Nature Podcast 18 May 2006

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Chris Smith: In this weeks show, a new antibiotic to tackle MRSA, there are interesting findings on chromosome one as the human genome project comes to a close, cheating bacteria re-evolve their social airs and graces, humans and chimpanzees turn out to be a whole lot genetically closer than we first thought, cells size up to the challenge of wound repair and the best prospect yet for extra terrestrial life: researchers have spotted a clutch of Earth-to-Neptune size planets orbiting a nearby start. Hello, I'm Chris Smith and welcome to the 18th May edition of Nature's Podcast. First up today a new form of antibiotic that might hold the key to dealing with MRSA and a whole host of other bacterial infections. It's called platensimycin, it's a natural product of the soil bacterium Streptomyces platensis and it works by blocking a series of key enzymes called fabH and fabFB which are used by bacteria to make fatty acids. Merck Research Laboratories' Stephen Soisson who uncovered this new agent with his colleague Jun Wang told me how they found out how platensimycin works. Nature 441, 358–361 (18 May 2006); Nature 441, 293–294 (18 May 2006)

Stephen Soisson: In bacteria fatty acid synthesis is generated by building up long carbon chains, these fatty acids consist of long carbon chains and the carbon chains are built up in two carbon units that are successively added on to the chain as it grows, and this antibiotic targets the enzyme which is the chain building enzyme if you will, it's the thing that adds on these two carbon components to the growing fatty acid chain. And by inhibiting that, very specifically, it shuts down fatty acid synthesis which is absolutely essential for the bacteria to grow.

Chris Smith: How did you go about proving that that's exactly how it was working?

Stephen Soisson: A mutant strain of bacteria was generated that expresses antisense RNA to the fabF gene and that has the effect of dialling down the amount of fabF protein that is produced in the cell which sensitises the cell to an antibiotic agent that targets that gene, so we had an inkling from the initial screen that the compound did specifically inhibit fabF but it took further confirmation using traditional biochemical methods and also we developed a direct binding assay where we could actually monitor the binding of the compound directly to the enzyme and, finally, the last thing was the determination of the atomic structure using X-ray crystallography of the antibiotic bound to fabF, seeing that it directly binds in the active site of the enzyme.

Chris Smith: This agent, though, only targets gram positives, is there any way in which it could be adjusted to make it have efficacy against gram negatives too?

Stephen Soisson: That's an interesting question. We know that the compound does bind with high affinity, to the fabF protein from gram-negative bacteria, at least E coli. So it doesn't appear to be a problem with binding to the target, it does appear more to be something that either the compound is not getting into the gram negative bacteria or it gets in and gets pumped out, so more studies are really needed to understand why it's not effective against the gram negatives and then, perhaps, a strategy could be developed to overcome that.

Chris Smith: Is this agent physiologically active though? In other words, if you inject it into the bloodstream, does it remain efficacious?

Stephen Soisson: Yes it does, and we do show that the antibiotic, when given intravenously, can clear a Staph aureus infection in an animal model.

Chris Smith: And highly efficacious or not?

Stephen Soisson: Yes it is highly efficacious and it appears to be very well tolerated.

Chris Smith: Steve Soisson from Merck Research Laboratories in New Jersey, describing how he and his colleague, Jun Wang, have discovered platensimycin, which works by blocking fatty acid metabolism in gram positive bacteria and it could prove very useful in dealing with, amongst other things, MRSA. Closer to home now, at least genetically speaking the champagne corks are popping this week as the human genome project completes it's remaining hurdle with the publication of the finished sequence of chromosome one. Here's Simon Gregory, who led the mapping of the bodies biggest chromosome at the Sanger Institute in Cambridge. Nature 441, 315–321 (18 May 2006)

Simon Gregory: The paper is about the production of finished sequence from chromosome one, subsequent annotation of the coding features like genes, looking at the genomic landscape of the chromosome and then using the sequence as the basis for looking at chromosome recombination, natural selection and also replication timing, along the length of the chromosome.

Chris Smith: There are still some gaps in this, though?

Simon Gregory: There are, there's probably about 26 gaps, I think we've got in chromosome one and probably... so chromosome one represents around 8% of the human genome and I think there is less than 200 gaps in the whole human genome at the moment, so when I mention gaps in it's the coding region of the human genome, so the euchromatic region.

Chris Smith: That's a big old chromosome then, if it's 8%, just one chromosome?

