some form until more recently, because you see in Native Americans, some groups have a little bit more shared affinity to this guy than others do, which suggests that they must have been carrying some Tandran-like ancestry, some of the groups when they were cross-a-year-old. the Bering Strait. This Tandrian ancestry, a big question, I think, still remains of like, how long did it last in China or mainland Asia? Who did it contribute? Is there any evidence left of their ancestry up until more recent times? And so a lot of people are interested in that question, especially in my lab in China. So he's not like a direct ancestor. He's like a cousin.

Yeah, yeah. A cousin, a first cousin, third cousin. You know, something like that. Or twice removed, maybe that's the right word. Twice removed, right? And then you said he's related to Native American populations? There was this interesting find in South America that solely comparing present-day humans with each other. What they found was that some groups in South America shared a little bit of a connection to groups in Papua New Guinea, in Australia, and in the Andaman Islands off the coast of India. And so these three groups that they were looking at, they split off really, really early

for non-African populations. They have this very old ancestry there that if you were to look at them, it sort of dates back into the first movements of modern humans across Eurasia. They have this connection, but it's really weird because they obviously weren't able to cross the giant Pacific ocean to get to the Americas. There's no evidence that suggests that could occur. And so they believe that potentially there was some ancestry that was related to them that was in mainland East Asia that contributed to them and that was carried over across the Bering Street as well. And it's something that we don't have an individual for. And it's when we saw that 10 year individual showed that same connection, that was sort of like a smoking gun of like, oh, there's definitely

things in mainland East Asia that sort of shares these very, very early ancestry like things. That's still just a vague hint. So I think we're still looking in. East Asia to find something else that, you know, really, really clearly shows this connection between now, Beijing, area, and then Papua New Guinea and Americas. But then the fact that we have something in mainland Asia was sort of a big find for us. So, yeah, so then what is, you know, your study and then, you know, finding Tengen, what is it filling in about our understanding of ancient East Asia? Pre-Nalithic, there was all these different types of. of very, very diverse Asian ancestries.

All of them are no longer found on their own today. They sort of maybe pop up, you know, in a few places in ad mixed form, but they're mostly not represented. And then you have this wave of some other ancestry that is now everywhere across present day, East Asia. Farming definitely played a role. I think we see that over here. But then it seems a bit more complex than that because there are non-farming groups

that are in the south that are more closely related to those farming groups and not to those Pillarlythic hunter-gatherers like Candoran. This is all speculation over here. But I think that sort of suggests that there's just a lot more population movement than people are normally typically thinking of with hunter-gatherers in mainland East Asia. But to like get at that genetically, we have to find a lot more samples and be able to get ancient DNA out of them. I'm Alexa Lim, and this is Science Friday from WNYC Studios.

there's like a lot of different ways to like study history even ancient history why the way you do it why is that interesting to you my interest in this states back to high school where I really became interested in archaeology because I was interested in all the different ways sort of how we can study humans like a giant mystery where you can ask these questions about how they live what were they eating you know what were they throwing away what were they sort of keeping and burying with them you know that were things of value and then sort of sort of get at their motivations for why. they were doing certain things. And I love that when I visited Jamestown when I was in ninth grade, and there was an archaeologist trying to tell us about that. And I was like, this is really neat that you can tell these things, not by looking at written texts. So I think that was sort of the first seed of being interested in human history. How did I end up on a computer coding trying to compare genetic patterns? Right. And so in college, I was trying to better understand the genetic aspects of this. And then what I was discovering is that people were better able to sequence humans, sequence anything.

And so you could start getting massive amounts of DNA from many, many different population. It's becoming a big data question. I was interested in how is it that I can look and analyze big data that's coming from DNA and assess individuals from across different regions, across the world, to address what I think is the most interesting questions about human prehistory, you know, like how their biological movements connect to what's observed culturally in their pottery and their tools and how that's shifted over time. You've studied another population in Asia.

I'm talking about pandas. You looked at the genome of a 22,000-year-old panda. Yeah. So when you learn how to do the methodology, humans really aren't that different from, you know, all the other organisms out there. But this individual, the specimen, was from, Guangxi, which is like one of the most southern provinces of China, and it's not an area where you find

pandas today. So, so 22,000 years ago, when this panda was alive, there was obviously the pandas that would lead to the present-day pandas that we don't have genetic samples for, but then there was also much, much different-looking pandas genetically. And so there was a high amount of genetic diversity that was present in pandas in the past. I don't know what. their fur color would have looked like. But the reason that we were even looking at this specimen is because it's skeletal morphology. So all we had was its skull was very similar to pandas. So I don't think that if we, you know, were to walk in and see this, this is a zoo. We would say like, oh, hey, this is a panda. But people who study pandas and who know what are the

important sort of features about them, you know, look at the skull when they were like, okay, this is definitely a panda that we had in the past. Like you said, you can apply it to anything. Thanks for joining us. Yeah, thanks for having me. It's cool to be able to talk about my research over here, especially since I think a lot of people don't know very much about northern and southern East Asia.

Melinda Yang is a professor of biology at the University of Richmond in Virginia. This is Science Friday. I'm Alexa Lim. And that's about all the time we have for this week. If you missed any part of the program or you would like to hear it again, subscribe to our podcasts or ask your smart speaker to play Science Friday. Every day now is Science Friday. Oh, and one more thing. Earlier this week was World Bee Day. If you missed out on the celebration, we have a lesson about the bots and the bees for you. I know video looks at RoboBee. Two Harvard

engineers have gotten a step closer to creating a fleet of the winged miniature robobees. You can watch the video at ScienceFriday.com slash RoboB. And you can say hi to us on social media, Facebook, Twitter, or email us. The address is, of course, SciFri at ScienceFri.com. Send feedback. Tell us what you'd like us to cover too. Have a great and safe weekend. I'm Ira Flato.