Gabriela Bishop (3:05)

Food production also needs space. Other land uses also need space. So we can't just keep expanding these natural habitats to infinity.

Roland Pease (3:13)

And autism is in the news, but for all the wrong reasons. The unfounded assertions made by President Trump earlier this week about painkillers, vaccines and autism have been widely fact checked here on the BBC World Service and most other reliable news outlets. Get your advice from health professionals if you're concerned. But his remarks ignore the extensive research into the complexities of the condition, which highlight the important role of genetics and inheritance. Several gene variants have been shown to be associated with an elevated risk of the mental condition, though that's only a starting point for further research. And their importance has been underlined in research this week showing how epigenetic controls acting early in fetal development shape the brain. Researcher Jonathan Mill of Exeter University explained to me the relation between genetics and epigenetics.

Jonathan Mill (4:14)

You know, every cell in your body pretty much has exactly the same DNA sequence, but each of those cells and tissue types that make up a human do very different functions. And so a different set of genes needs to be switched on or off in each of those cell types. And the processes that kind of mediate that switching on and off of genes are these epigenetic mechanisms. And that's what we studied in the context of development, aging and disease.

Roland Pease (4:43)

I sort of think of them as almost like a molecular Tippex that sort of just hides some of the genes so that they're not being expressed, or maybe it can even highlight them. But it's the sort of. The message isn't changed. It's just a bit muted in places.

Jonathan Mill (4:58)

No, exactly. I mean, it doesn't change the actual protein that's made. So these are not changes to the actual sequence. These processes just regulate how much of a given gene is switched on and then how much protein that makes.

Roland Pease (5:12)

And so in this study, you've actually got access to a huge number of brains, even ones from foetuses, before they're born. Just explain that a bit.

Jonathan Mill (5:21)

So we were very lucky to collaborate with the human developmental biology resource that has acquired a really unique collection of tissues spanning the early prenatal period. And we combine that with samples that have been donated by individuals to put their bodies towards research. So this is quite a unique set of samples. Our earliest sample was from 6 weeks post conception, and we have samples that go up to around about 100 years of age.

Roland Pease (5:51)

And so what with these tissues, you're. Then there are techniques, I take it then to see if this epigenetic silencing has been done.

Jonathan Mill (6:00)

Exactly. So what we'll do is we can purify different cell types. We're really interested in the differences that take place during development of different cell types in the central nervous system. So we can isolate those cell types and from those cells we extract DNA and then we can profile that for these chemical modifications that sit on top of the DNA sequence that really how genes are switched on enough.

Roland Pease (6:27)

I mean, these are ones which are known to be involved in brain development or.

Jonathan Mill (6:31)

Yeah, so it was a totally agnostic approach. We looked at every gene in the genome. So we didn't go into this, you know, expecting to find specific genes. So this is a, you know, what we would call a genome wide assay, you know, without any hypotheses about the specific genes we were going to identify.

Roland Pease (6:48)

And which sort of brain tissues was it you were looking at?

Jonathan Mill (6:52)

So we were primarily interested in the cortex, the region of a brain that's involved in many of the important functions that regulate cognition and executive function, et cetera. And it's a region of a brain that we know is important in a range of disorders and phenotypes of postnatal life.

Roland Pease (7:12)

And if I've understood your paper, right, and it is a complicated one, what you're really highlighting is that there's a lot of changes in, in this style of epigenetics, in the silencing very early on in development.

Jonathan Mill (7:26)

Yeah, and I don't think that's really surprising. So, you know, this is exactly the time that those epigenetic signatures that drive cell type differentiation and development are being laid down. So it's a really, you know, accelerated period of epigenetic changes that are really acting to temporarily switch on and off genes and bring about development of, of the human brain and the central nervous system.

Roland Pease (7:52)

So in other words, as the cells are sort of dividing in the early fetus, some genes are saying, right, okay, I've done my bit. Other ones are suddenly saying, right, this is where I need to start doing my bit. And that's how the character of all these cells has been defined.

