Breaking Science: Pink iguanas & mosquito love songs...

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Newly discovered pink iguanas, sustainable fibres, healthy eyes, mosquito love songs and do your eyes pop out when you sneeze?

By: The Naked Scientists (Guest)

  • Duration 30 mins
  • Updated Sunday 11th January 2009
  • Introductory level
  • Posted under Radio, Breaking Science
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The team explore how eco-friendly clothing could soon be made from chicken feathers and wheat; how mosquitoes use the harmonics of their wing beats to choose a mate; the new protein that could help fight blindness; a gene that may predict heart disease; the discovery of a new species of pink iguana on the Galapagos Islands; the discovery that the brain uses a tagging system to make us notice things.

Plus in 'Stuff and Non-Science', do your eyes pop out when you sneeze?

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Chris Smith: Hello and welcome to this week’s Breaking Science which is produced in association with the Open University. I'm Chris Smith from the Naked Scientists. In this week’s show is this the fashion item of the future?

Helen Scales: We've all heard of organic cotton but perhaps one day soon chicken suits could be the latest thing in eco-friendly clothes. This actually is a new process that could be developed soon to develop renewable fibres from the protein in chicken feathers, that’s a stuff called keratin, and it could also work from gluten which is found in wheat.

Chris Smith: But will it catch on, on the catwalk, I guess we'll just have to wait and see. Helen Scales will be here with that and some of this week’s other top science news stories in just a moment. Plus, can you guess what’s going on here?

[Sound of mosquitoes]

Chris Smith: Any ideas? Well it's actually the sound of two mosquitoes formally agreeing to date each other, and that’s because scientists have shown this week that they synchronise the beating of their wings to indicate to each other that they’re interested - a discovery definitely not to be sneezed at. And nor is this week’s ‘Stuff and Non-Science’ where we'll be finding out whether it's true that your eyeballs really can pop out.

First though let’s take a look at some of this week’s top science news stories from around the world with our correspondent Helen Scales. And, Helen, what’s this about a new gene that can help us to save people’s sight?

Helen Scales: We have this new protein that scientists have announced in a paper this week, which could help fight against blindness, and that’s all according to Bo Chen and Constance Cepko from Harvard Medical School in the US, and they’ve been looking at a protein called histone deacetylase 4, or maybe a bit easy off the tongue HDAC4, and that’s in a study that appears in the journal Science this week.

Chris Smith: But what does this gene actually do normally in a cell? What’s its role?

Helen Scales: It's a sort of gene tag if you like. It sticks itself onto the side of genes and determines essentially how much those particular genes are themselves switched on or not.

Chris Smith: I guess a bit like a cellular dimmer switch in that respect. They can tweak the function of different genes. So what’s it doing in the retina?

Helen Scales: What they found was that the expression of this HDAC4 protein really influenced how long certain types of photoreceptors seem to live and persist in the retina.

Chris Smith: These are the cells that turn light into electrical activity that goes into the brain?

Helen Scales: That’s right and, in particular, rod cells which are very important in playing a role in detecting low levels of light. They also seem to let another type of cell in the retina called bipolar interneurons live for longer, and these connect different neurons in the eye together, and that’s another very important stage in the visual pathway leading from the retina up to the brain.

Chris Smith: So how did the researchers find this and are they suggesting that we could manipulate this in order to affect whether people go blind in later life for example?

Helen Scales: Well what they did was they took mice, in which they were controlling the expression of this gene for HDAC4, and in the mice retinas where they actually under-expressed this, by using fluorescent dyes injected into the retina, they could see that these rod photoreceptors were dying off as well as these bipolar interneurons, and then when they actually over-expressed the gene for HDAC4 these cells lived for much longer and they actually slowed down the degeneration of retinas in mice that had diseased eyes. So we could imagine maybe one day we could do something similar like this in human beings.

