Nature Podcast 5 April 2007

This is a transcript of the 05th April 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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Ben Valsler: This week, Karl Deisseroth has found an illuminating way to control brain cells.

Karl Deisseroth: What we have discovered is a way to control the activity of brain cells using light. Blue light will turn the neurons on and orange light will turn them off. So, it is a little like a traffic light.

Ben Valsler: And I'll be on the verge of unleashing the power of the plant hormone auxin now researchers know how it works.

Ning Zheng: And with this structure we now can perhaps design better auxin-like analogues or auxin inhibitors.

Ben Valsler: More from Ning Zheng on that story coming up later in the programme. Also, Ulrich Wortmann explains how modern-day bacteria helped to solve an ancient mystery.

Ulrich G. Wortmann: I was working on a totally unrelated thing when suddenly I understood by looking at these bacteria we may be able to explain this data set from about 20 million years ago.

Ben Valsler: Welcome to the Nature Podcast. I am Ben Valsler and I will be sitting in for Chris Smith while he is off in sunnier climes. One of the best things about going on holiday is that you can put your feet up and switch your brain off. Before he left, Chris spoke to Karl Deisseroth, who has developed a technique for using light of different colours to switch neurons on and off. Kind of like a light switch for brain cells. This technique will allow scientists to accurately measure neural activity and potentially manipulate whole systems of neurons. Nature 446, 633–639 (5 April 2007) .

Karl Deisseroth: What we have discovered is a way to control the activity of brain cells, neurons using light and not only can we control them in the sense of stimulating them, we can also turn them off if we like as well, and we can do this with two different colours of light. So, blue light will turn the neurons on and orange light will turn them off. So, it is a little like a traffic light, except the colours are a little different, and the nice thing about this is light has a potential to be very well tolerated by the target cells, better than it would be if you were to stick a wire or electrode into the tissue, and it also affords us the ability to target specific subsets of neurons and that gives us incredible specificity in trying to probe neural surfaces for scientific purposes.

Chris Smith: I suppose that light is not so foreign to neurons, because after all the cells in the retina are well used to interpreting light and changing their activity in response to it, aren't they?

Karl Deisseroth: That's right, and not just our retinal cells, but many organisms in nature deal with light and have proteins which are designed to absorb light at different wavelengths and generate different sorts of outputs, and these tools that we have developed, the activator and the inhibitor of neural function, both come from microbes, one from an algae and one from a bacterium. They use proteins called microbial auxins, which we recruited and tuned and adapted for use in mammals like us.

Chris Smith: So, how did they actually wire into the function of the nerve cells so they can change its activity, in other words respond to the light you shine on them and then alter the behaviour of the nerve cell, how are you doing that?

Karl Deisseroth: What we do is we introduce the gene that codes for the protein that absorbs the light and the target cell will make the actual light response of protein. The cells then insert the new protein into their surface membrane. What happens then is when light of the right colour hits these little proteins, then on the surface of the cell that will trigger the flow of ions: in the case of the excitatory protein, there is a flux of sodium ions into the cell and that ends up stimulating the cell; in the case of the inhibitory protein, this is a chloride-ion pump and in this case, negatively charged chloride ions are pumped inside the cell and that ends up being an inhibitory influence on the cell.

Chris Smith: Have you done this both in the dish and actually in vivo, or is this just cells being cultured, where you can obviously control the situation for them very, very carefully?

Karl Deisseroth: Well, we started in culture, but we were very interested to move toward intact animals and we have two approaches towards that. First, we expressed it in nematode worms, C. elegans, and we were able to control the function of muscles and neurons in the worm; and in the mammalian branch of the work, we were able to introduce both of these genes to excitatory and inhibitory signals into the brains of mice and we were able to take out a slice of the brain tissue— a little like taking a circuit board out of a computer— and we were able to drive and control the neural circuitry in this intact mammalian brain tissue as well.

Chris Smith: I can see how this would be a massive boost for scientists because now you can non-invasively in real time see what nerve cells are doing just using light, so you don't have to harm them in vivo. Do you think there are any other applications though, I am thinking in terms of diseases and things and manipulating the diseased brain?

Karl Deisseroth: We are very excited about potential clinical applications as well as the basic science applications. For diseases one of the problems, particularly in psychiatric disease, there is no frank damage to the neurons in the brain, but there are more subtle changes in the high-speed dynamics of the circuit and it would be incredibly powerful to understand which specific cell types are working well or working too hard or not working well enough in particular diseased states.

