The chemical that turns locusts from Jekyll into Hyde

Host: Benjamin Thompson

Welcome back to the Nature Podcast. This week, the chemical that causes locusts to swarm…

Host: Shamini Bundell

And a project using music to study synchronisation. I’m Shamini Bundell.

Host: Benjamin Thompson

And I’m Benjamin Thompson.

[Jingle]

Host: Benjamin Thompson

As ever, our regular coronavirus-specific segment Coronapod will be appearing later on in the podcast. If you’re just here for that, I’ll put the timings in this week’s show notes so you can skip straight to it. However, I would suggest you stick around as there’s plenty of great non-corona science coming up. In fact, Shamini, what have we got first this week?

Host: Shamini Bundell

Well, over the past few months, plagues of locusts have been devastating crops across Africa. The sheer size of the record-breaking swarms is leaving farmers fearful for their livelihoods and communities with dwindling food supplies. And yet, locusts aren’t always so devastating. In fact, they spend most of their lives as solitary creatures. What triggers their swarming behaviour has been a long-standing mystery until now. A group from the Chinese Academy of Sciences in Beijing has discovered a pheromone which they believe is responsible for the change – the chemical signal that turns Jekyll into Hyde. We couldn’t get hold of the authors for this podcast, but reporter Geoff Marsh spoke to entomologist Leslie Vosshall from the Rockerfeller University in New York.

[Locust sound]

Interviewee: Leslie Vosshall

These insects are crazy. So, they start out as solitary, peaceable insects that nibble on food now and again, but once you get them together into a group of more than a small number, they turn into a mob. They change how they look. So, they change from this nice green grasshopper look to this menacing brown look, and then they take flight and migrate in enormous numbers and settle into agricultural fields and strip them of all crops. And then they get up and they fly to the next field, strip that crop, and keep going, and it has an unbelievably devastating effect on human agriculture and life. I’m Leslie Vosshall, professor at Rockerfeller University in New York, and I am a molecular neurobiologist and I really care about how humans smell smells in the environment and how insects smell smells in the environment and how they smell humans.

Interviewer: Geoff Marsh

A slight tangent then for you – we’re here to talk about how locusts smell locusts, essentially. There’s a real sort of Jekyll and Hyde vibe to their lifestyle, isn’t there?

Interviewee: Leslie Vosshall

Absolutely. They become completely different creatures. There’s almost no precedent in biology for their behaviour.

Interviewer: Geoff Marsh

And am I right in saying that it’s been long-suspected that there’s some sort of molecule or pheromone that forms a sort of master switch from that calm, solitary form into these devastating swarms?

Interviewee: Leslie Vosshall

Absolutely, and people have been searching for that pheromone for a very long time because it’s an interesting biological puzzle, number one, but also, number two, if you found that pheromone, you could of course use it to lure solitary locusts, trap them, and prevent the riotous mob from forming.

Interviewer: Geoff Marsh

Well, perhaps we should sort of cut to the chase. The authors have, it seems, fairly conclusively nailed their suspect and identified this pheromone as something called 4-Vinylanisole, which probably means very little to most people, but perhaps we could discuss how they got to that result.

Interviewee: Leslie Vosshall

This is an amazing series of experiments. When I was sent this manuscript, I just gasped. I thought, this is unbelievable. They’ve finally solved this long-standing, centuries old problem, and they did everything that one would expect of a pheromone hunt.

Interviewer: Geoff Marsh

What’s your checklist? How do you provide robust, gold standard evidence that this is the pheromone creating the switch?

Interviewee: Leslie Vosshall

You do that by sampling the air around the locust and finding the kinds of smell molecules that are in the air, do the analytical chemistry to generate the list of molecules, go down the list to find out which one causes them to aggregate. Then the key experiment, you chemically synthesise that molecule, so you make an artificial version of whatever the locust was producing and then you ask, ‘Does the chemical synthetic variant of what you think the pheromone is have the same effect?’

Interviewer: Geoff Marsh

And then the authors extend that, don’t they, and they go on to show specifically which receptor type and where the receptor type is. It sounds seriously involved, the research.

