Why peanut allergy is so common and hot forests as test beds for climate change
38:22 Share

This podcast is supported by the Icahn School of Medicine at Mount Sinai, one of America's leading research medical schools.

The school is the academic arm of the Mount Sinai Health System in New York City. It's consistently among the top recipients of NIH funding. Researchers at the Icahn School of Medicine in Mount Sinai have made breakthrough discoveries in many fields vital to advancing the health of patients, including cardiology, cancer, immunology, neuroscience, and artificial intelligence. The Icahn School of Medicine at Mount Sinai. We find a way.

This is the Science Podcast for June 12, 2025. I'm Sarah Crespi. First up on the show, staff writer Eric Stockstad talks about how scientists are probing the world's hottest forest to better understand how plants will cope with climate change. His story is part of a special issue on plants and heat, which includes reviews and perspectives on the fate of plants in a warming world.

Next on the show, convergent antibodies may underlie the growing number of people allergic to peanuts. Researcher Sarita Patil joins us to discuss her research on allergies and antibodies. She explains how different people actually appear to create antibodies with very similar gene sequences and 3D structures that bind to peanut protein. This is a big surprise given the importance of randomness in the immune system's ability to recognize harmful invaders.

This week in science, we have a special issue on plants and heat.

Some of the topics covered include how changing temperatures are reshaping plant microbiomes and safeguarding photosynthesis in crops. Be sure to check those all out. And also for the special issue, staff news writer Eric Stockstead wrote about studying how plants from the hottest regions contend with heat and how resilient they'll be as the heat gets turned up. Hi, Eric. Welcome back to the podcast. Always nice to be here, Sarah. Thanks for having me.

This is a really smart idea, I think, examining how plants from the tropical areas around the planet deal with heat and how they may or may not be OK as things get warmer. Can you start us with how plants in general deal when temperatures spike? What kind of mechanisms do they have? There are a lot of tricks up their sleeves. I mean, if plants have sleeves, they have tricks up their leaves. How about that? Plants have lots of tricks up their leaves.

to deal with heat. One is trying to avoid heat like we do. We try to stay out of the sun and they have ways of coping with heat if they can't avoid it. So that means if their leaves are getting hotter, they'll try to respond to that actively to keep the temperature inside the leaf at a comfortable level. I'm looking at this beautiful graphic from your story and it looks like there are kind of two main categories. There's what they do at the cellular level and then

And then there's also kind of these longer strategies involving changing up their leaves. Which one do you want to take first? First of all, it's a podcast. This is a beautiful, mostly visual graphic. So I'd encourage anyone who's interested in this topic and wants to know a little more to look at it on the web because the graphic really is a beautiful illustration

illustration on multiple scales of how plants deal with this from looking at leaves to looking at the surface of the leaf to zooming into inside a cell that's photosynthesizing. Here's what they do. Let's start with the zoomed in part. Let's start at the cellular level. What's going on when a plant is suddenly blasted with hot sun?

Plants turn to a really ancient strategy. In fact, it's so ancient that they share it with animals and bacteria. It's a tool called heat shock proteins. So when a cell is stressed by high temperatures, numerous bad things can happen. Proteins, they're just getting it done inside the cell, proteins are. But when it gets too hot, they can start to misbehave. They can unfold and

And you don't want that to happen. So heat shock proteins are what are called molecular chaperones. The plants are creating heat shock proteins to try and fortify these proteins for higher temperatures, repair ones that have already come a bit unstuck from the excessive temperature. They might release volatile organic compounds, right? And so those are produced in the cell. One is called isoprene and many, many plants will release this and it is in

in antioxidant. Harmful molecules get released inside cells and you want to mop them up before they do too much damage. Isoprene and other antioxidants will help reduce those. Oh, is there anything you want to say about the photosynthetic part of this? Plants, of course, have special organelles called cloroxes.

chloroplasts and chloroplasts have special membranes inside them, which is where all the reactions happen behind photosynthesis. When temperature goes up, all these membranes, they start to become more wiggly, more fluid.

So plants will change the fatty acids that they're synthesizing and putting into these membranes to help them stay robust at higher temperatures where they would otherwise need to start to leave. Let's move up in scale to what happens on the leaf itself when it gets exposed to a lot of heat.