Jonathan Mill (8:06)

Yeah, exactly. So this is what, you know, the neurons develop during this period. And so a neuron will have a specific set of genes and there are many different types of neurons as well. And each of those will have very specific functions that activation of specific genes.

Roland Pease (8:23)

But as well as seeing that they are being turned on and off, I presume these are genes Given the title of your paper, these are genes which are associated with neurodevelopmental disorders such as autism and schizophrenia. So these. You're suddenly saying this system is telling you these. Sort of confirming that these are the genes, which should be interesting.

Jonathan Mill (8:47)

Yeah, well, so, as I said, we didn't go into this expecting to find any specific genes. We were obviously able to show that actually there's very widespread epigenetic reprogramming during this period. And I don't think that's a surprising observation. What we did find were that genes that have been very robustly linked to neurodevelopmental outcomes like autism and schizophrenia through genetic studies, these genes were really enriched for these very dynamic developmental changes. And that just really reinforces the hypothesis that, you know, there are very early origins of these outcomes and that neurodevelopment plays a really potentially highly important role in the onset of these phenotypes.

Roland Pease (9:36)

I mean, you also looked at brains from adults much later in life. How did that comparison help you?

Jonathan Mill (9:44)

Yeah, so, I mean, in a way, this really highlights how striking the changes are during the prenatal period, because actually, the changes that we saw postnatally were firstly, you know, much attenuated in terms of their magnitude, but also very different. And so what that tells us is that the change is taking place during development aren't just, you know, the early parts of aging per se, but that's something very specific about development of the central nervous system. The changes postnatally are occurring in different gene regions and different kind of systems and are probably more about just general aging than development.

Roland Pease (10:29)

I mean, in the context of what's been in the news this week, I suppose part of what you're saying is that this just underlines the fact that so much of this could actually just be written into the genes. And, well, to be frank, you know, what a mother may or may not do, there's no good reason from your research to think that that's got anything to do with it.

Jonathan Mill (10:56)

Yeah, absolutely. I mean, we weren't really looking for changes associated with those types of exposures. It's not something that we could look at in this study. But I think the evidence is irrefutable that genetic variation plays a really significant role in autism and schizophrenia and other disorders of the central nervous system. Whereas I would say some of the epidemiological evidence pointing towards some of the things that have been in the news this week are probably much less robust.

Roland Pease (11:28)

If you're able to develop this line of research and so get a Better idea of what it is about which genes are being silenced and how and when and when. I'm still not quite sure how that will help clinicians deal with the disease that actually is a very serious one in children. Do you have a sense of how it fits into the sort of the bigger picture?

Jonathan Mill (11:53)

Yeah, absolutely. So, I mean, as I said, the intention of this study absolutely wasn't to study autism and schizophrenia. The aim of the study was to look at development of the human central nervous system. I think what it does is highlight some of the reinforces the fact that genetic variation is likely to play a strong role in these traits and outcomes. And what that does, I suppose, is really give us an indication about some of the underlying mechanisms that might be important in terms of how this relates to clinical outcomes and treatment. I think that's certainly not something that we're thinking about here and I think that's a long way down the line.

Roland Pease (12:44)

Well, that's one of the things my impression of the field is a. That it's incredibly complex. And here you're talking about things that in the past we would have no idea was going on in the brain because we didn't have the means to find these things and that the processes are so complicated. The idea that we ought to have had a treatment by now for something so deep in the brain is fanciful.

Jonathan Mill (13:11)

Yeah, well, I mean, firstly, I would refute the claim that we really wanted treatment for something like autism. I mean, autism is a, at the end of a spectrum of a personality trait, whereas something like schizophrenia, where there really are kind of severe consequences of having a diagnosis with schizophrenia. I mean, that is something where potentially, by understanding the developmental causes, by understanding the cell types that are involved in the disease, that we can then maybe, you know, tap into targeting some of those dysregulated patterns of gene expression and hopefully make symptoms better for patients who are suffering.