Chris Smith: I think also quite important is that there are some drugs around that actually block those genes, some of the anti-epileptic drugs block histone deacetylases, and so there’s a risk, I suppose, that they might translate into long term loss of sight and so this is a useful finding because now we can develop versions of these drugs that don’t have that side effect. So it's important to know this I guess. Well let’s move from eyes to hearts, and heart disease is important. What have people found out about that this week?

Helen Scales: Researchers this week have pinpointed a gene that may help us predict whether or not someone is at risk from something called early onset coronary heart disease, which basically means they’re more likely to have a heart attack, and we might be able to use this gene to actually detect that there could be a problem, long before we have any idea of it really.

Chris Smith: So what’s the gene and what does it do?

Helen Scales: Right well for a while we've known that there’s a certain part of chromosome 7, a particular Neuropeptide Y gene or NPY, that’s closely associated with this disease, and we've thought for a while that it's actually heritable so it's passed on from generation to generation. What this latest study has found is that there are actually six versions of this particular NPY gene that seem to be very closely associated with the early onset coronary artery disease, and it was a study that’s published this week in the open-access journal PLoS Genetics, and it's basically led by Svati Shah and Elizabeth Hauser from Duke University Medical Centre where this research was carried out.

Chris Smith: So in this particular study how did they home in physically on that particular gene and identify that one as the cause on chromosome number 7?

Helen Scales: Well what they did in this study was they took a huge number of different people, starting off first of all with a group of about a thousand families that have a history of this condition, and they looked at chromosome 7 and in particular these NPY genes that seem to be associated with the disease, and looked at basically what those people had.

They also took a group of people who weren't related but had actually been to the Medical Centre at Duke University to have an angiogram, and then followed that up and asked whether or not they actually did end up having actual heart attacks, or also whether they had a history of that in their family, and by looking at that and comparing it to people who didn’t have heart attacks and a heart associated with a disease, they were able to hone in and pin down the particular variants, these six variants, which were very closely tied and associated with these people who either had had a heart attack or it was in their family and it was likely that they also had inherited those genes.

Chris Smith: And what do they say the implications of this are and what do they propose to do next now they’ve identified this hotspot?

Helen Scales: Well it's clearly a step closer to understanding these very complex factors that actually lead to the chances of someone having these heart attack conditions. So if we can pinpoint this even earlier and know this is going to happen we can take steps to actually stop this condition from developing. It's not an all or nothing thing. It's not just because you have this gene you’re definitely going to suffer from a heart attack.

Chris Smith: So a useful early warning system then. Thank you for that. And let’s look to Australia now and find out about why we might be dressing in a chicken suit in future.

Helen Scales: Yes, we've all heard of organic cotton but perhaps one day soon chicken suits could be the latest thing in eco-friendly clothes.

Chris Smith: You’re talking real sort of chicken skin and feathers and all that kind of stuff?

Helen Scales: Well, I'm afraid not, no. Lovely as that may sound and rather fun, this actually is a new process that could be developed soon, to develop renewable fibres from the protein in chicken feathers, that’s a stuff called keratin, and maybe this could be a solution to all of the oil-based fibres that we use at the moment to make our clothes.

Chris Smith: Good because chicken feathers are a big problem because they are generated by the ton load but there haven't been that many uses for them have there?

Helen Scales: In fact most of these millions of tons of feathers that are produced in the chicken meat industry are buried in landfill sites so it really is a problem and it can even become contaminated waste. It's really nasty stuff if you don’t deal with it properly. Well, Andrew Poole, Jeffrey Church and Mickey Hudson, all from CSIRO Materials and Science Engineering in Australia, have been looking at this potential in the journal Biomacromolecules, and how it works essentially is by using these proteins molecules to make fabric.

Back in the 1930s several companies were trying to make fibres out of various things like milk, peanuts and soya beans, but the problem they encountered, and the same problem that we have now, is that these fibres are extremely weak when they get wet. Basically that means it won't survive a journey through your washing machine.