Interviewee: Leslie Vosshall

That’s right, so this paper compresses what would be decades of work into a single paper. So, not only identifying the molecule, showing that the synthetic variant has the same activity as the stuff that the locusts make. Then they ask this question of how are the locusts smelling it, and so they do recordings of individual cells on the antenna – there are thousands of different cells – and then they puff over these individual compounds, 4-Vinylanisole, and identify cells that respond to this putative pheromone. They then have a long list of odorant receptor genes that could be detecting the pheromone, so these would be the proteins sitting in the neurons in the locust antennas that are actually binding to the pheromone, and in these really beautiful experiments, they put these genes into cells, force those cells to express this locust receptor, so you have tissue culture cells smelling the putative pheromone and then they make a match. This particular receptor is the closest match to what the locust is actually using to smell the compounds.

Interviewer: Geoff Marsh

And then as if that wasn’t enough evidence, they then, in a world where CRISPR gene editing is more easily applied, they knocked out that specific receptor and lo and behold, the behaviour was stopped.

Interviewee: Leslie Vosshall

That’s right, so a key prediction, if you have the right receptor, if you make an animal that lacks the receptor, it should no longer respond to the pheromone. The mutant retains a little bit of activity, probably because there’s additional chemical components that have a little bit of activity, but the mutant is very, very defective, so that was a beautiful genetic validation using modern techniques to make a locust that’s impervious to the pheromone.

Interviewer: Geoff Marsh

Obviously, it’s very cool that we’ve now got the specific identity of this pheromone that we’ve been searching for for such a long time, but beyond that pure science factoid, how can this new knowledge be useful in terms of stopping these devastating swarms?

Interviewee: Leslie Vosshall

The authors have already shown the way toward the deployment of this molecule. So, you can put the molecule out on bait traps, as they’ve shown in their paper, and you will attract locusts. I think that the key is to come up with something that has the same activity as 4-Vinylanisole but is amped up, so it’s 100 times more potent, and then use that as a super juiced-up pheromone version.

Interviewer: Geoff Marsh

As you said, you come from a background of mosquito biology. I suppose an idea could be borrowed from that field in terms of yeah, releasing knockout locusts into the wild that don’t respond to this pheromone.

Interviewee: Leslie Vosshall

Yeah, this is another idea, again, that could be borrowed from insect friends, the mosquitoes, that are probably an even more intractable problem, so the authors in this paper have generated mutants that don’t respond to the pheromone. You could, in principle, generate a whole race of locusts that take over the populations and now they will neither produce the pheromone nor smell it, would be the prediction.

Host: Shamini Bundell

That was Leslie Vosshall. You can find a News and Views article she’s written about this, along with the paper, in the show notes. Also, thanks to Baudewijn Ode for the migratory locust field recordings.

Host: Benjamin Thompson

Next up on the show, it’s time for Coronapod, where myself, Noah Baker and Amy Maxmen discuss the latest coronavirus updates. Now, in the past, we’ve kept the regular Nature Podcast a corona-free zone, so if you want to skip this segment then make sure you check out the show notes for the timings of everything else that’s coming up. But for now, Amy and Noah, hi, thanks for joining me.

Amy Maxmen

Hi.

Noah Baker

Hi, Ben.

Host: Benjamin Thompson

This week, we’re going to be talking about potential treatments. Now, we’ve talked about vaccines a lot, and there are ways off yet, so until they’re available it seems like treatment options for COVID-19 are limited. We’ve got dexamethasone, which seems to help if you’re seriously ill, and there’s remdesivir, which maybe shortens someone’s time in hospital if they are sickened. But there’s another group of things that researchers are looking at and that’s monoclonal antibodies. Now, they have been used for a while now for different diseases, but they’re really under the spotlight when it comes to COVID-19.

Noah Baker

Yeah, so we’ve talked a lot about antibody testing, so that’s looking for these immunoglobulins, these little proteins that are produced in the body in response to antigens, which are these little markers on the outside of the virus, and antibody therapies are an attempt to generate these antibodies artificially to sort of help kick start people’s immune systems and, I suppose, piggyback off that natural defence to try to give people a fighting chance against COVID. And people have been looking into these for quite some time and it’s plodding along. They could potentially be quite important. Usually, monoclonal antibodies are mostly used for things like cancers and autoimmune diseases.

Host: Benjamin Thompson

Yeah, there are a couple of efforts in particular to produce therapies using these monoclonal antibodies that are coming along.

Amy Maxmen

Yeah, there was a recent preprint out showing that one of them, made by Regeneron Pharmaceuticals, which is sort of a newer company that uses humanised mice in order to kind of generate what these antibodies are. They have some early results from monkeys showing that monkeys who are exposed to SARS-CoV-2 that were then treated with their Regeneron cocktail of antibodies, that these monkeys clear the virus much faster than monkeys who are treated with the placebo. So, that’s some early promising results, and they’ve started a clinical trial.