Roland Pease (13:55)

Epigeneticist Jonathan Mill, whose study was just published in Cell Genomics, let's say with genes, their fluid character and disease, but turn to infections, bacteria in particular. Antibiotics are our primary weapons against bacterial infections, molecules that can disrupt a key aspect of a bacterium's life processes. But even as penicillin was first being rolled out in the 1940s, bacteria were mounting countermeasures to disarm the antibiotic. And the ease with which bacteria find new forms of antibiotic resistance is a constant worry for clinicians. Genetic packages called plasmids seem to be at the heart of their adaptability. And evolutionary biologist Samir Iqbal et al have managed to get an intriguing view of what plasma look like before antibiotics, thanks to a rare collection of historic samples from over a century ago.

Zamir Iqbal (14:57)

It's amazing. It's amazing that it exists. So Everett Murray was a microbiologist around the turn of the last century, and he worked during the first World War on various infections, and he collected samples from patients. And over the years, he collected some. Between 1917 and 1954, he collected several hundred. And at the time, they were used for comparing different strains of bacteria. And then they were frozen, essentially for decades before my colleagues at the Sanger center basically revived them, sequenced their DNA, and started studying how the DNA of these bacteria has evolved over these hundred years, the hundred years when humans have really industrialized the use of antibiotics.

Roland Pease (15:40)

The key word in your papers is plasmids. And these sort of toolkits, are they almost that bacteria carry around alongside them? You know, give me your description.

Zamir Iqbal (15:54)

So I think the way to think about it, or the way I think about it now, is that a bacterial cell is actually sort of run, if you can say, DNA runs. A cell is run by a kind of committee, and at the head is the chromosome, and this is the DNA of the actual species. But there's a bunch of foreign DNA that's come in. They're sort of lodgers. They've come in and they stay in the cell for generations. And they can be either like a toolkit, They've got some genes that are useful, or they can be a kind of manipulator, and they can control the chromosome and get it to do different things. So there are a lot of examples of plasmids, for example, altering gene expression on chromosomes and that allowing particular bacteria to be infections of humans or to survive in human serum or things like that. Plasmids can do different things. They can either be very passive and they provide useful tools, or they can be sort of controllers of the gene expression of the chromosome. And so this is the strange thing. They're not parasites, like malaria is a parasite inside us, or malaria is a disease, but they don't have their own cells. They're just DNA. But they are evolving organisms because their DNA changes, and those changes affect its fitness. And most importantly, because they can move from one bacteria to another, they could start off for several generations in E. Coli, and then it looks like, you know, they're not doing too well there. They can basically form a bridge between that cell and another cell, push themselves out, get into another cell, and start living out life there. And they may find you know, the grass is greener in another species, so they're actually independent organisms. And that was the whole idea of the project, is normally when we think about antibiotic resistance, we think about strains of bacteria that are spreading in the hospital and how has that evolved and that kind of stuff. And we don't think of the plasmids as anything more than just like a taxi that's moving around some drug resistance. But because it's an evolving organism in its own right, we can ask, how have they adapted to the fact that humans are using all these antibiotics over these hundreds of years?

Roland Pease (18:02)

And so the point is, you can actually see differences, can you, in these plasmids over the period when we didn't have antibiotics, and now they're all over the place.

Zamir Iqbal (18:11)

Yes. And I think what we learned is not just that there are some changes. So what we found is that a minority of them evolved to pick up drug resistance genes, and they became the key vectors of drug resistance today. And that is sort of what we expected to find. I mean, we were going to look and we were going to see how they changed. What we didn't expect to find was we understood the rules of the game better. So the way plasmids work is instead of picking up mutations gradually, and these being useful or not useful, they wholesale restructure their genomes so they can eject chunks of the genome. You can get two unrelated plasmids can merge to form a bigger one. It's a bit like the example I give is a bit fanciful, but it's a bit like lions and eagles mating to form a griffin. The griffin is fertile, and then the griffin competes with the lions and the eagles and it takes over. So because plasmids can shuffle their DNA in such dramatic ways, it means they just test out all kinds of different options, and over time, most of them die out, but sooner or later, one of them turns out to be useful. So now, if we look at what's happening today, 50% of the drug resistance genes that we find in our modern data are lying inside plasmids, which have been obviously fitted together, you know, built up out of smaller ones from years ago.