Chris Smith: But you’re saying that they’re making the material out of keratin which is what the feathers are made of. That’s the same stuff that our own hair and fingernails are made of, and we don’t dissolve when we go in the bath. You don’t get out the bath or the shower bald, thankfully - although it feels like it sometimes. So why should there be a problem with the water effects?

Helen Scales: It's the same molecule but it's in a different arrangement in our hair and nails, it's tightly bound together. But when you’re looking at a fibre that’s long and thin there is that much more of a potential for the molecules not to stick together. So we've got these long thin molecules that we need to be able to stick together when they’re wet, and we could use things like clay, another very promising nanoparticle we could use is cellulose - whiskers they’re called.

Chris Smith:

But Helen, as someone with an immaculate taste in fashion, can you see a coat made of chicken feathers and stuck together with clay really catching on in the high street?

Helen Scales: Well it does sound pretty yucky doesn’t it, to be honest, and I'm a vegetarian too so I might have problems with the whole fact that it came from farming. It's going to have to have a good marketing drive behind it I think. But perhaps if we focus on the fact that to some extent this really can be a renewable option, maybe we could go for it. I'm sure Karl Lagerfeld could do something chic with it, perhaps, but we'll have to wait and see I think.

Chris Smith: I just remember Ali G saying to a vegetarian, “Here you eat this chicken or I’ll kill another one.” But anyway, moving on, tell us about this final item, pink iguanas, the Galapagos are in the news this week.

Helen Scales: This is a newly discovered species of iguana that sits pretty in pink on the Galapagos Islands, and it might be offering us new insights into how the islands came to be such a fabulous, famous hotspot of unique biological diversity.

Now, as many of you know, this year is the 150th anniversary of the publication of Charles Darwin’s revolutionary book on the Origin of Species, and when he visited the Galapagos Islands in 1835 Darwin was astounded by the abundance of unusual species living on the dozen volcanic outcrops that make up this Archipelago, but he missed a rather strange iguana with colourful pink skin. In fact, surprisingly, no one noticed this so-called “rosada” iguana living in the slopes of the Volcan Wolf on Isabela Island until 1986 can you believe.

Chris Smith: It's quite hard to believe that given you’ve got something that’s bright pink it could be missed. Is it very, very small then?

Helen Scales: It's not very small at all. I think it lives in quite an isolated area. But it is quite amazing to think that a big, you know, a couple of foot long iguana might have gone overlooked all this time. But what’s happened now is genetic studies have revealed that it's not only a separate species, but this is the oldest species of land iguana and the ancestor of all the other land iguanas in the Galapagos Islands. And we know all this thanks to a study led by Gabriele Gentile from the University of Rome, Tor Vergata, in Italy, along with her colleagues from the Charles Darwin Foundation and the Galapagos National Park Service in the Galapagos.

Chris Smith: So what did they actually do to find out where in the evolutionary pecking order of iguanas on the Galapagos this one sits then?

Helen Scales: Well they looked at the DNA. The amount of DNA essentially that they share the same can really tell you how long ago it was that they split from a common ancestor. And by doing that they discovered that it was maybe as long as 5.7 million years ago that the Galapagos iguana family tree cleaved in two. One side you’ve got these pink iguanas and on the other side you’ve got all the others. And it's amazing that the pink iguanas that are left actually live now on one island that wasn’t actually there 5.7 million years ago. It was still under water and that volcano hadn’t come up yet. So something really interesting is going on in the Galapagos with these iguanas, and I think this is just the first part of us really starting to understand that.

Chris Smith: So pinker than a dodo but not quite as dead as one. Thank you very much Helen. That was Helen Scales from the Naked Scientists with a roundup of some of this week’s top science news stories. And if you’d like to follow up on any of those items the details and the references are on the Open University’s website. The address is open2.net/breakingscience.

In just a moment how scientists have uncovered the code that your brain uses to make you pay attention to things, but first to the science of love songs. In some countries it's traditional to woo or serenade a woman by singing beneath her balcony. Well now it turns out that things aren't so different in the insect world. Here’s Lauren Cator.