Simon Gregory: It is, so human chromosome one is the largest human chromosome, so the chromosomes are numbered one from the largest to 22, which is the smallest autosome and then you've got X and Y. And so, effectively, this publication marks the end of the chromosome publications and the fine scale analysis because it is, in fact, the last human chromosome to be published, so it's the largest and the last.

Chris Smith: Now, when you actually did this fine mapping and the annotations, there must have been some surprises?

Simon Gregory: Definitely, so the annotation is superimposed on top of the chromosome sequence manually, so we have a lot of instances where we have gene families, novel genes, expansion of genes in the specific regions of the genome. When we overlay fine mapping details that, say, originate from sources like the HapMap project where overlaying existing information, we were able to identify the fact that you can localise regions of recombination on the chromosome.

Chris Smith: And what's the significance of them?

Simon Gregory: It's the recombinations, effectively, where you are slicing and dicing chromosomes that originate from either a mother or a father inherited in the offspring, so we are able to identify regions of high and low recombination which is previously associated with the enzochromosomes, but we were able to narrow down the fact that recombination occurs away from genes, which you would expect because you don't want to disrupt genes too much, so something like 80% of the recombination of chromosome one occurs within 15% of the genome, of the chromosome.

Chris Smith: Were there any finding that were highly, medically relevant?

Simon Gregory: What the sequence of the chromosome one data enables researchers to do is to look at genes that are implicated, for example in mental retardation there's a syndrome of 1P3536, so that's at the top of our chromosome. Chromosome one is also frequently lost on the short arm in cancers and amplified in the long arm, on the Q arm in other sorts of cancers. We've got disease loci, which are associated with Parkinson's and Alzheimer's and things like that.

Chris Smith: So given that you've now polished this off, does this mean you're out of a job?

Simon Gregory: No, not at all. It's sort of a labour of love, it was very sad to see the end of the project because it really saw a collection of individuals working as a team, hundreds and hundreds of people working the lab, throughout the world, towards this common goal. And, really, the production of the sequence, the annotation of the genome and the overlapping of available resources like the HapMap, they either provide resources for additional work or the fact that we've got all the sequence now, we can actually start looking at the mechanics for the diseases that we're interested in.

Chris Smith: Duke University's Simon Gregory, who this week announced the completion of the sequence of chromosome one and, with it, the human genome project. Now, as a general rule no one likes cheaters, but Greg Velicer from the Max Planck Institute in Tübingen, Germany, seems to be the exception. He's been studying the Myxococcus xanthus, bacterium. Forms of this bug can appear which are incapable of growing on their own and they depend upon the help of the surrounding bacteria for their survival, including the ability to make spores, they are referred to as social cheaters, but are these individuals destined to be freeloaders forever? Well, apparently not because flicking a single genetic switch enabled these bacterial sponges to regain their social skills. Nature 441, 310–314 (18 May 2006); Nature 441, 300–302 (18 May 2006) |

Greg Velicer: We've been using the social bacteria Myxococcus xanthus to study the evolution of cooperative behaviours and in particular we have shown that a cheating genotype of Myxococcus xanthus,a strain that is unable to aggregate into fruiting bodies by itself, but is able to exploit other genotypes that can do so, that such a cheater, which is obligatory dependent on a co-operator, is able to re-evolve independent social autonomy, namely it's able to re-evolve its own ability to undergo development and no longer needs the co-operative sponsor.

Chris Smith: So it's almost like a passenger, a genetic passenger amongst the more competent forms of its own species?

Greg Velicer: Exactly.

Chris Smith: So how did it get like that in the first place?

Greg Velicer: It got like that during a previous evolution experiment, which was my first evolution experiment back when I was a graduate student. I had started playing around on the side, with these bugs because they looked interesting and I did a very simple experiment where I allowed multiple populations to evolve under conditions where they didn't have to go through development. So I gave them lots of food, in liquid, so they were shaking for a 1,000 generations and out of 12 populations that evolved, all of them evolved major losses in their social abilities and so, later, then I took some of these evolved genotypes that had lost their developmental ability and screened them for cheating behaviour and found that some of them, which make no spores in isolation can actually exploit their co-operative ancestor very strongly.

Chris Smith: So how did you end up finding out that they could then revert back to the spore-forming phenotype?