Ben Valsler: Karl Deisseroth there from Stanford University. One of the futuristic applications of this work is that we may one day have brain implants capable of manipulating the activity of different parts of the brain using just light. You can hear more interviews and watch some videos of that technology in action on the Nature website at http://www.nature.com/nature/videoarchive/braincellonoffswitch. Now, to focusing in more depth on some of the implications of that technology. Nature's Kerri Smith caught up with correspondent Alison Abbott. Nature 446, 588–589 (5 April 2007) ; Web Focus: http://www.nature.com/nature/focus/neurobreakthrough.

Kerri Smith: The Illuminating approach to brain control reported by Deisseroth and his team is also featured in Nature's News section this week. Our correspondent Alison Abbott has written a story covering the wider implications of the work. Clearly, the clinical benefits to be gleaned from a technique are likely to be profound, but basic science will also be receiving a huge boost and the life of many neuroscientists may start to look rather different as a result. Alison is on the line from Munich. Alison, first off, how is this new technology going to help scientists studying the basic nuts and bolts of neurons?

Alison Abbott: Basically, what neuroscientists have always wanted to be able to do is to control exactly the type of neuron and exactly the place that they are interested in at the moment. A lot of brain scientists work with electrodes, you put the electrodes in a position which can indeed be very precise, but whereas a stimulant stimulates everything around it and of course an electrode cannot inhibit, it can only stimulate. What this new light-activated protein technology offers are 'on' and 'off' switches that can be placed in any type of neuron that the investigator can define or in any tiny or large brain area. Eventually, this will also give the scientists the opportunity of switching these neurons on and off at any particular time they want, so they have absolutely full control.

Kerri Smith: Well, so this is a real boost to the techniques that scientists currently have at their disposal. Deisseroth's group, as he mentioned, appreciate the potential clinical benefits of this technique, to say the least. What are the big things that this technique is likely to be useful for?

Alison Abbott: Basically to replace and supplement the clinical techniques that we have at the moment and deep-brain stimulation, but also things like lesion therapy, which is used to control epilepsy. So, what we have in deep-brain stimulation is they search and place an electrode in very precise position deep inside the brain to stimulate it. When you do the stimulation, like all electrodes it stimulates everything in its vicinity. So, we still don't know exactly what we stimulate and we could be stimulating activating neurons, we could be stimulating inhibitory neurons. All the more, it somehow works, but it is rather crude and crudeness inside the brain is something that we want to avoid. In the distant future, we have to say one could conceive of actually exchanging the electrode for some sort of optical cable, of transfecting these channels into the human brain and therefore being able to switch on exactly what we want in these defective neural circuits. This is one critical application way, way down the road and second application in particular this new channel, the inhibitory channel, which we are most excited about is the possibility of switching off any aberrant overactivity in the brain, for example in epilepsy. Mostly, however, I think we would like use this technology to understand the diseases better and therefore to develop targeted therapies, like drugs that hit the right targets rather than anything that is involved in putting in the brain.

Kerri Smith: All in all, now researchers, perhaps not surprisingly, have high hopes for that technology and I understand they are not just keeping it to themselves.

Alison Abbott: Yes, absolutely hundreds of labs around the world now have clones of these proteins. Many, many, many groups have started to use them. The results are now starting to creep up. There is a lot of excitement in the field. There is a possibility of a huge breakthrough and so people are attempting to work as fast as they can, now that they have this exciting new tool, to be the first in their particular field. It is really taking off in a big way.

Ben Valsler: That was Nature's Kerri Smith talking with Alison Abbott about the impact of Karl Deisseroth's work on the control of nerve cells using light.

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Ben Valsler: Now, the nervous system is not the only way for an organism to regulate itself. There is also a complex system of hormones. Auxins are amongst the most important of plant hormones because they regulate plant growth and show a lot of promises herbicides, but until now finding out how they work has been a challenge. Here is Ning Zheng. Nature 446, 640–645 (5 April 2007) ; Web Focus: http://www.nature.com/nature/focus/plants.

Ning Zheng: What we have discovered is following the identification of the receptor for this important plant hormone auxin, we have used X-ray crystallography to solve the 3-D atomic structure of this receptor in complex with the plant hormone, and that reveals the mechanism of how the hormone works on this receptor.

