Nature Podcast 10 January 2008

This is a transcript of the 10th January edition of the weekly Nature Podcast. Audio files for the current show and archive episodes can be accessed from the Nature Podcast index page (http://www.nature.com/nature/podcast), which also contains details on how to subscribe to the Nature Podcast for FREE, and has troubleshooting top-tips. Send us your feedback to mailto:podcast@nature.com

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Kerri Smith: This week, forming baby planets.

Johny Setiawan: This is the first time that a planet is discovered in its nursery with its disc of dust and gas around a young star.

Adam Rutherford: Good news for scientists tackling parasitic diseases such as toxoplasmosis and malaria.

David Sibley: Parasites use a hormone that is normally found in plant cells. The pathway that this hormone is produced by offers a promise of a potential new drug target.

Kerri Smith: And scientists have found a gene that lowers the risk of cancer while studying Down's syndrome.

Roger Reeves: This is something that we owe to the people who have trisomy 21. It is their genetic legacy, if you will, that has really led us to finding a potential way to reduce cancer incidents in everybody.Music

Kerri Smith: This is the Nature Podcast. I am Kerri Smith.

Adam Rutherford: And, I am Adam Rutherford. Kicking off our first podcast of 2008, here is Geoff Brumfiel on the ongoing search for a magnet with just one pole.

Geoff Brumfiel: You've probably never wondered why magnets have both a north and a south pole, but physicists have. Their models predict that magnetic monopoles, a north or south pole by itself should exist somewhere in the universe, but nobody has ever seen one. This week, a paper in Nature suggests monopoles might exist in an exotic material called spin ice. I spoke to author Claudio Castelnovo of Oxford University to learn more. Nature 451, 42–45 (3 January 2008)

Claudio Castelnovo: So, we have objects in our world that have a north and a south pole and we learnt by brute force that if we break them apart still we don't find a north and a south pole separate, but we find little objects that still have a north and a south pole. So, that doesn't work, but another thing that one can think of doing is taking a fridge magnet or a bar magnet and say by exerting a strong force, pulling it apart and imagine that you have actually the ability to do this without breaking it. And you know, with a bit of an imagination, imagine you are able to stretch it as far as you want, then it is true that you have an object that has a north and a south pole. But the moment you stretch it so much that what is in between is as thin as a hair, if you want, you can bend it or pull it as much as you want, it doesn't matter. Then, you really can leave one end at home and then work around with the other end and to all effects, you have a monopole in your hand. If you think of it in our ordinary world, if you want to pull them apart, it costs a lot of energy. It is very difficult. Usually, you break them. So, really this is just a segment of an imagination.

Geoff Brumfiel: So, they haven't found them out in the wild as it where, but you are saying in this paper I think ,that there is a case for monopoles existing in a condensed matter system, i.e., in a material, maybe you can tell me a little about the material and where you think these monopoles are?

Claudio Castelnovo: Okay, so, spin ice, the material that we studied is essentially an ensemble of tiny little magnets with a north and a south pole. The beauty of it is that they are arranged naturally at low enough temperatures, so that they essentially form a head to tail, so north-south, north-south lines that are closed. So, you can imagine this essentially like a soup of these loops.

Geoff Brumfiel: So, you are saying that you have norths and souths and they sort of curl back on themselves so you have like a loop, a closed magnetic loop sort of?

Claudio Castelnovo: Exactly.

Geoff Brumfiel: Okay.

Claudio Castelnovo: And, when you create an excitation, when you let rise the temperature a little bit or you use a magnetic field to create an excitation in the system, these excitation corresponds to taking one of these loops i.e., north-south, north-south, etc., and inverting all the north-south little magnets that you have along that portion and you end up with the same object, but now instead of having north-south that follow each other entirely, you have two pinch points, where you have a north-north and a south-south.

Geoff Brumfiel: So, how would you observe these in spin ices, because I don't think anyone has seen them yet?