Noah Baker

I guess these monoclonal antibodies, essentially what they are is like a designer, custom-made, bespoke created version of the convalescent plasma treatment that we’ve talked about on Coronapod before. That very much aims to just throw these antibodies into a person, but they do it direct by just taking blood from people that have survived coronavirus infection and hoping that the right antibodies are in there, whereas these kind of monoclonal antibody treatments are trying to actually isolate specific antibodies and generate a specific response which is more targeted, could potentially be much more powerful, but is also much more complicated, takes more time and is much more expensive.

Amy Maxmen

Yeah, the median price for antibody therapies in the US according to a story that will be out by Heidi Ledford is US$15,000-US$200,000 per treatment, so they’re quite pricy to manufacture. Also, apparently, it’s not simple for generic manufacturers to just jump into the game either.

Host: Benjamin Thompson

And these things have to be injected as well or infused in some cases, I guess, which maybe adds another layer of complexity, and it seems like there are worries that there could be some disparity in different parts of the world. The monoclonal antibodies that I’ve read that have been sort of licensed and are being used seem to be disproportionately used in high-income countries who can afford these sorts of prices.

Amy Maxmen

Yeah, for sure, I mean remember how long it took to get antiretroviral drugs to Africa – years and years and years. So, there’s that and then also there’s some question about what about low-income people in the US, low- and middle-income people? Sure, maybe we figured out how insurance can cover treatments that are expensive for rare diseases, but COVID is so prevalent. Even making sure that everyone has enough access to this is going to be an issue, which is sort of why in our latest story, Heidi writes about how, as with vaccines right now, they’re trying to ramp up manufacturing in advance of figuring out which vaccine works. Some people are saying what needs to happen is there needs to be sort of business agreements and efforts to figure out how to manufacture antibody-based therapies rapidly now and to put in the work to figure out what arrangements could help this move faster on the science side and also what kind of deals could be made.

Noah Baker

I think that’s something that’s been quite I wouldn’t say unique, but it’s been something that’s been characteristic of the scientific response to a lot of things in COVID, is that people have been thinking not just about how can we develop therapy, but there have been calls at almost every stage to think about the distribution, think about the manufacturing, all in one go. In most pharmaceutical development, those things happen in stages, whereas everything has been happening kind of concurrently here and for good reason because these things take a long time.

Amy Maxmen

Yeah.

Host: Benjamin Thompson

I mean clearly some hurdles to overcome, not to put it bluntly, but it does appear people are quite excited, if that’s the right word, about these potential treatments.

Amy Maxmen

Yeah, and they make a lot of sense. I mean they’re exciting enough that, for example, when I went up to Seattle in the beginning of March and I met with somebody named Helen Shu, an infection disease specialist, she wasn’t just working on this home-based test that I wrote about, but she was also involved with a study to isolate antibodies from people who are infected with COVID for this very reason. So, from the very start, infectious disease people had been thinking that this is one potential powerful treatment. It’s worth pointing out that Regeneron – one of the companies involved now – they ended up having a successful Ebola drug that actually was proven to be better than remdesivir. Now, this if for Ebola – a totally different thing from COVID – but again, antibody therapies have had some successes.

Noah Baker

And there are certainly a lot that are being worked on. Right now, I think there is an estimate that there are more than 70 antibody therapies that are currently being developed to treat and prevent COVID, and there is clinical trials on the way. Again, it reminds me of there are equally large numbers if not more vaccine trials, but there’s a lot of effort going into these and so something is likely to happen. We just have to wait for that thing to happen at some point.

Amy Maxmen

Yeah, and I think what I’ve seen is that early results from the Regeneron antibody cocktail, those are expected in September, which is very soon, and Eli Lilly’s single antibody that they’re testing out, that should have data in the fall, so we should know a lot more in the months to come.

Host: Benjamin Thompson

Well, it does seem like the back half of the year is going to be fairly important for a lot of different results as well, vaccines and what have you, and I’m sure we’ll explore a lot of those later on. But for the time being, I hope you’ll both join me next week for more of the latest coronavirus news. Noah and Amy, thank you so much.

Amy Maxmen

Thanks.

Noah Baker

Thanks, Ben.