Greg Velicer: To be honest it was an accident! We were doing a set of competition experiments in which we were trying to determine what effect cheaters would have on longer term population dynamics, if you mix cheaters and co-operators together in a mixed population and allow them to go through multiple cycles of development. We were interested in how well do the cheaters succeed, do they cause big crashes in the population size when they get up to high frequency? Those kinds of questions and to our surprise, within just five or six cycles of development, in this one particular case, we saw this evolutionary transition happening.

Chris Smith: Have you got a handle on what's going on genetically to make these things either cheaters or revert back to full virulence, if you like?

Greg Velicer: We have the beginning of a handle, and a very important beginning. We have, for the first time, sequenced the entire genome of a laboratory evolved bacterium, so we took this strain that had re-evolved co-operative development and we sequenced its genome and we identified, what we believe, are all of the mutations that differentiate this evolved cooperator, not only from its parental cheater but also from the original ancestor from which the cheater evolved and there were 15 such mutations but only one of them distinguished the re-evolved cooperator from it's cheating parent and that one mutation, we were able to demonstrate, is the cause of arrestoration of development by transferring it from the re-evolved cooperator back into it's cheating parent and conferring the evolved cooperative phenotype.

Chris Smith: Greg Velicer from the Max Plancke Institute in Tübingen, Germany showing that, under the right conditions, obligate parasites do seem to be able to re-evolve in an autonomous lifestyle.On the way we will be hearing how chimpanzees seem to have mixed their genes with humans a lot more recently than we first thought, how cells size up a repair job and how the wobble of a nearby star has revealed three rocks and, potentially, watery planets in orbit. First though, with a look at some of this week's other major science news stories and talking to Anna Lacey, here's Nature's Jo Marchant.

Jo Marchant: Thanks, the first news story I'm talking about today concerns some exciting results coming out of a genomes conference in New York. Researchers say that, for the first time, they have managed to sequence nuclear DNA from ancient Neanderthal fossils. Now, we've had mictochondrial DNA before, but not nuclear DNA and certainly not as much of it. It's obviously very difficult to sequence the DNA, it's very fragmented, very degraded. So Svante Pääbo at the Max Plancke Institute for evolutionary anthropology in Germany and his team, looked at around 60 different Neanderthal specimens, to look to see whether the DNA in the fossils was likely to have survived. They identified two that were promising and the results that they reported last week, from one of those fossils found in Vindija Cave outside Zagreb in Croatia. Nature 441, 260–261 (18 May 2006) |

Anna Lacey: But when people want to be looking at ancient DNA usually it is, like you say, very degraded. How to they manage to fit it all together?

Jo Marchant: Yes, that's really a problem with this ancient DNA. The normal way that you sequence DNA involves inserting segments of the DNA that you want to sequence into bacteria to grow the bacteria up, so that you've got enough DNA to sequence. That's really difficult when you've got tiny fragments and very small amounts of DNA so Svante Pääbo's team used quite a new method of sequencing DNA which, rather than cloning it into bacteria first, actually sequenced fragments of DNA in an emulsion directionally, kind of in tiny little wells in a slide.

Anna Lacey: And are they going to be wanting to compare this with human DNA now?

Jo Marchant: Absolutely, yes. The big question that everybody always asks with Neanderthals is did they cross breed with humans at all? We've had mitochondrial DNA before which is DNA from little organelles in the cell that produce energy and there the sequences look quite different. That suggested that there wasn't any cross breeding but having the more extensive nuclear DNA sequences will give us a better handle on that and confirm whether or not any isolated genes might have made it across.

Anna Lacey: Well, let's move now from DNA to CO2 and some rather promising figures for climate change.

Jo Marchant: Yes, this is the latest economic modelling of what it would cost us to actually stabilise the levels of greenhouse gasses in the atmosphere. I mean basically to do that you would need to transform the world's energy industry and costs of tens of trillions of dollars are often cited, perhaps three to 15% of the world's GDP over the next 100 years, but in a special issue of the energy journal they have brought together 11 different models, looking at the latest thinking of, well what effect would this have on the world's economy? And the results are quite optimistic. Nine of the 11 models predict that, if you were to stabilise carbon dioxide levels at 450 parts per million, which is widely seen as the most ambitious target worth discussing, that would set back global GDP by only 0.5% or less, over the next 100 years. Nature 441, 264–265 (18 May 2006) |

Anna Lacey: I mean, that sounds absolutely great, but how did they actually work out this model, what did they incorporate?