Chris Smith: Why has it been such a problem? Because, as I understand it, people have taken a very long time to work out how auxins work and finally have arrived at this point. So, what has really been the stumbling block?

Ning Zheng: Actually, the identification of the receptor has taken a very long time mainly because the receptor does not work in the general way where other receptor works, and this has to be reviewed by the structure and after solving this structure, we understand that the receptor cells doesn't have very high affinity to the plant hormone.

Chris Smith: It seems rather counterintuitive that you should have a receptor that doesn't seem to have a very high affinity for its ligand because if you look at most systems when the ligand locks onto the receptor it does so really quite strongly. So, why should auxins be different?

Ning Zheng: Right, the auxin is different because the mechanism of how auxin works involves enhancing protein–protein interactions. So, the receptor cell, even though it does sense the auxin, it doesn't have the high affinity to the auxin because the true receptor consists of the receptor cell and its protein substrates.

Chris Smith: So, the auxin is forcing another protein to interact with the receptor and therefore causing the effect, and therefore you don't see this very strong interaction between the auxin and the receptor because that is not so much the critical thing that is going on with this other protein?

Ning Zheng: Yes, and additional to that is that when the substrate binds to the receptor in the presence of the auxin, it gets degraded, that's why biochemically it's very hard to isolate a complex consisting of three molecules.

Chris Smith: Because, of course you've got to try and work out what they all are, and then work out which one is which in isolation, to then work out a structure, presumably?

Ning Zheng: Yes, so we basically produce the receptor in insect cells, but not in E. coli or bacteria because bacteria actually doesn't have the necessary cofactor that is required for the receptor to assemble. So, production of the protein was done in the insect cell, and after we purified the protein, crystallization was rather straightforward, but we ran into a problem — which is that, after we crystallized and resolved the structure of the receptor, we found a mysterious density in the middle of the receptor and we couldn't figure out what it is. So, after consulting with several senior scientists, we had an idea that it might be a chemical called inositol phosphate; however, inositol phosphate has several forms and we were not sure which one is the right one, so that is why we had to borrow the expertise from another group, which is Dr Carol Robinson from University of Cambridge.

Chris Smith: Well, Carol is here with me now. So, Carol, how did you manage to get around these problems that held up Ning and his team?

Carol Robinson: It is a very interesting problem for us because the molecule that he was interested in looking at was bound very tightly in the complex. So, although we tried very hard, we couldn't actually release it from the protein that was holding it very tightly in its inner core, and so what we did was we used mass spectrometry and we took the whole complex of three molecules, and then we put it into the mass spectrometer; and what we normally do is try to maintain protein interactions, but in this case we tried to break them apart and to release this small molecule that was bound within and what we found was we could quite easily break the two proteins, but the inositol molecule was actually bound so tightly that it wasn't keen to come out at all. So, we actually measured it in its complex with one of the proteins and from that molecular weight measurement, we were able to identify it.

Chris Smith: Did you actually know at that time it was probably inositol?

Carol Robinson: Actually, I do not think we did, but we sort of came on to the same conclusion independently over many miles.

Chris Smith: So, there was this mysterious thing stuck in the middle of all the protein. It looked like it could be inositol, but it took your work to prove that it was?

Carol Robinson: Yes, I think that is true, and I think then everything fitted.

Chris Smith: And, certainly once you ended up with Carol's data showing that this definitely did have inositol jammed into the middle of the structure of this protein receptor, how did you then take it forward?

Ning Zheng: So, then we had to solve a series of structures with the receptor together with this inositol phosphate cofactor in complex with three different auxin compounds and the substrate protein to obtain a final complete picture of how this complex works; and from the structure, what we can see is that the auxin that's present induced conformational changes within the receptor. So, this is totally in contrast to other hormones. What it does is it binds to a surface pocket on the receptor, which also holds the substrate and they bond to the very bottom of that pocket. Therefore, it sits in between two proteins and promoting protein–protein interaction like a molecular glue.

Chris Smith: And, now you have got this amazing piece of evidence and involving obviously an international multidisciplinary team, how is this going to build on what we know about auxins and how they work and what sort of applications might there be, I should think that there were lots of industrial uses, aren't there?