Claudio Castelnovo: It is a difficult task. So, it turns out that these monopoles don't obey the quantization condition for the fact that they are very tiny. So, it is a matter of principle it is possible to measure them, although it requires level of accuracy that is achievable, but it requires very, very fine-tuned experiments, which are not yet set up.

Geoff Brumfiel: Okay.

Claudio Castelnovo: On the other hand, one can say, if we have many of them, we can maybe hope to see effects that are collective and this has been done already as discussed in the manuscript and by using a magnetic field to generate significant density of these monopoles in the material in spin ice, one induces a face transition in the material and that has no other explanation so far. There is no theoretical understanding of it, but for the understanding via the monopoles.

Geoff Brumfiel: So, I suppose my last question then is where does this get us in terms of actually finding these free monopoles in the universe? I mean, does this really solve that problem or is this just an interesting condensed matter sort of phenomenon?

Claudio Castelnovo: The lead point is, it is an interesting condensed matter phenomenon. In essence, it does not help us finding or answering the question of why we do not see magnetic monopoles in our ordinary universe, but it shows quite interestingly that if we change the properties of the vacuum we live in, we can actually generate them naturally, and this was maybe something that people were expecting as a matter of principle, but showing it in practice is always something very, very interesting.

Adam Rutherford: Geoff Brumfiel talking to Claudio Castelnovo of Oxford University.

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Kerri Smith: Finding new drugs to treat tropical parasites is an important task given the number of people affected and the constant battle with drug resistance. A quarter of the world's population, for example, is infected with toxoplasmosis caused by a parasite related to plasmodium, which causes malaria. Working with Toxoplasma, David Sibley from Washington University in Missouri and his colleagues have found that its ability to spread through its unfortunate host is controlled by a hormone found until now only in plants and some sea creatures like sponges. This plant's origin makes it a potential target for drugs that will combat the parasite without affecting the human host. Sibley told me about Toxoplasma's life cycle and what the team has now discovered about its plant-like parts. Nature 451, 207–210 (10 January 2008)

David Sibley: It is a very common parasite. It infects about 25% of the world's population relatively non-pathogenic fortunately. So, it only causes disease in immuno-compromised individuals, but it can cause a latent or chronic infection in many individuals. One of the mysteries about this parasite is it has very complicated developmental cycle. It grows in one form in a very fast replication type of process. This form is really responsible for expanding the number of parasites and disseminating the infection, but then it switches to a slow growing semi-dormant form and the signals that it uses to decide which form of growth it's going to use are not particularly well understood. We knew that calcium was involved in some of these signalling and as it turned out the ABA pathway that we discovered, this plant-like pathway is involved in regulating that calcium signal and basically this allows them to decide when are they going to grow fast and when are they going to switch to a dormant form. Maybe one of the interesting things about it is that it allows individual parasites to communicate, so they can collectively make a decision about their fate together.

Kerri Smith: Now, tell us a bit more about why this was unexpected then, there have been reports, haven't there, of the similarities between parasite and plant hormones?

David Sibley: Yes, that's true. There was a precedent for plant-like pathways in these parasites and we knew that it came about by an endosymbiont that they acquired in their past, in their ancient history. I think the reason this was unexpected is that it wasn't obvious in the genome, for example, how calcium signalling would work, how certain types of communication would work and so although we knew it they had these pathways, it wasn't obvious that in this case that the pathway we were looking for would wind up as a plant-like pathway.

Kerri Smith: Is this pathway that you have elucidated here, a new one, then in addition to what we already knew that they had in common?

David Sibley: Well, it is not new in the context of higher plants. Abscisic acid production is common in higher plants and it is used to control development, flowering, seed dormancy, a variety of different developmental steps. What was new is the fact that it is conserved in these parasites and here it is being used for communication again, but in a slightly different way.

Kerri Smith: Tell us a bit then about what role abscisic acid plays in this pathway?