Lauren Cator: I'm interested in how mosquitoes choose their mate, and my hypothesis is that they may use flight tone as a way to get information about the quality of potential mates.

Chris Smith: So in other words how fast the wings are flapping?

Lauren Cator: It's not a direct relationship but that sound that’s created by the wings flapping, yes.

Chris Smith: So what was the big unknown then that you were trying to investigate here?

Lauren Cator: There was a paper published in 2006 by Gibson and Russell, and they found that in Toxorhynchites, a large non-blood feeding mosquitoes, that a similar behaviour was occurring, and, as a medical entomologist, I was interested in seeing if medically important mosquitoes, mosquitoes that feed on human blood and transmit pathogens that infect people, were doing similar things.

Chris Smith: Well this seems like a very good time to bring in Ben Arthur who’s another researcher on this paper. Ben, how did you actually investigate what was going on with these mosquitoes to see how they were tuning into each other’s wing beat frequencies?

Ben Arthur: Well it was a two-part study. We had behavioural methods and some physiological data as well. In the behavioural data, what we did was we tethered individual mosquitoes to a fine insect pin with some glue and positioned them next to a special microphone which could sense the wing flight tone very finely and just listened to what they were doing.

[Sound of mosquito]

So what you’re listening to right now is a male mosquito singing along at around 600Hz, and he’s next to a microphone. And we’re going to bring in a female here.

[Sound of mosquito]

And she’s singing at 400Hz. And the higher harmonics at 1200Hz, the shared harmonic, if you listen real close, you can hear the beats produced because those two frequencies are so close together. And that’s what’s happening when they’re courting.

Chris Smith: So which sex is changing its wing beats in response to the other?

Ben Arthur: They both do. So if the male’s relatively stationary and the female comes in she’ll modulate her tone up or down to match his, or if the female is stationary and then the male can move his and they’ll just synchronise to actively both match each other.

Chris Smith: You’re saying it's not actually the frequency the wings are beating at, but the harmonics, the multiples of the frequency the wings are beating at, which seems to be important?

Ben Arthur: That’s right. So the natural occurring frequency of the female wing beat is at 400Hz and that of the male’s at 600 and those are different enough that they don’t try to match the fundamental but rather the shared harmonics are the integer multiple at 1200Hz.

Chris Smith: How does the mosquito that’s the recipient of these frequencies, how does it actually detect them, and how do you know that it's actually responding to the frequencies, and then how does it then know, right now I need to mate?

Ben Arthur: Right, well it has these very plumose antennae, and these antennae sense the movements of the particles in the air, and there’s a sensory organ at the base of the antennae called the Johnston’s organ which transduces that movement of the antennae into an electrical voltage that the nervous system can then use to detect where the sound is, and what it is and whether it's a mate or not.

And the second part of our study then recorded from the Johnston’s organ and saw these electrical voltages and we found that we could measure electrical voltages all the way up to 2kHz which includes that shared harmonic at 1200Hz.

Chris Smith: Wasn’t there some claim previously by other people though that mosquitoes a) were deaf anyway and b) that they couldn’t hear sounds that high in frequency, so you’ve really scuppered both those myths haven't you?

Ben Arthur: That’s right, exactly, and we've shown it with both behavioural data and physiological data in the same paper.

Chris Smith: Lauren, what do you think that the major impacts - apart from obviously this being academically very interesting - what do you think the main other impacts are from a medical point of view?

Lauren Cator: Well just generally we know very little about mosquito mating behaviour, and we have no idea who’s choosing who or how they’re choosing them, and one of the control strategies that’s been proposed is to create transgenic mosquitoes - so mosquitoes that through genetic manipulation are either unable to transmit pathogens or are sterilised. The idea would be that if you release these into the wild that males carrying your desired genotype would be able to compete with wild males for female mates, and drive the genotype through the population. Unfortunately we have no idea what constitutes a sexy male mosquito.