Ning Zheng: Yes, absolutely. As a matter of fact, a number of companies in agriculture and horticulture have contacted us because, as it turned out, there are number of naturally occurring or synthetic compounds that have auxin activity and with this structure we now can perhaps design better auxin-like analogues or auxin inhibitors.

Ben Valsler: The University of Washington's Ning Zheng and, before that, Cambridge University's Carol Robinson sussing out the structure of the plant auxin receptor, and this week Nature updates a plant biology web focus featuring this latest work and others in the field. You can find that at http://www.nature.com/nature/focus/plants/index.html. Now climate scientists are just starting to understand what happens when the amount of atmospheric carbon changes and what events causes this variation. The records of the early Cretaceous atmosphere show a huge change in carbon and sulphur levels that until now no one could explain. Ulrich Wortmann from the University of Toronto told Chris how he solved the problem. Nature 446, 654–656 (5 April 2007) .

Ulrich G. Wortmann: We found out that microbes living below the sea floor actually play a very important role in regulating the global carbon cycle, say, the content of oxygen in the atmosphere, and also how much sulphur is in sea water.

Chris Smith: Surely we knew that already, didn't we? The Earth's biomass, if we break it down how much there is in the ocean, there must be at least a third or a half of the total planetary biomass?

Ulrich G. Wortmann: Typically, when we speak about these things we speak about plants or we speak about algae living in the ocean, but we found that below the surface of the sea bottom, right, if you go below the sea bottom, there is a vast area of biological activity you can go down to at least a kilometre and you will still find bacteria living happily down there, and this totally new ecosystem is very active and plays a very active role on our planet and that is a fairly new discovery, and we show here what role it actually does have for, say, planetary cycling of carbon, sulphur or oxygen.

Chris Smith: How they are actually contributing to the levels of those things on Earth?

Ulrich G. Wortmann: On the Earth you have algae. Algae do photosynthesis and by that they produce carbon and oxygen. When the algae die, they settle down and few of them actually go into the sediment and there they are eaten by little bacteria and turned back into CO2, and by that process they are either using up oxygen or sulphur. So, that is how they influence oxygen, sulphur and carbon cycles.

Chris Smith: So, how did you actually come across the findings that you did when you did your study?

Ulrich G. Wortmann: Pure serendipity or happenstance, call it that way. We were sitting on a data set that we couldn't explain for a long, long time. About 120 million years ago, the early Cretaceous period, we have a very detailed record of a massive positive carbon isotope excursion accompanied by a massive negative isotope excursion recorded in sulphur isotopes, and that is a big puzzle. With our modern understanding, this should not be the case — they should be positively coupled and not negatively, and I was working on a totally unrelated thing, the deep biosphere and the modern sediments, when suddenly I understood that by looking at these bacteria we may be able to explain this data set from 120 million years ago. So, we actually connected two seemingly unrelated fields.

Chris Smith: So, putting it all together what do you think did happen a 120 million years ago then?

Ulrich G. Wortmann: Well, what happened is when the South Atlantic Ocean opened, it was a very warm sea and lot of gypsum was deposited during that time. Gypsum contains sulphate and sulphate is the main fuel for these deep subsurface bacterial ecosystems. Because of the opening, the bacteria lost their food essentially, their energy source, and stopped working and because they no longer converted organic matter back to CO2, they completely changed the way carbon was recycled on this planet.

Chris Smith: And are there any other spin-offs from your model, other areas where it now makes predictions, which we can go out physically and test and therefore hopefully shed some more light on this part of history?

Ulrich G. Wortmann: If you look back in time we had a lot of carbon cycle excursions and none of them was really well explained so far and I think what we can do with this model is we can go back and test now each single one of them, whether it was happened by microbial action or by some catastrophic volcanic event, for example. There is a huge very similar event happened between Palaeocene–Eocene about 50 million years ago. It is just the exact opposite. It is very well coupled with a huge thermal anomaly that was called 'Palaeocene–Eocene hothouse' and it is not very well understood. It could well be that something in these lines would explain the Palaeocene–Eocene climate.

Ben Valsler: That was Ulrich Wortmann with the answer to a 120-million-year-old mystery — the opening up of the Atlantic Ocean robbed a whole ecosystem of its food, causing a big shift in CO2 levels. Now, more recent, but every bit as mysterious, is the story behind the remains of Joan of Arc. Here is Nature's Kerri Smith. Nature 446, 593 (5 April 2007) .