Roland Pease (19:34)

Were the plasmids very different 100 years ago, before the antibiotics? I mean, were there things that you could recognize as antibiotic resistance because they were needed in the sort of for the fight between bacteria and fungi and things in nature, or have they sort of taken a different character?

Zamir Iqbal (19:53)

That's a very good question. So we do find some antibiotic resistance genes back then. And that's not a surprise because antibiotics have been used by fungi and bacteria for millions of years. So it's not a surprise that the genes were there floating sort of in the environment. But what kicked off is accumulating more and more of them in a small set of plasmids, which obviously, you know, they decided that the best way for them and for their host to survive is to accumulate more of them. Beyond that, I wouldn't say that there's obvious characteristics that I can say. 100 years ago, there were, you know, plasmids were very different back then.

Roland Pease (20:30)

I mean, were they bigger? Were they bigger smaller or more or. I don't know.

Zamir Iqbal (20:34)

Well, we spent a while looking at that and they weren't bigger or smaller. I mean, I tried quite hard. I was quite convinced for a while that they were going to grow bigger, they were going to bolt together different plasmids that all had different genes, and together they'd be a super plasmid, which was much bigger. And you do see those bigger things, but you also see that happening in plasmids that don't have drug resistance in them. So what happens is they fuse things together and they see if it's any better and if not, it will just die out. And there's this continual turnover of trying. It's like a crazy, crazy free market where all kinds of companies start up all the time. They go bust a lot, but sometimes.

Roland Pease (21:13)

You have massive successes, mergers and acquisitions in the bacterial world. Amazing. Presumably, in a sense, it sounds to me like the plasmids are a brilliant way to accelerate the adaptability that just waiting for point mutations to affect this gene or that gene's much slower than saying, oh, I'm just going to throw it all up in the end, reshuffle this toolkit I've got and see what happens.

Zamir Iqbal (21:38)

That's exactly right, yes. Because they're collections of functioning tools already and then all you're doing is shifting them around and working out. Sometimes you can't have this combination because they interact with each other badly or, you know, sometimes they're not useful. And that's why lots of bacterial species are very generalist. They can live, you know, E. Coli can live in your gut, it can give in the soil. And so across a whole species, you will find hundreds of different plasmids, depending on where that particular strain is living. Whereas, you know, across our species, we all have the same DNA. It's a very different world.

Roland Pease (22:12)

Bath University's Zamir Iqbal, impressed by the flexibility of bacteria. Go to Science magazine for more of the details. A reminder, this is Science in Action from the BBC.

Go Turkia Advertiser (22:28)

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Jonathan Mill (23:45)

This is the story of the One.

Gabriela Bishop (23:47)

As a custodial supervisor at a high school, he knows that during cold and flu season, germs spread fast. It's why he partners with Grainger to stay fully stocked on the products and supplies he needs, from tissues to disinfectants to floor scrubbers, all so that he can help students, staff and teachers stay healthy and focused. Call 1-800-GRAINGER, click grainger.com or just stop.

Jonathan Mill (24:09)

By Granger for the ones who get it done.

Roland Pease (24:17)

Eight months ago, science in action led with the alarming swarm of earthquakes in the Aegean Sea, and that led to the evacuation of many from the Greek island of Santorini, the relic of a volcano that spectacularly exploded in classical times 3 1/2 thousand years ago. Santorini last erupted in 1950, followed a few years later by a major earthquake at nearby Amorgos that triggered a deadly tsunami. So no wonder the constant shaking caused alarm in February. The German Centre for Geosciences quickly sent a team with sensitive equipment to learn more about what was going on, and they report this week that magmatic rumbling deep below the seafloor was driving all that activity. Seismologist Maris Iskun led the analysis in.