Host: Benjamin Thompson

Noah and Amy there. Coming up later in this show, we’ll be hearing what 16 headphone-wearing violinists sitting in a circle have revealed about synchronisation. Before that, though, Noah Baker is back, this time with the Research Highlights.

[Jingle]

Noah Baker

There are more emperor penguins in Antarctica than was previously thought. Despite being the largest penguins around, emperors are tricky to find as they breed on sea ice in some of the coldest and least hospitable parts of the planet. But researchers at the British Antarctic Survey have been using high-resolution satellite imagery to discover unknown colonies, often at the edge of the known emperor penguin breeding range. In a recent paper, they’ve reported eight new colonies and confirmed the existence of three more, bringing the total across the continent to 61. This suggests that there may be between 5-10% more emperor penguins than previously known, but the researchers warn that many of these new colonies are in places that are particularly vulnerable to the effects of climate change. Read more on that in Remote Sensing in Ecology and Conservation.

[Jingle]

Noah Baker

Microsoft Excel – the widely-used spreadsheet software – has been causing some headaches for geneticists by autocorrecting the names of genes. For example, if a researcher inputs the name ‘MARCH1’, which is short for membrane associated ring-CH-type finger 1, Excel has an unfortunate tendency to reformat the name into a date – 1 March. These kinds of reformatting problems are surprisingly common, with one 2016 study finding that a fifth of papers had some kind of Excel error. The solution: renaming the genes. Over the past year, some 27 human genes have renamed to avoid Excel errors, and this week, the HUGO Gene Nomenclature Committee have announced new guidelines for naming genes and proteins so as to avoid autocorrect issues. Read the full announcement over at Nature Genetics.

[Jingle]

Host: Shamini Bundell

Next up, reporter Ali Jennings has been finding out how an unusual instrumental arrangement has revealed new information about how humans synchronise.

[Violins playing]

Interviewer: Ali Jennings

Sixteen violinists sit in a circle. They’re each playing this repeating 12-note melody. The whole group is trying to play in synchrony, but each violinist can only hear their two immediate neighbours. This is because they’re wearing noise-cancelling headphones and playing electric violins. The signals from each violin are sent to a control desk, behind which sits Moti Fridman of Bar-Ilan University in Israel. Moti controls what each violinist hears. This unusual setup comes from a collaboration between art and science.

Interviewee: Moti Fridman

Actually, in the beginning, this experiment started as a demonstration by a science museum that wanted us to do something about synchronisation and only after we did the experiment, we realised that we found new science.

Interviewer: Ali Jennings

People synchronise in many aspects of daily life. Audiences synchronise their clapping. Crowds synchronise their attention. Moti himself researches synchronisation. In this setup, he connects 16 violin players in a network and precisely controls what each violinist hears. By gradually adding a time delay between what a musician plays and when her two connected neighbours hear it, Moti can upset the synchrony of the violinists in the network. Then Moti can see what the musicians do to try and resynchronise.

Interviewee: Moti Fridman

And this is something that people that try to actually play over the internet found out, that when you have a small delay, what happens is that everybody starts to slow down.

Interviewer: Ali Jennings

And this is what Moti sees with his violinists.

[Violins playing]

Interviewee: Moti Fridman

When you start to encourage the delay more and more, when the delay is half a second or a second, and you’re trying to play what you hear from me and I’m trying to play what I hear from you, there is no way.

[Violins playing]

Interviewer: Ali Jennings

As the delay increases further, different patterns of synchronicity emerge across the whole network as the violinists valiantly try to synchronise with their immediate neighbours.

[Violins playing]

Interviewer: Ali Jennings

Then when the delay reaches two seconds, the network suddenly stabilises. Each violinist believes he or she is playing in synchrony with both neighbours. But in reality, they’re actually perfectly out of synchrony. When one violinist is at the beginning of the melody, her neighbours are both half way through, and vice versa. They are now in what is known as anti-phase.

[Violins playing]

Interviewer: Ali Jennings

But the effect only works in groups of an even number. And here’s where Moti observed something that had never been seen before. In odd-numbered networks, violinists would sometimes end up with neighbours who weren’t in anti-phase, but that neighbour would be ignored, and as a result, the network would remain stable and often a violinist wouldn’t even realise they were ignoring anyone.