Jo Marchant: Well, basically they are looking at the mechanisms that lead to technological change, so they have basically been saying, okay, what policies would lead to stabilisation of greenhouse gasses at 450 parts to a million? And then they've looked at what then happens to industry and what they found in these models was that, as the private sector shifts investment into low carbon technologies, these then evolve and become more competitive with traditional energy sources becoming a lot cheaper and, actually, it ends up not costing that much at all. In fact two of the models, actually showed that global GDP was actually higher after 100 years than it would have been if we'd have carried on business as usual.

Anna Lacey: If cutting back all this carbon and getting new technologies is going to be so beneficial, why aren't we doing it already?

Jo Marchant: Well, the researchers certainly hope that their results are going to reach governments and may influence the next assessment from the intergovernmental panel on climate change, which is due for publication next year. But we have to add a note of caution, that they're just models, we don't know that this is going to be the case so it's interesting and it's an optimistic message, but I think there is a long way to go yet.

Anna Lacey: Well, there has been even more number crunching this week, but this time in the world of physics.

Jo Marchant: Yeah, that's right. It's another story about scientific rankings basically. We ran a story last summer about a ranking system called the H Index which looks at the highest number of papers a scientist has published that have each received at least that number of citations, so for example, a researcher who had 50 papers that have each had at least 50 citations would have an H Index of 50. Now, Michael Banks, who is a PhD student at the Max Planck Institute for Solid State Physics in Stuttgart, has adapted the H Index for topics within physics, he's basically used the same index but then divided that by the number of years over which papers involved in a particular topic have been published to come up with a way of answering the 'hot or not' question for his discipline. Nature 441, 265 (18 May 2006) |

Anna Lacey: So, the obvious question is: what's the top of the charts?

Jo Marchant: Actually the whole of the top five is really dominated by nanotechnology. We've got carbon nanotubes at the top and then nanowires and quantum dots and then fourth and fifth place are fullerenes and giant magneto resistance.

Anna Lacey: But people are always coming up with new indices, is this one really that new, is it going to really change ranking systems?

Jo Marchant: Well, it's a bit of fun really. The H Index that it's based on was only described for the first time last year and it's attracted interest but it's still to be studied in depth and I would say that the same is true, probably, of this one. I mean, there are obviously other ways that you can rank it. One thing we are doing is inviting readers to tell us what they think, both of this ranking system and of the top five. If you go to then you should find the story and you can comment and tell us what you think.

Chris Smith: Nature's Jo Marchant talking with Anna Lacey. This is Nature's podcast from the 18th May edition of Nature, with me, Chris Smith. All of the stories we are covering this week are, of course, available on the Nature website, and there is also a text transcript of this show which is available from And now to a man who has thrown a genetic spanner in the evolutionary works because Harvard Medical School's David Reich has compared the human genome with sequences from some of our other primate relatives, including chimpanzees. The study hinges on the fact that, as two species diverge, they slowly accumulate independent DNA mutations, and this genetic clock can be used to work out when the divergence first took place. But, unexpectedly, some parts of our genome are much closer to chimpanzees than our present understanding of hominid evolution would have suggested. And this is especially marked on the X chromosome which appears to be over a million years more similar to chimps than it should be. This had led David Reich and his colleagues to suggest that, after we diverge from chimpanzees, there was a subsequent remixing before we finally split apart for good. Nature advance online publication 17 May 2006 | ;

David Reich: We've compared DNA sequence from the human, the chimpanzee, the gorilla, the orang-utan and a monkey, a macaque monkey. And what we found were two things. One, that human and chimpanzees share genetic ancestors that range very dramatically from some sections of the genome to the other, so that in some sections we share a common genetic ancestor, four million years more recently than in other places in our genetic material. The other thing we've found is that the X chromosome, the chromosome that, along with the Y chromosome, determines sex, humans and chimpanzees have a common ancestor about 1.2 million years more recently on the X chromosome than the rest of the genome, that's about 16 or 17% more recent than the rest of the genome and that means that, in the population, just prior to the split of humans and chimpanzees, there was a very different time to the common genetic ancestor of humans and chimpanzees on the X chromosome, compared to the rest of the genome.

Chris Smith: That's a very surprising finding, isn't it? How do you account for it?

David Reich: So, one way that we thought we could explain this is by a model of population history where human and chimpanzee ancestors initially separated then were separated for quite a long time, then they became differentiated and possibly began evolving some different traits and then remixed back together. If that happened, in a kind of hybridisation event, human and chimpanzee genetic ancestry would range over a very wide range of times.