Maris Iskun (25:07)

The beginning of the year. In January, there was an intense earthquake sequence starting in Santorini, and this was felt by the people and the tourists on Santorini island. And this very intense shaking was really concerning for the people because we didn't know what was going on at the time. We didn't know whether this process was tectonically driven or whether it was magma movement in the earth crust.

Roland Pease (25:35)

As I recall at the time, you had to take new instruments and so on to try and get really detailed measurements.

Maris Iskun (25:41)

So colleagues from my institution GFZ and from Geomar, they went to Santorini to deploy new seismometers as well as ocean bottom seismometers.

Roland Pease (25:53)

So you need a really close up look to get all the detail. Because you say there are a lot of earthquakes. They were sort of quite small compared to the ones we normally report on, on the program.

Maris Iskun (26:02)

There were a lot of small ones, but they also reach magnitudes of 5, which is really intense. So those, you can really feel the shaking. And this was going on day and night. So people were really terrified, they couldn't sleep at night. So also our colleagues which went to Santorini for measurements with the seismometers, gas measurements, and they did drone flights to see changes in the system of Santorini, they couldn't sleep because of the shaking. So what they, they were terrified and slept in the car for, for many nights. We were activated during this. So I was in Potsdam and I was looking at this crisis and the data in real time and what we did with new algorithms, AI driven algorithms to track the seismicity and to image where the Sesame City is really coming from. And pretty quickly we learned that it looked like a movement of magma. So when magma is injected into the rigid rock, it's cracking open new pathways. And this is really generating thousands of earthquakes. So very small ones, but also some bigger ones. And these come in waves. So when the dike is inflating, we call this a dike, a magma dike. You have an overpressure, you have. And when this pressure exceeds the strength of the rock, then we crack it open. And this is what you feel as earthquakes.

Roland Pease (27:20)

And how far down or how far near to the surface was this activity going on?

Maris Iskun (27:25)

Yeah, so this is very interesting. So the activity really started at 18 kilometer depth. So this is really, really deep. This is what we image.

Roland Pease (27:32)

Okay, that's twice as far down, let's say almost as Everest is up.

Maris Iskun (27:37)

Oh yeah, yes, it's pretty deep. It's pretty deep, but the magma is more buoyant and so it's coming up. So it's making its way to the upper levels of the crust. And this is what we Tracked. So it was going up and it was moving away from Santorini, but in an oblique fashion. And it came to rest at like 4 or 5 km beneath the sea floor.

Roland Pease (28:02)

You talk about the magma rising. Where's it coming from in the first place?

Maris Iskun (28:06)

So the magma is really coming from depths. So we have a subduction zone there. So there is. The African plate is being subducted beneath the GAM plate. This is melting up at great depth. So we're talking about like between 60 and 80 kilometers. So we have molten rock coming up, but we cannot see it. So we only know this from the models we have, and we have geochemical evidences. This is plate tectonics. Right. At large scale. Then we have batches of magma that is rising up and these common pulses. So it's only the last step where the magma can really break rigid rock. So below the rigid rock, it's viscous. It's like play doh. Right. So you cannot generate any earthquakes, so you don't see them. So just bubbling up there like a lava lamp. Right. It's only these top 15, 18 kilometers where we can really track it using seismicity.

Roland Pease (29:04)

The magma, which did move last February, last January, has that just cooled down? Has that gone hard? Now if it just looked like some kind of basalt, if you could get down there with a chisel.

Maris Iskun (29:16)

Yeah, that's a great question. So most likely it's when these magmas in place, they're full of gas, so they dissolve these gases. And the cooling process really takes a long time, so particularly at these steps. So now it's sitting at like 4 or 5 km, and the solidification takes a long time. So this can take a decade or more or way more, because in the beginning. So this ascent of magma from 18km to 4km was pretty quick, actually. And then it was arrested there in 4-5km and blowing up or bloating up like a balloon. So it was accumulating and also growing. And this is what we saw in almost real time.