David Sibley: So, the model is that the parasite produces abscisic acid, it builds up to higher and higher concentration so the more parasites that are found within a given cell the higher the level of ABA would be. Ultimately, this triggers the calcium rise, which is a signal for them to exit the cell, and what we showed in this study is if you block their ability to make ABA, they now don't exit the cell and instead they develop into this more dormant form that remains inside the cell.

Kerri Smith: The signalling pathways in plants and in parasites have this abscisic acid in common and so, how did you go on to use that similarity to then combat this Toxoplasma gondii?

David Sibley: Well, that was kind of a fortunate circumstance, I guessed it. In plants, if you block production of ABA, you can prevent a number of things, but one of them is seed germination. Because of the necessity of ABA synthesis for controlling development in plants, there have been inhibitors developed that will block the production of ABA and they act at a specific step in the biochemical pathway that produces this hormone. Those inhibitors are often used as herbicides and because that pathway is unique to plants and not found in animals, these herbicides have very low toxicity. They have been shown to be very non toxic to animals. So, we took advantage of this and obtained one of these compounds called floridone and we were able to show that floridone blocks production of ABA in the parasite and so, it alters its program of development and makes it much less pathogenic and so when we were treating that infections with floridone we were able to show that it would decrease the severity of the infection.

Kerri Smith: And this was in mice?

David Sibley: This was done in mice, yes.

Kerri Smith: And, so, I mean, presumably, you haven't tried this on humans yet, but is there something that you could move into human trials?

David Sibley: It's possible. There also are previous studies showing that this same herbicide, floridone will block the growth of malaria of the malaria parasite Plasmodium and we believe the pathway is also conserved in, in Plasmodium and so perhaps, this would be a lead for development of new drugs that target a unique pathway in the parasite. Then, infections with floridone, we were able to show that it would decrease the severity of the infection.

Adam Rutherford: David Sibley at Washington University in Missouri. As we heard in that report, new avenues for drug development sometimes emerge from unexpected results. The surprising parallels between hormone signalling in plants and parasites might lead us to a potential new drug target. In another study published in Nature last week, a gene associated with Down's syndrome is found to lower the risk of cancer with a potential to reduce the incidence of tumours in everybody. Charlotte Stoddart reports.

Charlotte Stoddart: The relationship between Down's syndrome and cancer has been studied for more than 50 years, but researchers can't agree on whether people with Down's syndrome, who have an extra copy of chromosome 21, suffer from cancer more, the same amount or less than the general population. Roger Reeves and his colleagues from Johns Hopkins University School of Medicine in Baltimore tried to resolve this conflict using a mouse model of Down's syndrome or trisomy 21 as it is also known. Their mice had three rather than the normal two copies of some genes. One of these genes appeared to lower the risk of getting cancer in their animal models, which is surprising given that this gene Ets2 is generally considered to be cancer promoting. Roger told me how they pinpointed the Ets2 gene. Nature 451, 73–75 (3 January 2008)

Roger Reeves: So, we initially took a mouse model with Down's syndrome. Like people with Down's syndrome, it has three copies of the number of genes, in this case, about a 108 genes and when we cross that Down's syndrome mouse model to a mouse model that gets cancer, we found that the number of tumours was significantly reduced. We had another mouse that had three copies of just 33 of those genes and when we crossed it to the same cancer model, that mouse also had a significantly reduced number of tumours. And so we/the next examined the individual 33 genes, came up with a candidate that we thought might be contributing to the lower tumour frequency and that gene was the Ets2 transcription factor and sure enough if we had mice that had a triplication of a subset of genes, but not Ets2, their tumour number went back up. So, the number of copies of Ets2 was directly correlated with the number of tumours that we saw in the mice.

Charlotte Stoddart: In your experiment, you have been looking at intestinal cancer, but do you think that this Ets2 gene could offer protection from other kinds of cancer?