Kerri Smith: Her life and death are among the most celebrated in history, and so it is only natural that the supposed relics of Joan of Arc, who was burnt to the stake in 1431in the town of Rouen in Normandy, have been treasured ever since they were discovered languishing in the attic of a pharmacy in Paris a century-and-a-half ago. But it turns out that the relics are not what they seemed. The charred-looking human rib and the remains of some linen and wood found in the site of Joan of Arc's execution did not belong to the French heroine at all, but to an Egyptian mummy. Our Paris correspondent Declan Butler has been exploring this story for Nature. Could you tell us first of all what exactly these relics consist of?

Declan Butler: It is a small jar containing the rib of a human, there is a fragment of linen 15 cm across, and then very unusually, there was a femur of a cat alongside, but this was consistent with the medieval practice of throwing black cats on to the pyre of supposed witches.

Kerri Smith: So, people were pretty convinced this was Joan of Arc then, what do they now feel it to be and why have people changed their minds?

Declan Butler: Well, for Philippe Charlier, who is a forensic scientist at the Hospital Raymond Poincaré in Paris, first of all it became immediately suspicious that it was not Joan of Arc because when he looked in detail at the actual sample after he got permission from the church last year: he found out that this had not been burnt at all, but virtually impregnated with a black kind of crusty resin which was consistent in fact with the Egyptians' way to embalm people, so that got them on to the original source of this. So, they brought a series of techniques to bear, including mass spectrometry, electron microscopy, pollen analysis. Among them the most historic was carbon-14 analysis dated the remains to 3 to 7 centuries before Christ, so that hardly fitted with the idea of a 15th century martyr. So, then they did a spectrometry profile of the rib and chunks of carbon and the cat femur and they compared this with compounds and they also did it with the Egyptian mummies and, lo and behold, the actual profile was exactly the same as that of a mummy.

Kerri Smith: As far as the modern scientific techniques that the forensic scientists spoke about and the remains, they also were using an analysis of smell, is that correct?

Declan Butler: Considering the open bodies before, they were impressed by the variety of odours, so he decided this time to get somebody to sniff the remains. So he got two of the experts, Sylvaine Delacourte from Guerlain and Jean-Michel Duriez from Jean Patou, to actually smell the samples — and of course they were trying to do this later with mass spectrometry of the air samples, but this is just to get the first note. What he found was they both independently in a blank study concluded that it smelled of burnt plaster and vanilla. Now the vanilla is inconsistent with cremation because vanillin is actually produced during decomposition of body. So, the fact that we will all produce it one day is consistent with decomposition and rules out cremation as well. But it is also very consistent with the mummy and likewise burnt plaster is actually the smell of objects like gypsum mixed with the embalming solutions.

Kerri Smith: Wow, so do we have any idea what on Earth the remains of a mummy were doing in a jar in an attic in Paris?

Declan Butler: One is that in the middle ages, mummies were used widely in medicine to create potions etc, and in fact there are entire volumes of 15th century tomes describing lots of recipes based on the blood of mummies; and then after this was the find in 1867 in the attic of a pharmacy, so that tells it nicely as well.

Kerri Smith: Certainly does. And are these the only such relics that are reported to be belonging to Joan of Arc?

Declan Butler: Yes, these are the only relics that are reported to be from Joan of Arc. Legend has it that, in fact she was, we knew that she was burnt three times because they wanted to be sure nothing was left over and the legend has it that some of her organs resisted and were found missing from the funeral pyre manifestation at the stake; in fact it is a scientific reason that it could be true, according to a study it is extremely difficult to burn a human body completely. So, there was a kind of possibility that some relic has remained and there was only one ever to have resurfaced in the past, in a jar in an attic and it was written on it "Remains found under the stake of Joan of Arc, virgin of Orleans" and was recognized by the Catholic church at the beginning of the century.

Kerri Smith: So, how significant is this finding that they did not belong to Joan of Arc?

Declan Butler: Well, clearly it is not as famous a relic as for example the Shroud of Turin, which as we know has been subject to major forensic analysis. It is of interest though, first of all for this whole palaeopathology field, what's interesting is bringing in lots and lots of modern techniques today on the studies actually carried out by people who actually have been able to uncover the past. It is really just one more case in an important area for science that has been used actually to reveal this history of tricks behind individuals. In this way, we can actually pair together a lot of history and clearly in some case the symbolic factor that the relics of Joan of Arc are in fact a fake. It is of just great public interest, I think.