Plants are pretty dynamic in their leaves. You might notice, right, if you have an office plant and you've moved it into the sun, that as it grows new leaves, they'll look different from the old leaves. If a plant's in too much sun, it will have a lighter colored leaf. If you've moved it into the shade, the leaves will be darker. As it's growing leaves, the leaves are adapting to those changing conditions of light levels. It will also do that with temperature changes.

The most important way that leaves can cool themselves is by opening pores in the leaf that allow evaporated water to escape. You could think of it like sweating. I was about to say you got there first. That cools the leaf off. So plants can open and close these stoma, these stomata to regulate how much they're cooling, how much water they're losing for

for the goal of keeping cool. If this is a longer heat wave than a few days, as they grow new leaves, they can have leaves that have more of these. So that increases their capacity to cool themselves. So that's one. You might change the color. Some plants will change the angle of the leaf as it's growing to have it exposed to less direct sun. These are all the tools in the plant's back pocket.

These are all the tricks up their leaves that allow them to kind of deal with these short term bursts of heat. But they do have kind of this safe operating temperature outside of which things start to kind of fall apart. And this can happen for different reasons. Can you kind of talk about some of the main effects that occur when a plant just gets too much heat for too long and none of these things are working? If temperature keeps going up and, you know, I think we're talking in the high 40s, it's different for every species. Right.

But generally, 45 degrees Celsius, getting hotter and hotter, the photosynthetic machinery inside the leaf starts to get irreversibly damaged.

At that point, the leaf's figuring out, is it worth trying to save this leaf? Should this leaf just die? Chlorophyll, the green pigment, that will start to break down. That's why they go from green to brown. I am just making you describe a leaf dying in like minute detail right now. That's right. But the death of a leaf is not the death of a plant, right? So plants can lose leaves. In fact,

leaves die here in the temperate zone where we're talking to each other. We see that in the autumn, in the fall. They come back. In the tropics, right, it's often a stress response. I've heard people say, oh, well, plants will move uphill or they'll move north to cooler areas or they're going to evolve to adjust to these higher temperatures along with climate change. How realistic is that for the tropics? It depends a bit on where we're talking about the tropics. So if

If you're in the tropics near the Andes, for example. You got some mountains nearby. In mountains nearby, your seeds can travel further up the hills, the foothills, the mountain, and they will be in a cooler environment. So that is one way that plants can move to...

to find a temperature range that's more suitable to what they're adapted for. If you're in the lowlands, in the middle of the Congo Basin, in the Amazon, your seeds have to travel a lot farther. So it's just not practically feasible for plants to move fast enough, right, on their generation time to get to cooler further north, further south, or up.

So there are real limits and there are studies coming out that suggest that given the response that plants have made, that the pace of evolution and the pace of migration just isn't fast enough for the forecasted temperature rises. The thinking is there are real constraints on whether plant communities will be able to cope with higher temperatures faster.

How will these communities change over decades up to the end of the century as temperature goes up degree by degree? That's a hard prediction to make because if you look back in time, we do find in geologic time,

tens of millions of years ago, the climate was a lot warmer than now. And we know from the fossil record that the tropical forests were still present, right, and expanding. So it's hard to handicap that bet, isn't it? Well, let's talk about what the researchers are doing to kind of tease this apart, because it is a very tough question. To do that, we're going to do a tour of the tropics. Let's start with the

the Boiling River in Peru. This is the first thing I heard about this story was that there was a very, very hot river and that researchers are studying it and the plants around it. How hot is hot? How does it get so hot? What's going on there? This is one of the hottest forests around.

Plants live in hotter environments, right? In Death Valley, in the deserts. But in terms of forests, this is a freakishly hot forest. That's due to geology. For some unknown reason, there are deep geothermal sources of water, of hot water coming up, and they end up in this river at dangerously high temperatures. You would not want to fall in to this river. It would burn you immediately.

What's amazing is it's flowing through a forest. There are trees that are surviving at 5, 6, even up to 11 degrees Celsius above the average for similar forests that are further away from this geothermal water. The scientifically beautiful thing about this place is that they go up and down this river as more or less geothermal water is in it and the temperature changes.

So they can study the forest and see how it differs at temperatures that are much hotter than other tropical forests experience. And so what kinds of changes did they see in the hottest part of the hottest riverbed? I guess the good news is, right, that there are trees there. So it is a forest. I'll take it. But it's different.