Roger Reeves: That is our guess at this point and we are trying to test that now in additional models of different kinds of cancer. In people with Down's syndrome, the studies that show less cancer, show less cancers of many different origins and types, and so if the mouse model is truly representing this aspect of Down's syndrome then we would expect the same thing in the mouse model.

Charlotte Stoddart: How do you think the Ets2 gene works, what is the mechanism?

Roger Reeves: We think that what Ets2 might be doing is making the cells very sensitive to program cell death that is a normal occurrence, when cells begin to undergo the process of transforming from normal cells to cancer cells. Whatever Ets2 is doing, it makes sense to us that it must be very early in their transformation pathways since it works in so many different kinds of cells and tissues in humans.

Charlotte Stoddart: In the general population only about 1 in 1000 people have Down's syndrome and so benefit from this protection, but for people who do not actually have three copies of the Ets2 gene, do you think it might be possible to produce the same protective effect by up-regulating the gene?

Roger Reeves: I certainly hope so because I only have two copies of that too. So, we think that in fact Ets2 is a good potential pharmaceutical target if we could up-regulate that or something else in the pathway that is being activated by Ets2, just a little bit in those of use who only have two copies of chromosome 21, perhaps we could lower our risk of cancer by 95% as we see in people who have Down's syndrome. If trisomy 21, Down's syndrome weren't compatible with survival, we probably would not have found this potential way to prevent cancer in everybody for quite a long time, because I do not think most people would have taken genes that are supposed to cause cancer and increase their expression to prevent cancer. So, this is something that really we owe to the people who have trisomy 21. It is their genetic legacy, if you will, that has really led us to finding a potential way to reduce cancer incidence in everybody.

Adam Rutherford: Roger Reeves ending that report by Charlotte Stoddart.

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Kerri Smith: You are listening to the Nature Podcast. This week's Podium is from Ehsan Masood who writes about science in the developing world. Published online 2 January 2008 Nature 451, 8–11 (2008)

Ehsan Masood: Last month, driving in Jakarta, I was struck by just how bad the traffic can get. In rush hour, a 20-minute car journey can take up to 2 hours. If Jakarta was the capital of a developed society, a device on how to speed up the traffic would fly in from universities, from research centres, industry, environmental groups, and think-tanks, lone inventors even; not so, in large parts of Africa, Asia, and the middle east. Informed scientific advice is rarely available, where it is most needed. To improve the appalling standards of public transport, reduce hunger or ensure that everyone has access to medical care and good schools the World Bank is so concerned about the lack of quality analysis from indigenous institutions that is considering setting up its own research centre. One of the main differences between rich and poor countries is in the amount of knowledge that's generated for economic and social development. Learning, good practice, research, and innovation are critical for poor countries and this is no longer an issue for debate. This was not always so. For years, governments and development agencies believed that for poor countries to become richer the best thing was for them to loosen state control over their economies. Everything else, so the thinking went, would fall into place. 20 years ago, four remarkable individuals defied the sceptics and committed themselves to creating institutions for policy research and analysis in the developing world. Calestous Juma had to establish the African Centre for Technology Studies in Nairobi, in his spare bedroom. Saleemul Haq founder of the Bangladesh Centre for Advanced Studies in Dhaka in Bangladesh did not always have the funds to pay his staff. Today, these institutions, which also include the Alexander von Humboldt Institute in Bogota and the Sustainable Development Institute in Islamabad in Pakistan, are influential sources of knowledge and ideas with good international reputations. Of the many lessons from these four stories, two stand out. The first is that to build a knowledge-based institution in a developing country. It is a good idea if you are young and obstinate. It also helps to have a few friends in high places to help with fund raising or to defend you from the odd military dictator. The second lesson though is a more depressing one. Despite the success that each institution now enjoys the state of impartial policy advice in poor countries is pretty dire. This is not the fault of the West or of agencies like the World Bank or even and you often hear this as of colonialism. The fact is that the development of young people with analytical skills is being held back in many poor countries, because governments, the private sector and individual families do not see this as a priority. They either regard it as a luxury that they cannot afford or admit that critical thinking is too difficult to instil in societies were deference to elders is rewarded. Anyone who wants their country to become more advanced must understand that building public transport and enticing Microsoft to build research labs all have one thing in common. They need a steady supply of bright young people, who are bold enough to think. Now, if this needs a social revolution as much as a scientific one, I say bring it on.