Ben Valsler: Kerri Smith and Declan Butler with what it turns out are not the remains of Joan of Arc, but in fact is an ancient Egyptian mummy.JingleEnd Jingle

Ben Valsler: Now, just as Egyptian mummies were protected from the elements in sarcophagi and their tombs, the Earth is protected from the ravages of the solar wind by its magnetic field. Rory Cottrell from the University of Rochester has used the miniature magnets locked up in some of the Earth's oldest rocks to show that it has been with it for at least 3.2 billion years. Nature 446, 657–660 (5 April 2007) .

Rory D. Cottrell: We have been interested in a very long time about when the Earth's magnetic field actually started. The Earth's magnetic field is important because it helps to protect our planet from solar wind, which can be very deadly in terms of radiation and other nasty things that we do not really want to be a part of, and the Earth's magnetic field is one way that protects us from this.

Chris Smith: I think Mars has become cropper because it does not have a magnetic field any more, does it? And it has become a dried-out prune of a planet as a result.

Rory D. Cottrell: Right, Mars and Moon actually both had evidence of a magnetic field very early in their geologic history four billion years ago, but now they no longer have a magnetic field and we think that it stopped in both Mars and the Moon because the planet cooled too quickly. They no longer had a liquid iron core like we do or, in our case, liquid iron outer core that convects, and convecting electronic fluids will create a magnetic field, we have a magnetic field, and since it froze on Mars and the Moon they no longer have a magnetic field.

Chris Smith: So, is it not intuitive to think that because the Earth has been hot ever since it was created it should have had a magnetic field since it was created then?

Rory D. Cottrell: Intuitively yes, that is what you would think. It takes a little bit more than just a simple heat exchange from the centre of the Earth to the surface to create the magnetic field simply a temperature difference between the inner core, which we now know is solid and the outer core, which is liquid, is it really enough necessarily to create a magnetic field? So, one of the questions that our study can answer is when might the solid inner core have started to form — that compositional difference between the liquid outer core and a solid inner core may have been enough energy to actually kick start the magnetic field.

Chris Smith: How can you tell that? You are looking, for instance, for the magnetic signature written into rocks which date back right on time, for example?

Rory D. Cottrell: Yes, one way to indicate that there was magnetic field is to see how that can be measured in the oldest rocks present on the planet is, for example, the samples that we looked at are 3.2 billion years old and they retain evidence of a magnetic field. There are rocks from the Moon also that retain evidence of a magnetic field that are about four billion years old, but younger soil samples do not retain that. The same can be said for Mars.

Chris Smith: How did you actually do your study? How do you trace magnetism in ancient rocks?

Rory D. Cottrell: It is a very tricky question in that most rocks have seen many of geologic events throughout their history and we do not want the younger events, we want the original event and what we did was to crush these very old rocks, these 3.2-billion-year-old rocks, so that we could selectively take out certain minerals, quartz, which you see as beach sand and feldspar. These minerals can contain very tiny magnets within them that record the Earth's magnetization.

Chris Smith: How do you measure that, because if you are just getting individual grains from bigger bits of rock, how do you actually tell how these miniature magnets are behaving, and how do you know what their orientation is relative to the rock they came from?

Rory D. Cottrell: Well, the rock itself has an orientation. We will take core samples that we know how they were situated in the rock and then what we will do is create a very thin section of that rock about a millimetre thick, with that known orientation on it. Now, this thin section of rock will have all sorts of minerals in it, the ones that we want, quartz and feldspar, and the ones that we don't. So, we mechanically etch away everything that we do not want from this orientation slide and leave behind just the minerals that we want, and then what we do is we put that or heat that up with carbon dioxide laser because one way to get this information out of the rocks is to slowly heat it up and see its response to being measured in a zero magnetic field environment.

Ben Valsler: And the way she did that was using a squid magnetometer or a superconducting quantum interference device, which is capable of measuring tiny magnetic fields. Now, finally this week, it is not just the Earth that experiences climate change, but also Mars, as Lori Fenton of the Carl Sagan institue explained to Chris. Nature 446, 646–649 (5 April 2007) .