It's much less diverse. So fewer species manage to survive there. Fewer plants are growing on the ground. There are fewer animals. It does seem like it's pretty intolerable for most life. But the plants there, they seem to be doing okay. There's no real signs of stress. So that's encouraging. There's another experiment in Puerto Rico where they're warming up plants and trees with heaters. So they go out into the forest and they are like warming them up over time for years.

What has that shown about plants' resilience to heat, their growth in the presence of excess heat, that kind of thing? What they've seen are some mixed signs. And most of these experiments that we're talking about, the evidence is not clear cut in terms of saying plants are doomed or plants are going to be fine. The evidence is mixed. And that's true in Puerto Rico. They find some signs in some species that plants are doomed.

acclimating to these higher temperatures, right? That they're adjusting their photosynthetic machinery to be optimized at higher temperatures, which is a, that's a good sign. The plants will cope with it. But they also find that some species are not growing as tall. So that suggests that they're stressed by the temperatures.

Now, under Rwanda, this is where scientists are moving plants around from cooler areas to warmer areas. What were they looking for? This is a really nice design, and it's happening not just in Rwanda, but in South America as well. The idea is to take advantage of the natural temperature gradient as you go up in elevation, right? So these are in the foothills, and they take species that normally live at lower elevation and hotter temperatures, and they bring them up into the cooler temperatures and they

for our purposes of thinking about how plants will respond to a warming world, they do the opposite. They take species that have been used to growing in higher, cooler temperatures and

and they move them downhill into lower elevation places where it may be five degrees warmer on average during the day. They can move these plants, they can watch them as they grow, study the leaves, and look at how they're changing compared to the controls back up at the normal cooler elevations. And they see...

But they see a cloudy picture with some species coping better than other species. You know, the takeaway, I know mixed evidence can feel unsatisfying as an answer. And I think one message that I heard

trying to squint and say, well, what does this mean for the future? Is that they're expecting that there will be chaos is too strong a word. What's the word I'm looking for? Winners and losers. They'll be winners and losers, right? So you'll have communities shifting. That might also sound a bit ho-hum, right? Because communities change and that's the nature of the world. But they do find that changes seem to be happening in a way that could have larger consequences.

and consequences, right, that humanity should pay attention to. And are the temperatures that people are talking about, these global increases, and specifically in the tropical regions, are those in range with the threat to these trees? Like, are they at their upper limit for survival? It's a simple question, isn't it? It is. I thought of it, yeah. But it gets complicated because...

Because what is the temperature of a leaf? You can measure the average air temperature of a tropical forest in space. But what matters is the temperature that the inside of the leaf is at. That's what matters for photosynthesis. You have to figure out how many leaves are experiencing those critical temperatures.

How often? Right. So it becomes complicated. And a lot of researchers are trying to figure out how hot are these leaves actually getting? And then they have to figure out how much of an impact it makes. Are they going to be heated up to these dangerous temperatures for the plants, like based on what we know about climate change models of the tropics? Yes, certainly some are. And it doesn't seem to be an alarmingly high number right now. But...

You have to think it's not just the gradual increase in temperature that is happening from increases of carbon dioxide to the atmosphere. But down the line, it might become worse. Especially with heat waves. So this sounds like very much a story in process. Researchers are looking at this question in all different ways. They're heating up plants. They're moving plants around. You even invoke biochemicals.

Biosphere 2, which I didn't realize was in operation at this point. What should we keep our eyes out for? Like what other kinds of experiments or findings are you going to be looking for in

in the near future? I think a really key one is hard to do. And that is, at what point do tropical trees die? They're not seeing it in the boiling river. They're very unlikely to turn up the heat so much at Biosphere 2 that they kill their tropical forest.

Because they probably aren't going to do that. For listeners who aren't familiar with Biosphere 2, Google it now. It's 1991, I think, when they put it together. It's an incredible story, how it came about. It's...

frankly, just as incredible that it is still being used for research. It's run as an educational and research center. You can take tours of it. I've been. It's worth the side trip from Tucson. It's just amazing what they're doing there. So they have gigantic rainforest trees inside this greenhouse in the desert in Arizona. They have done

where they deprive them of water and see what happens. They've done experiments where they increase the temperature up to 50, 55 degrees at the top of this greenhouse and see what happens. The leaves die.

but they grow back. So a key question is at what point do these tropical trees start to die? Because they can lose their leaves and regrow them, not over and over again, presumably, because it takes their resources, their stored resources to do that. So what point do these trees die? You know, we're unlikely to find out. Well, hopefully we won't find out from Biosphere 2 that those trees will continue to stay alive. That's a tough one to answer.