Chris Smith: Why do you think the effect is seen in the X chromosome of this remixing, but not in other bits of the genome then?

David Reich: This was the unexpected result from our study. What we found was that, by looking at the scientific literature, that there was a very unusual feature of the X chromosome that's been found by scientists who study speciation, this is not my field, this is another field. But scientists who study speciation, they found that when they mixed back populations that have separated for a substantial period of time, the genes that are unusually responsible for the incompatibility between the species, the sterility, the hybrid and viability are unusually concentrated on the X, this is called the 'large X effect' and it's one of the empirical rules of speciation that seem to occur. There's a concentration of genes associated with hybrid, a viability on the X chromosome. This means that if you separated two populations for a long time, half a million years, a few hundred thousand years, a million years, and remix them back together and they formed a hybrid population, what would happen is they would have to resolve incompatibilities on the X chromosome, which would be an unusual selection for the X chromosome.

Chris Smith: That sounds like a pretty viable explanation, but how does this sit with the fossil record then?

David Reich: So, if you use what we know about the fossil records, for when humans and orang-utan's split from each other and for when humans and Macaques split from each other, you can actually extrapolate, calculate what the time of separation of human and chimpanzees genomes were and then, since the species separated 1.2 million years more recently, calculate that. The number you get is that humans and chimpanzees split from each other more recently than 6.3 million years ago and probably more recently than 5.4 million years ago. 5.4 million years ago is incompatible with several fossils that have been identified as walking upright, so it's hard to reconcile these results with current interpretations of the fossil record of when human ancestors first speciated from the ancestors of chimpanzees.

Chris Smith: Harvard's David Reich with an intriguing explanation as to why our sex chromosomes are so much more similar to a chimpanzee than they should be. And now to John Hopkins School of Medicine where Pierre Coulombe and colleagues have been looking at how the cytoskeleton, the meshwork of proteins that work a bit like the poles of a tent to keep the cell in the correct shape, can directly control protein synthesis and therefore cell growth. The finding has obvious implications for wound healing and in a number of other important medical conditions. Nature 441, 362–365 (18 May 2006) |

Pierre Coulombe: Protein synthesis is key to cell growth and tissue growth as well and is complex to a very tight and complex regulation and what we have uncovered is a new facet to the way protein synthesis is regulated in epithelial cells.

Chris Smith: And specifically what aspects of that?

Pierre Coulombe: Well, we have discovered that a keratin, that is a structural protein that is part of the cytoskeleton in epithelial cells, contributes to regulate a kinase that is key to determine how much protein synthetic activity is going on in epithelial cells.

Chris Smith: It's quite unusual to think that a structural element and an intermediate element, at that, this part of the cytoskeleton, should have this regulatory role?

Pierre Coulombe: Yes, and this is a new facet of this function of these intimated filaments that have come into light in recent years in numerous labs throughout the world and I think that ours is really a wonderful example of this new, non-structural support function that these filaments provide.

Chris Smith: How did you actually make this discovery, what did you do?

Pierre Coulombe: Well, it was a bit of serendipity so one of the wonderful advantages in working with skin as a model system is that you can seed the cells in culture and study them in various ways and when we did that and seeded the cells from a transgenic mouse model which are lacking this particular keratin known as K17, we noticed that the cells appeared smaller and we've measured them and we confirmed that they were smaller. And in previous studies of this mouse model we had come across the notion that these animals are defective for their ability to repair wounds, but we had not been able to determine why is it that they had this defect in wound repair? And with the cell culture finding, we then went back to these wounds that we had stored in the lab and we looked at the cell size and the margin of these wounds, and sure enough, the cells were smaller. So those were the initial events that prompted a more careful investigation as to whether cell growth and protein synthesis, in particular, could be altered in these keratin or skin epithelial cells.

Chris Smith: Pretty unusual finding, there must be some obvious spin-offs from this one?

Pierre Coulombe: Yes, so I think that one of the key issues now is to determine as to whether this function that we've uncovered for this specific member of the super family of intermated filament genes and proteins applies to other members of that family in other cells and tissue context and good place to look for this kind of function would be the central nervous system and the muscle where injury to these kinds of tissues does trigger rapid changes in the intermated filament gene expression and regulation. Another spin off is that the keratin that we have been studying in the context of this project is upregulated in the context of very important diseases such as psoriasis, as well as various forms of cancer and the question is, is that could keratin be contributing to aspects of cell growth in the context of these disease processes?