Lori Fenton: Scientists had noted from the Viking mission of the 1970s and on comparing global maps of the surface of Mars with what they have served in 1990s when Mars Global Surveyor got to Mars, there were changes in what the surface looked like. There were some dark places that had become bright, some bright places that had become dark, and really this is something that did not surprise anybody because the astronomers had noticed for hundreds of years observing Mars through a little tiny telescope from the ground, that there are known changes in the surface of Mars from time to time, although there are features that are known to be studied over time as well.

Chris Smith: And when you say they are known, Lori, do we actually know what those features are that are provoking these changes, or are they just anomalies that we till now could not really explain?

Lori Fenton: I think we have known for the past 20 or 30 years of what they might be. I think early on astronomers attributed them to changes in vegetation, but now we know there is no vegetation on Mars, so we know it is much more mundane than that, it is dry dust on the surface moving around, either covering up or exposing darker surfaces that are underneath them.

Chris Smith: So, how will you find that? How do you know it is down to dust moving around and what was your approach to trying to work out what was going on?

Lori Fenton: One of my co-authors, Paul Geissler, wrote a paper where he looked at these changes and tried to understand what was causing them and he gives a lot of support for the fact that it is dust moving around on the surface. He looked at the places that changed between 1970s or 1990s with high-resolution images and showed that these are places where we see a lot of tracts from dust levels where there had been a lot of dust-level activity and places where it looked like wind had blown strongly and perhaps lifted up some of the dust, and he wrote a paper on this, then he came to me and he said what if this is due to the climate and what if this is due to wind circulation, or it might just be due to global temperatures for example and so, what we did was to take the Viking albedo maps, basically just a brightness map of the surface of Mars, and put it into a climate model and take the same thing for the first year of the thermal-emission spectrometer data, which was an instrument on the Mars Global Surveyor in the 1990, and also put it into the climate model. So, we ran the model twice exactly the same, changing only the input albedo maps and then just take the difference after we ran the model and see what happens.

Chris Smith: And what does that show?

Lori Fenton: Well, places that darkened warmed up. Anybody who has walked barefoot on an asphalt road knows that it gets hot and that it hurts to walk on, and that maybe if the surface where it looked brighter would not be quite so hot, maybe the concrete which is brighter is a little bit cooler.

Chris Smith: Is it the dust that is provoking these changes as it moves on and covers things that were previously reflective and makes them darker and therefore they soak up more heat?

Lori Fenton: Yes, that is exactly what is happening. When the bright dust gets eroded away and removed, it exposes an underlying darker surface and that darker surface is going to absorb more heat from the sun and it is going to warm up and that in turn is going to radiate and warm up the atmosphere above the surface and so in places that darkened (and most of the surface did darken), there was net global decrease in albedo of 2%, so 2% darkening of the surface, if you will. So, that is going to cause an increase in temperatures.

Chris Smith: So, does this mean that we are going to see some kind of cycle on Mars where the warming leads to more extreme weather, this moves more dust around, this affects the weathering even more and the whole thing goes running on big circle?

Lori Fenton: Very probably, yes. I do not know if we could exactly call it as a circle, but yeah what we did find was that an increase in heating is going to encourage dust level formation. It also increases the wind stresses. So, these are two processes that we know remove dust from the surface. So, there is a positive feedback going on where the darkening of the surface enhances the processes that darken the surface. The only thing that I can think of that really resets the whole system are big dust storms and Mars is prone to regional and even global dust storms.

Chris Smith: But why should a big dust storm reset the system? You would have thought that it would make it even more powerful wouldn't you?

Lori Fenton: Yes and no. Dust storms seem to whisk dust off the surface and redistribute it randomly and then, in the coming years after a big powerful dust storm, the regular seasonal winds and dust levels come and sort of clean up, if you could imagine people cleaning up after a quick but wild party.

Ben Valsler: Lori Fenton telling Chris Smith about how Mars has its very own form of climate change caused by the movement of dust over the surface. Well, that is all for this week. Next time, I will be finding out what causes some cancers to be superspreaders. In the meantime, if you have any feedback about this programme, please e-mail us on mailto:podcast@nature.com. If your ears crave more science, this week's edition of the Naked Scientist's podcast has a cardiology theme, exploring what causes a heart attack, how blood vessels react to drugs, and answering your questions quite literally on matters of the heart. That is the Naked Scientist Podcast, available for free from http://www.nakedscientist.com. This week's show was produced and presented by me, Ben Valsler, and Chris Smith. So, until next week good-bye.

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