All right. Thank you so much, Eric. You bet, Sarah. Good to be here. Eric Stockside is a staff writer for Science. You can find a link to the story we talked about and the special issue on plants and heat at science.org slash podcast. Stay tuned for a chat with researcher Sarita Patil about why peanut allergy might be so common.

Why is peanut allergy so common? Is it something about the peanut or about us? This week in Science Translational Medicine, Sarita Patil and colleagues wrote about what's happening at the exact spot where peanut allergen meets human antibody and why so many of us react. Hi, Sarita. Welcome to the Science Podcast. Hi, thanks for having me here. Let's just do some background here on allergies. I think sometimes I might be hyper aware of peanut allergy because it

comes up so often for parents with kids in school. But is peanut allergy really a very common one, a very serious one? And is it all around the world? It's not just your imagination. We really are seeing an increase in peanut allergy. And that's been globally, not just here in the United States. The frequency of peanut allergy has been climbing, particularly in children. And the challenge with peanut allergy is that it tends to be one of the more persistent forms of allergy.

And so it really makes it a challenge to manage. You could have a childhood allergy that goes away, but peanuts going to stick around probably. Peanuts a little bit more persistent than some of the other really common allergens. Yeah. There is this big study. Everyone said, oh, if you give your baby peanuts early in life, this is going to protect them from having a really scary reaction to peanuts later. Has that proven out over time? And is it kind of

helping us with this increase. That is a landmark study and it is an amazing study for our field in general because it is true the early introduction of peanut, both in people who would have a higher risk than normal of developing peanut allergy, as well as just sort of in general, really does decrease the risk of peanut allergy and not just by a little, by a lot. So as a clinician, we recommend early introduction of peanut to all of our patients.

patients. And we really are strong proponents of making sure that we get it in early and often. Let's get into the nitty gritty here, where the epitope meets the peritope. You may have heard of an epitope before. It's this bit of a protein that the immune system recognizes. It's a specific structure on the surface, the feature that the antibody locks onto. The part of the antibody that's doing that recognition is called the peritope.

And this is part of an antibody protein that has the right bumps and dents and charge on the surface to lock on to the target protein. And this is the interaction that we're going to focus on. So let's first talk about the most common epitope from peanut. What do we know about this little piece of peanut that seems to raise so many reactions?

So in peanut allergy, where the antibody and the antigen, in this case, a peanut protein, meet is really the critical interaction that really fundamentally underlies the way that the body reacts. And we know a lot about descriptions of how the more regions of the protein that you recognize, the worse the reaction is.

We know that some people recognize some and some people recognize a whole lot of different regions. What we didn't have a lot of insight in and where advances have really been made in the last, I would say, couple of years has been in trying to figure out those molecular interactions. Because for the longest time, work that was really spearheaded by some giants in the field, we could take the peanut protein, chop it up into little peptides and

and look at where there are continuous regions of the peanut that are recognized by antibodies, because we can look at where the circulating antibodies in someone's body could bind to those peptides. But what we didn't know was what surfaces on top of that peanut protein could be recognized. Because a peptide could just be a little piece of whatever, but the structure and the surface are a lot more elaborate and different.

depend on a lot of other conditions. And we know from immunology that those are the most commonly or frequently recognized regions. So we didn't know that and we wouldn't know that until we could actually get human antibodies from people and then figure out how they molecularly bind to the peanut allergen. That's where I started a long time ago. And so there is like a fragment of peanut that seems to at least get a lot of binding from human antibodies, right?

A special fragment. There's a region on top of the peanut protein that's a 3D, what we call conformational epitope, that is recognized really commonly by peanut antibodies. I discovered this about a decade ago. And at the time, it was a sheer accident of the way that I coded my analysis.