Adam Rutherford: Ehsan Masood, and you can read Ehsan's feature on the same subject at http://www.nature.com/nature. Now, one question of planetary science that remains unanswered is that of how planets actually form. One of the theories is that space dust and gas accrete or slowly stick to a planetismal a tiny sub-Pluto-sized protoplanet. This week, Johny Setiawan and colleagues from the Max-Planck Institute for Astronomy in Heidelberg, Germany have discovered a baby planet sitting right in its nursery, i.e., a planet orbiting a star that is less than 10 million years old. It is a huge baby, 10 times the size of Jupiter and it is right next to a massive ring of stellar dust giving credence to the accretion theory. I spoke to Johny Setiawan and started by asking him what the conflicting theories of planet formation are? Nature 451, 38–41 (3 January 2008)

Johny Setiawan: Basically, there are two scenarios, the one is, say that, planets form from a planetesimal or from the planet's embryo, which then accrete the gas and the dust or this planetesimal and this process takes quite a long time from few million years up to even 100 million years and the other theory say that planets form from this instability of gravitational collapse, let us say that a planet can form only within a few thousand years. So, this is a quite contradiction, but there is no direct proof of that. There are only theoretical models. There is no observation evidence of both theories.

Adam Rutherford: So, you found this new planet orbiting a star, which is less than 10 million years old. Can you describe what this system is like?

Johny Setiawan: Well, the system consists of the star, TW Hydrae. It is a young star and then circumstellar discs are around the star. The disc is quite massive. It goes from very close to the star to 200 astronomical units and then what the latest discovery is then, the planet is between the star and the disc. So, the planet is in orbit of only 4% of astronomical units, which is a distance between the sun and the Earth. Before this, we know already there is only the star and disc and now we know that this disc formed planets. So, that makes this discovery interesting.

Adam Rutherford: Okay, so you have a very young star, less than 10 million years old, and then a very massive planet orbiting close to it and then this huge disc of dust further from that.

Johny Setiawan: Yeah, exactly gas and dust that is around the star and the planet.

Adam Rutherford: And the theory is that the dust seeds the planet formation and it begins to suck in matter from the disc of dust and that is how the planet forms right?

Johny Setiawan: Exactly yes, the theory says that this disc can be called as protoplanetary disc, but until this discovery nobody knew if this protoplanetary disc indeed protoplanetary.

Adam Rutherford: I understand that looking for extra solar planet is actually pretty difficult, how do you go about finding this huge planet?

Johny Setiawan: Well, if you want to detect exoplanets around young stars then you have to analyze all other things like the activity of the star and also the characteristics of the circumstellar discs around the star. It is different from the exoplanet around quiet stars like our Sun. And that's why not many young stars had been detected to have planets, at least until the TW Hydrae.

Adam Rutherford: What does this actually tells us about the formation of, say for example Earth?

Johny Setiawan: What the discovery tells is that, the planet formation and the migration should be finished or complete within 10 million years or even less than that, and circumstellar discs really form planets. It is the first time we see the connection between the young stars, planets, and environment around the system.

Kerri Smith: Johny Setiawan from the Max-Planck Institute for Astronomy in Germany. That is all for this week. Our Sound of Science is from Bjorn Nielsen from the Technical University of Denmark. He sent us the sound of the muscle protein myosin.

Adam Rutherford: Bjorn explained that by assigning a particular sound frequency to each amino acid, he and his team can hear how the modelled proteins react to simulated changes in temperature in solvent composition. I am Adam Rutherford.

Kerri Smith: And I am Kerri Smith. Thanks for listening.

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