Roland Pease (30:01)

I mean, in a sense that's quite important because if this happens again, people who are being alarmed because they're feeling their house shake and they know that they live in a dangerous place to have. The experts say, don't worry, we are watching it and we know where this is happening. And at the moment it's not an immediate threat to you. And we'll let you know when in an evacuation is necessary. We can let you know. In a sense, you feel that you're getting towards that kind of capability.

Maris Iskun (30:24)

Yes. So on the One side, we have the scientific curiosity to, to learn more about these systems and how these volcanoes work. But what is really important is that the methods that we develop, that they scale and that they are key to better protection of the population. And we can try to contribute to this by shaping an improved and better situational awareness when these systems awake.

Roland Pease (30:54)

That's what I call science in action. And that was Maris Iskun, whose analysis just appeared in Nature Geosciences. Finally, the plight of insects whose populations have been declining alarmingly. The details are hard to pin down. So many species, so many habitats, so hard to track, especially when people only recently started to count them seriously. But a German study noted a 70 decline since the late 20th century. A global meta analysis speaks of a 45% drop. And in Europe, a third of hoverflies, a tenth of bees and a tenth of butterflies are all on the Conservation Red list. In other words, in danger of extinction. For these pollinators, it's the encroachment of vast agricultural monocultures into natural habitats that's destroying the flowers they need to survive. Land restoration is the watchword. But how much Gabriela Bishop has been trying to find an acceptable balance.

Gabriela Bishop (31:56)

It's kind of this push and pull. Agriculture needs pollinators, but agriculture, at least the way we do it now, also harms pollinators. And I think especially in Europe as well as in the uk, we've become really conscious of this and a lot of work has been done to improve policies to make agriculture more sustainable. So we're moving in the right direction. But what we tried to do here is provide more concrete recommendations of what might be needed.

Roland Pease (32:22)

I mean, the good news, in a sense, if I understand it from your paper, is that some kind of restoration of natural lands, grasslands or woodlands and so on, can actually make a huge difference.

Gabriela Bishop (32:34)

Yeah, exactly. And we were really advocating for kind of reaching a certain percentage of these types of natural habitats within agricultural areas to kind of move away from this completely cleared landscapes where we just have monocultures and very intensive farming. So bringing back in these patches of natural areas in order to maintain the pollinator populations there. And we hope that this guidance kind of provides some targets that managers or policies can look at in terms of trying to reach those.

Roland Pease (33:08)

And you say there's a kind of a threshold, a percentage.

Gabriela Bishop (33:12)

Yeah, exactly. And some people will definitely not agree with how we've defined it here, but we kind of just aim to get one type of definition which can be used, which is, in our case, a threshold percentage, where after this threshold, it would actually be more beneficial to start improving the quality of these habitats. And when we talk about quality, we're mainly talking about flowers, because that's what the pollinators need. So we're kind of looking at it from an aspect of, let's expand these natural areas up to this certain point, and then we can start working on quality, because we know that food production also needs space, other land uses also need space. So we can't just keep expanding these natural habitats to infinity.

Roland Pease (33:57)

And the percentage. I mean, for example, you say that for hoverflies, it's 6% of the area needs to be some kind of wildland.

Gabriela Bishop (34:04)

Yeah. So a key finding of this paper was that different species groups had different thresholds, and that's because they have different needs and different uses of agricultural areas. And the reason why hoverflies is so low is because they actually. Well, several species and several of the most abundant, the most common species that we see are making use of the agricultural fields themselves, whereas other species, for example, solitary bees or bumblebees, they need a little bit more room because they're more reliant on the natural habitat patches.

Roland Pease (34:38)

So when the agricultural crops are flowering, they can go there and they can use the nectar, pollen and so on from there. But that's only a small part, I guess, of the annual season.

Gabriela Bishop (34:48)

Exactly. So once those crops are done flowering, they can no longer be resources. And it's also not necessarily a nice place to set up a nest or to live permanently, because the tractors are coming through those fields. So we really need these patches of natural habitat where the bees can live from year to year.