Chris Smith: John Hopkins' Pierre Coulombe who has found that the cytoskeleton plays a key role in controlling genes associated with cell growth. Now finally this week we leave the solar system destined for the excitingly named star HD69830 around which the Geneva Observatory's Cristophe Lovis and his colleagues have found orbiting three rocky planets about the size of Neptune. They're to small to see directly but it was the wobble they provoked in their home star that's given them away and, intriguingly, at least one of them is in the habitable zone, like the earth, so it might be home to liquid water. Nature 441, 305–309 (18 May 2006) |

Cristophe Lovis: We have discovered a multi-planet system with three very low mass planets and it's the first such system with such low mass planets and, of course, we are now beginning to discover planets that are only a few Earth masses in mass, so we are approaching planets of a really small size and its become very interesting.

Chris Smith: So, you're into the kind of size which is almost Earth-like and, therefore, very similar in terms of their capacity to support life perhaps?

Cristophe Lovis: Yes, for example. So we are not sure now what is their exact composition, but of course if the mass is very low then these planets are very likely to be mostly rocky and in that case they would really look like the Earth.

Chris Smith: So, where are these planets?

Cristophe Lovis: They are around a nearby star. This is quite a bright star that can be seen with the naked eye and it's about 40 light years away from the earth and so these three planets are orbiting this star, which is quite like our sun, a little bit less massive, a little bit cooler, but still much like our sun.

Chris Smith: And how did you actually make these observations?

Cristophe Lovis: We used dedicated instrumentation which was developed with the goal of being able to discover possible extrasolar planets by measuring, very precisely, the radial velocity of the stars. All stars are moving across space and each star has its own velocity in space, and so when observed from the Earth we can measure the component of this velocity along our line of sight. So some stars are just receding from us and some stars are approaching. And on top of that, when they are orbited by planets, these planets will induce a little gravitational wobble on these stars and they will make oscillations around their centre of mass velocity and we are able to measure these very tiny radial velocity changes.

Chris Smith: So you saw this star, literally, wiggling a bit in space?

Cristophe Lovis: Yes.

Chris Smith: But if it wiggles a bit, how do you know there's three planets then if you can't see them?

Cristophe Lovis: The signal curve by a planet is expected to be like a sinusoid curve and when we observe this star we noticed that the radial velocity showed complicated changes that could not be only explained by one sine curve and after accumulating enough measurements and trying orbital solutions, we found that the best solution was when we fitted three planets on these radial velocity curves.

Chris Smith: And where are these planets, in relation to the star itself?

Cristophe Lovis: The first one orbits with a period of nine days, it is very, very close to the star. Much closer to the star than, for example, Mercury in our own Solar System. Then the second planet orbits in 30 days which is a little bit further away and, most interestingly, the third planet which orbits in about 200 days which becomes quite similar to the Earth and so it's about 60% of the Sun/Earth distance.

Chris Smith: Is that within what we call the habitable zone, for this particular star then?

Cristophe Lovis: Yes, for this particular star it would be at the inner edge of the habitable zone so that means just at the border where the temperature is low enough for water to become liquid and that's one of the definitions of the habitable zone.

Chris Smith: Do you think there is water there? Or do you not know anything about the composition of these particular planets?

Cristophe Lovis: At the moment we have to be very careful. From the observations we have now published, we cannot say anything about the composition of these planets but we have made some theoretical calculations that show these planets, actually the first two, are mainly made of rocks and the second one and the third on also contains a lot of ices, that means there is a lot of water, but this water is not necessarily in the liquid form, it could be in ice.

Chris Smith: So literally watch this space for more fertile findings from HD69830 and its clutch of rocky words. That was Cristophe Lovis from the Geneva Observatory. Well that's it for this week. If you have any comments or feedback on this weeks show, do drop us a line to Next time, explosive news on the volcano front, but in the meantime if you are in the mood for some more science, this weeks edition of the Naked Scientist podcast takes a look at the origins of BSE or mad cow disease, how the toxoplasmosis parasite could be linked to schizophrenia and we'll also be meeting the inventor of the cervical cancer vaccine. That's the Naked Scientist podcast which is freely available from Additional production this week was by Derek Thorne and Anna Lacey and I'm Chris Smith.AdvertisementThe Nature Podcast is sponsored by Bio-Rad. At the centre of scientific discovery for over 50 years. And on the web at