I found these similar antibodies across multiple patients, and I was totally shocked. And when you say the antibodies are similar, what's the same about them? The sequences look fairly similar, especially in the region that we know typically contacts between the antibody and the antigen, in this case, the peanut protein. We should mention why we're talking about sequences here. This is something if you're into immunology, you probably know about, but if you don't, you don't. And basically, there is this process where we kind of

jumble up genetic material to make these different surface structures for antibodies. Yeah, I think it's worth kind of thinking about the fact that we learn that humans can make a huge number of diverse antibodies because we've got to recognize everything that's out there in the universe and protect ourselves. And so the diversity of antibodies comes from two ways. One is that we all have lots of different genes and they can recombine or rearrange in different ways. And

result in a multitude of different antibodies. But there's also this process of natural selection that we call affinity maturation, where individual pieces of the antibody get altered, mutations drop into the antibody to help it become better or have a stronger binding to a particular protein. And because of that, we all individually end up having kind of a unique set of antibodies, like kind of a unique fingerprint.

It's so interesting. Like if you think about it, these recombinations, you're just creating physical shapes, just different physical shapes. And it's going to be different both because people encounter different things, but also because how you elaborated and matured those things are different. So it's very cool, but also very complicated to then say, oh, look, these are similar person to person, right? That's kind of a surprise. It's a total statistical anomaly. And so when it happened, I was totally shocked and

kind of almost unprepared to know what to do with these antibodies. So we published it. But, you know, in the next 10 years, other people would find these antibodies and their cohorts. We'd find that these convergent antibodies is what we call them, convergent or public antibodies, would be found in lots of other disease contexts too. And so we began to understand that this was a real phenomena that

For some reason, we as a human population had really eerily similar antibodies. Once you make the physical structure, do you also see similarities there? Yeah, so it wasn't until our

our work led us to really start to interrogate how antibodies and peanut proteins interact in the 3D world, that I really began to think about convergence from not just a sequence-based level, but to really think about it as a 3D, where in physical space are these connections, these energetics being made and how are they similar?

One of the big pieces of this paper is looking at x-ray crystallography and then also modeling that interaction on a computer and saying, well, it looks the same, it looks different across antibodies collected from different people. So what did you see was the same or different about these interactions using those tools

on antibodies from all these different people. One of the things that we noticed right away is that when we looked at the models, the places, the interactions were all happening. They looked almost all identical. Like you could barely tell the antibodies apart. We thought that was strange. Then we interrogate the energetics and the same thing. You stack them all on top of each other. And the way that these two proteins are binding is almost exactly the same.

Then the next question was, did these antibodies evolve to all have the same interactions? Or were they like this just even before this process of affinity maturation had happened to them? So do we just make this? Is this kind of one of our templates that is just super common and then maybe it gets improved, but it's kind of just omnipresent in people? That's right. So to do that, we simply looked at our sequences and took out all the mutations. We reverted them back to their

pre-mutated state. You unshuffled the cards to find out what they looked like before they shuffled. And then we were super shocked because they could bind the peanut protein again with a pretty fairly strong binding. And this is where you start talking about germline keratopes, like germline binding. Can you talk a bit more about that term here? What we were actually referring to is the fact that these interactions between these antibodies that have been taken all the way back to what they would have looked like just from

from the genetics themselves. Their binding patterns were, again, eerily identical to each other. And so they were germline encoded, these interactions. So the genetic sequences not matured through affinity maturation. The structures they code for are binding strongly to peanut protein right out of the box. So this really just raises a lot of questions. You talk a

with peanut is something that you've seen with other antibodies and other disease states. So can you talk a little about how that's like a common theme that's starting to appear in allergy and immunology? One of the puzzles with peanut specifically is making it a little bit different than the other

that we had seen was in most of these other disease contexts, and I'm going to refer to like COVID, for example, the antibodies that were identified as conversion or public antibodies had the same identical genes that were used, that were rearranged, and very, very similar regions that again, bind to the protein. And there's very strict definitions around that because what you're really trying to capture is

is the ability of these antibodies to bind to the protein in similar ways, but what you have is a 2D sequence.

When we looked at the peanut sequences, they didn't use the exact same antibody gene. They used different antibody genes, which was super puzzling to me. You say they have a sequence convergence, but it's not. The sequences aren't the same or they are the same. So this is where it kind of breaks the rules a little bit. The sequences all look the same in the regions where they bind to the peanut protein.

But the genes themselves that were used to recombine, they actually used different antibody genes. Oh, that's so strange.

Do we need to talk about whether or not peanuts are some kind of special trigger for humanity? Is there something going on? Do we have a deep, dark history with peanuts? Or is it just similar to something that we were kind of encountering a long time ago? Or is this just a coincidence? What do we know? I would love to know the answer to all of those questions.