Interviewee: Moti Fridman

When I talked to them afterwards – ‘Did you find something different? Did you hear something different?’ – they didn’t have a clue what I was talking about. From their point of view, it was exactly the same. They didn’t even notice that they ignored one of them. Their brain did it automatically.

Interviewer: Ali Jennings

This result shows that human networks don’t work like other networks. Humans can choose to simply ignore certain connections to preserve the stability of the network. In this case, to keep playing in anti-phase with their neighbours. Designing artificial networks like this could help in other situations. For example, autonomous vehicles on a motorway can be considered a network of cars. If one car slows down to change lanes, it’s better that the other cars ignore them rather than everyone slowing down in synchrony and making you late for work. But it’s not just about the science, explains Elad Shniderman, a musician from Stony Brook University in the US.

Interviewee: Elad Shniderman

The art and the science really, really depend on each other. The science kinds of needs the art to do its experiment, and from the other way around, there is a kind of breakthrough in the artistic approach here which I need the scientists.

Interviewer: Ali Jennings

Elad worked with Moti to design the experiment. For Elad, this represents a new way of making music.

Interviewee: Elad Shniderman

I did hear minimalistic music where the phase is coming back over and over, and they play with phase, but this is different because minimalistic music, the composer controls the big picture so he decides everything. So, here, this is a totally different thing. What will come out will be something that I don’t have total control over – not me and not the musicians.

Interviewer: Ali Jennings

The setup allows the network itself to control elements of the music, and that’s what gives rise to such original and complex performances. And in the future, Moti and Elad plan to use different melodies and different instruments to explore what other compositions this setup can create, and to investigate the decision-making processes that underlie the conscious and unconscious choices the musicians make. But for now, sit back, relax, and enjoy the sound of 16 professional violinists playing in imperfect synchrony.

[Violins playing]

Host: Shamini Bundell

Ali Jennings there. To find out more about Moti and Elad’s work, head over to the show notes where you’ll find a link to their paper.

Host: Benjamin Thompson

Finally on the show, it’s time for the weekly Briefing chat where we discuss a couple of articles that have been highlighted in the Nature Briefing, and that is, of course, Nature’s daily pick of science news and stories. Shamini, what’s caught your eye over the past few weeks?

Host: Shamini Bundell

Well, you know how I love strange and quirky animals, so my pick for this week is about an anglerfish, which is kind of maybe as quirky as you can get. So, quick quiz for you, Ben. Do you know any good facts about anglerfish?

Host: Benjamin Thompson

Right, um, they have appeared in Finding Nemo. They’ve frightened me quite a lot, I think, as a child, when I saw one on a nature documentary because they’re weird looking things, right? They have that kind of lure, don’t they, in front of their heads, and this mouth just full of jagged teeth. What’s not frightening about that?

Host: Shamini Bundell

Yes, exactly. So, they dangle this sort of strange bioluminescent organ out the front of their heads and use that to tempt in prey. But another weird thing about the anglerfish, or at least about some of them because there are actually hundreds of species but the story I’ve been looking at is about a few of these species, have really weird, I was going to say mating rituals but it’s not so much a mating ritual. It’s that in many species, the females are really huge, the males are really tiny, and when a male finds a female, it will bite on to her and then fuse with her body. So, it’s like attached to her body, like often, sometimes, permanently.

Host: Benjamin Thompson

I mean I’m kind of speechless. That is a bit out there. Is that parasitism? I mean how are we defining that?

Host: Shamini Bundell

So, I don’t think it’s bad for the female. So, the sort of extra nutrients she has to provide to the male are kind of small, and she can have multiple males and just have like them producing any sperm that she might need, depending on the species, but the reason that it’s generally good is that when you’re swimming around in the deep sea because this is a deep sea species of anglerfish, is that once they’ve found a mate, they kind of want to stick with it because apparently it’s just really hard to actually find mates down there, so if you find one, don’t let them go. And for the male, it kind of fuses its tissue with the female. It actually atrophies away loads of other bits of its body that it doesn’t need and gets all its nutrients from the female’s blood supply, and then it’s there. When their eggs get laid, they can be immediately fertilised. But as well as just kind of being this weird and slightly creepy way of mating, there’s been this mystery. Because of the fact that their tissues fuse together and are using the same blood supply, there’s always between this question of how their immune systems worked because if you think about if you have an organ transplant, even if you match the donor and the recipient really well, if you put foreign tissue in someone’s body, their immune system is just going to be like, no, no thank you, don’t want this, which is why you give people immunosuppressants to stop the immune system attacking things that you don’t want it to attack. So, with anglerfish, we’ve got two completely separate individuals with their tissues fused together, so the question was, how do they manage this?’