Roland Pease (35:06)

I'm wondering the scale of these patches. Let's say I've got 100 hectares that I'm farming. So for the bees, it looks like I need about 15 of those hectares should be set aside for wildlife. Does it matter? Is it one big patch that you're talking about within that area, or are you talking about the hedges in between and maybe having some additional free spaces?

Gabriela Bishop (35:27)

So we didn't look at that specifically in this paper, and of course, it's going to be up to the land managers how it might best work in their landscapes. But in general, as ecologists, we would recommend definitely a mix of some larger patches, some smaller patches, and then these linear elements, like hedges like you mentioned, that are connecting these patches because that allows the landscape to function well in terms of connectivity.

Roland Pease (35:53)

And then you're saying that on top of having a minimum amount of land, you then can do a better job because by encouraging different kinds of plants within them.

Gabriela Bishop (36:04)

Yeah, exactly. So conservation doesn't just stop at setting aside land, we also need to manage that land to be diverse itself. And in some areas that can look like just letting the land do its thing. But in other areas, for example, in the Netherlands or in the uk, you might have a very intensive system to begin with, so you have to apply management that will allow the plants to recover, allow to have more diversity of flowers there, and then you get a habitat with a higher quality.

Roland Pease (36:36)

If some of these targets are met in farms, is this a question, then, of sustaining the current populations, or are you looking at whether that you can actually return them to the abundance that they would have been? Because presumably, you know, a thousand years ago, when most of the land was wild, the populations would be quite different.

Gabriela Bishop (36:56)

Exactly. I don't think we necessarily have the ability to do some sort of restoration to a previous state when the agricultural system looked completely different. There's been a certain level of loss and readaptation of the system to how it is now. But the main goal is to just augment the populations that are still left in order to make sure that they don't continue to decline.

Roland Pease (37:21)

So those insects which are on the red list that you're talking about, you would. You'd hope that they would at least remain on the Red List, not go extinct or hopefully become less endangered?

Gabriela Bishop (37:31)

Exactly, exactly, yeah.

Roland Pease (37:33)

This comes with a cost, as you. I think you say, and I don't know if it's not in your paper, but maybe it's in other papers. For farmers, will they incur losses in their crops, but by doing this, by setting land aside, or actually, does the pollination benefits offset, as it were, the land use?

Gabriela Bishop (37:54)

That's a great question. And yes, it's going to look different in different contexts, because if a farmer actually doesn't have any crops that they farm that need pollination, it's not necessarily in their benefit to have a really targeted piece of land for pollinators next to their crops. And in that case it would really only be for biodiversity conservation. However, generally, what we encourage is for these support schemes, like, for example, the Common Agricultural Policy in the eu, to reward this type of land management on farms in order for it to be worthwhile for farmers to do. And farmers are not only farming food, they're also stewards of the land themselves, they are the land managers. So in a way, they have the power to not only produce things, but they can also manage the land for other things that are beneficial to people. For example, biodiversity.

Roland Pease (38:51)

One other thing, because this is not all of us are farmers, but this summer in particular, I think it's been a good summer in my garden. I've seen, I think, a spectacular range of small insects and they give me real joy when I see them hovering around some flowers or something in aggregate. Can individuals with their homes and their gardens and so on, can they make a difference here?

Gabriela Bishop (39:17)

Yes, totally. That's something that has come up in previous research, that people's gardens actually play a really big role in supporting pollinators, not only in urban areas but also in suburban areas. And that's because the rest of the landscape can sometimes be so poor because of this agricultural intensification. So if people are maintaining nice gardens with lots of diversity of flowers, they can really play a key role in supporting pollinators throughout the year.

Roland Pease (39:45)

Nice to know that I'm doing my bit. Gabriella Bishop is at Wangeningen University and her study with over a hundred global collaborators was just published in Science. And that's it for Science in Action this week. I'm Roland Pease, the producer is Alex Mansfield. Go to our back catalog@bbcworldservice.com for that prize winning edition and another three decades of global science reporting.

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