I don't think we know yet. And I think these are the first steps to really thinking about how we as humans on a population basis have these antibody genes that might be predestined or pre-programmed to bind to certain proteins in the world in pathways that are eerily similar. It's freaky because we've thought, oh, it's random. It's not inherited except for in very special ways.

It's trained by your environment. Like we had all these preconceived notions about how the immune system worked. Like it would be great if we were all born resistant to malaria. We're not. We're born semi-resistant to peanuts for some reason. It does boggle the mind, right? Why does this happen? How does it happen? It looks so predefined and so predetermined that you have to think that there has to be a reason for it. And I think all those questions, why do we have these? How did they develop? Are unknown and it's,

Really, the fun thing about this project is it's right on the edge of our understanding of so many different concepts. We're just coming into our own in terms of understanding how proteins interact in 3D space. We're just learning more about human antibody genetics worldwide. We're just learning about how convergence evolves or develops. We found one

pathway to antibody conversions. But there are undoubtedly other pathways that probably have really important implications for how we think about many other diseases. What can we do with this information clinically, dietetically? Is there a way to take advantage of this understanding? And maybe it's too soon to think about that. Oh, I don't think it's too soon at all. It's really fun because this molecular map that we now have puts a whole new set of tools in our hands.

First of all, in the field of food allergies specifically, our ability to define antibody convergence on a population basis is

allows us to understand how many people have antibodies that recognize peanut, including those disease-causing antibodies, and lets us disrupt those interactions meaningfully, not just for one person or two people, but again, on a population basis. This work builds or helps contextualize our previous work that we've done on the discovery of neutralizing antibodies and tolerance to peanut allergy. But I think

being able to have this map lets us go one step further than just even developing, you know, molecular tools to disrupt that interaction. We now have the opportunity to maybe develop antibody gene targeted approaches to shape the antibodies, the body's response, right, towards something that's more favorable or we're

We can also, you know, we can't forget about the protein, right? We can now, with this, you know, atomic level map, engineer with molecular precision, potentially what we eat or what we take in to tailor the response. Because there's going to be a top 10, right? There's going to be the top 10 things that people respond to. So interesting. Yes. It's just opening up that window, right? Opening the window to the opportunity to be able to understand what are we encoded?

to recognize. A lot of us have a response to peanut like our body recognizes it, but some of us tip over into this allergy response becomes bad for us. Do we know about that switch? And does this relate at all to our better understanding of that? I think that's a fascinating question. I don't think we know yet. There's been a beautiful set of work that kind of starts to map out how your body can tip into having allergy.

and specifically how these, the cells that make antibodies can be convinced to convert over, switch over to making antibodies that are not so good for you. It's an emergency. There's a peanut in here response. Correct. I think how that happens and where that happens and what are the multitude of ways that we can get there is a great question. Do you want to talk a little about your surveys about what babies have and what adults have and like what the different reactions look like? We didn't know.

where the antibodies that babies make bind to the peanut allergy. But we did know from that study of early peanut introduction that babies who eat peanut, they have some antibodies to peanut. So are these the same antibodies was our question. So to study that, we actually turned to our collaborators here locally who have been following healthy infants who had started eating peanut early, just as we recommend.

And we were able to look at their blood. Then we found that indeed about half of these babies made these IgG antibodies to peanut. And almost all of those, except for one, made these responses, these conversion antibodies. So that doesn't mean they're allergic. It just means that they are

They're forming these predicted antibodies that, you know, everybody tends to have. And it's very early in life. That's super cool. All right, Sarita, we're all done. Thank you so much for talking with me. Excellent. Thanks so much for having me. Sarita Patel is the co-director of the Food Allergy Center at Mass General Hospital and assistant professor at Harvard Medical School. You can find a link to the SCM paper we discussed at science.org slash podcast.

And that concludes this edition of the Science Podcast. If you have any comments or suggestions, write to us at sciencepodcast at aaaas.org. To find us on podcasting apps, search for Science Magazine or listen on our website, science.org slash podcast.

This show was edited by me, Sarah Crespi, and Kevin McLean. We had production help from Podigy. Our music is by Jeffrey Cook and Nguyen Coi Nguyen. On behalf of Science and its publisher, AAAS, thanks for joining us.