Host: Benjamin Thompson

Which begs the question, how do they manage this?

Host: Shamini Bundell

Ah, I’m glad you asked, Benjamin. So, yes, this is what the new research has been looking into, and it’s basically a genetics study of a whole bunch of anglerfish species, and what they’ve found is, particularly with the species that do the fusing, they have lost key genes in certain parts of their immune system so that whole sections of their immune system is missing, to the extent that if I was a person and I didn’t have this much of my immune system, like I would be in serious trouble.

Host: Benjamin Thompson

Well, the immune system is a fabulously complicated thing in general, but you mention sort of transplants and stuff there. One can see that there may be some benefit from this finding sort of further down the road for human sort of tissue transplantation and what have you.

Host: Shamini Bundell

Yeah, and I think that’s why they’re particularly interested in this because if we can work out to some extent how the anglerfish can survive with this massively dampened immune system, maybe that could be of use for medical interventions in the future. But that’s still very much the open question here on this one.

Host: Benjamin Thompson

Well, let’s stick with sort of animal odysseys this week, Shamini, and let’s imagine you were a beetle in a pond and you’re eaten by a frog. What do you imagine would happen?

Host: Shamini Bundell

Well, I was really happy being a beetle in a pond until you ate me with a frog. Okay, so, it’s not going to be good is it. I guess I’ll die slowly from digestive juices?

Host: Benjamin Thompson

Well, that’s what I thought too, right? But it’s not the case for one particular sort of aquatic beetle, and there’s a researcher in Japan who’s been feeding these beetles to a pond frog that it often encounters as it sort of goes about its daily life, and something rather peculiar happens. Now, it turns out more than 90% of them survived and they passed through the stomach and the stomach acid and through the intestines and all the rest of it, and made a bit of a – well, how can I put this – back-door exit. There is a video that you can watch of this. I mean, I can’t read froggy facial expressions, but I’m detecting a little bit of surprise from the frog’s face when this beetle sort of pops out and off it goes on its merry way.

Host: Shamini Bundell

Oh, man, was this just someone feeding beetles to their pet frogs and then it accidentally came out the other end?

Host: Benjamin Thompson

Well, this story did stand out to me because it reminded me of something else, and it was a toad that was fed a bombardier beetle, and this beetle sort of spews out this kind of noxious fumes, and then the toad few it up after an hour, and it turns out that it’s the same researcher who’s done this work, and it looks like he’s really, really interested in sort of insect defences, and it turns out there are a multitude, it looks like. And in this case then, with the sort of pass through situation, it seems like the legs of the beetle are important. If the legs are stuck together, the beetle gets digested. And maybe its stimulating the muscles at the back of the frog to maybe sort of release or relax and let the beetle escape. There’s a lot of important questions that I think remain to be answered with this research.

Host: Shamini Bundell

Wait, so it’s actually like actively doing something. So, if it can’t move its legs, it’s just going to get digested, therefore it must be physically doing something inside the frog to get it through unscathed.

Host: Benjamin Thompson

Yeah, apparently so, and it’s quite the journey – six hours on average from one end to the other, but the record was six minutes, which is… goodness me.

Host: Shamini Bundell

It’s definitely an unusual evolutionary response to this whole predator-prey dynamic, just like, ‘Yeah, eat me, go on then.’

Host: Benjamin Thompson

Well, I’ve been looking into this, as you might imagine – and it’s totally ruined my YouTube search algorithm, by the way – but it kind of turns out that survival of digestion is kind of rare but it does exist in snails as well and, obviously, these beetles too. So, yeah, I’m sure there’s many, many more kind of weird and wonderful ones to be discovered.

Host: Shamini Bundell

See, this is why I love evolution because it’s so cool.

Host: Benjamin Thompson

And that is why people should sign up for the Nature Briefing, to get more stories like this delivered directly to their inbox. We’ll put up a link of where to sign up and links to today’s stories in this week’s show notes.

Host: Shamini Bundell

That’s all for this week. As always, if you want to get in touch with us then you can reach us on Twitter – we’re @NaturePodcast – or send us an email – we’re podcast@nature.com. I’m Shamini Bundell.

Host: Benjamin Thompson

And I’m Benjamin Thompson. Thanks for listening.