Chris Smith: Hopefully they’ll find out soon. That was Lauren Cator and before her Ben Arthur. They’re both based at Cornell University, and they’ve published that work in this week’s edition of the journal Science. And if you’d like to read a bit more about how animals use sounds to track down a mate or find their way around there are links to a number of articles about those subjects on the Breaking Science website. That’s at open2.net/breakingscience.

Now from the harmonics that mosquitoes use to the frequency that our brain cells fire out when we’re interested in something.

Scientists have discovered that the brain uses a special nerve firing rhythm like a code to tag information that it needs to pay attention to. For instance, when we’re looking at a picture a part of the picture that the brain wants to analyse at any given time is labelled with this code to signal it out as important, and it turns out that this code consists of pulses of nerve activity which occur about 50 times per second. But rather than relying on the brain to add these tags to important information itself Brunel University’s Andy Parton wondered whether hiding the same code in the thing a person is looking at can make it much more attention-grabbing.

Andy Parton: So we presented three small striped patches on a computer screen, and we told the subjects that what they had to do was detect a change in width of the stripes on one of the patches - a very subtle change. What they didn’t know is that one of the patches was flickering at 50Hz. The other two patches were, well, either stable or flickering at 100Hz because that’s the natural rate at which the screen flickers. And what we found was that even though the subjects couldn’t say which patch was flickering at 50Hz, they were invariably faster at responding to a change in the width of lines at that location. That indicated to us that attention, if you like, was drawn to that particular patch rather than the other two patches.

Chris Smith: Why do you think 50Hz is the magic number? Why has the brain jumped on that frequency, 50 cycles a second, to make that the number which is particular for attention?

Andy Parton: I don’t know whether 50 per se is the magic number, I wouldn’t want to say that, but what we’re interested in is what’s called gamma frequency oscillations. That goes from 40 up to maybe 70 mid-range gamma, and there seems to be a lot of evidence from the animal literature and human EEG that it's very connected with visual processes activity in this range.

Chris Smith: And given that you’ve discovered this do you think that there’s therefore grounds for redesigning car dashboards to alert people to important things they need to pay attention to quickly, or road signs or some other kind of alerting systems so that it forces people to pay attention, or from a more nefarious advertising point of view do you think advertisers will jump on this and we'll start seeing TV commercials that are much more distracting than they were previously?

Andy Parton: Well of course that’s an interesting question about whether it would be more distracting because by it's nature if it's unconscious, I don’t know whether it is distracting. But certainly it has potential I think for covertly, without your knowledge, drawing your attention to things, and I think that’s very important both for, as you say, things like driving and things like that maybe for alerting people, or even there are a number of disorders that occur to do with attention, sometimes following a stroke, sometimes following other neurological conditions, and rehabilitation of those conditions might work much more effectively from things that cause people to automatically reorientate their attention, than some of the more sort of conscious processes that are traditionally used.

Chris Smith: In people who have things like ADHD (attention deficit hyperactivity disorder) where they seem to struggle to discriminate the important things from the less important things, do you think there might be a role in that that this system or something related to it is playing?

Andy Parton: Most definitely actually, yes. My personal experience has been with a neurological condition called visual neglect. That’s an attentional problem that occurs after a stroke, where people don’t notice one side of space. And I think there is definitely a good reason to think it might help in that, and there’s some good strong evidence to actually say there are links between neglect type syndromes and ADHD. So I think there’s every reason to think that something like that might help draw attention to things that are important.

Chris Smith: I suspect there'll be teachers everywhere wondering how they can rig up that system in the classroom. That was Andy Parton from Brunel University, and he’s just published that work in the journal PNAS.

You’re listening to Breaking Science with me, Chris Smith, and it's time now for this week’s ‘Stuff and Non-Science’ where we murder urban legends. And with a myth the magnitude of which could make your eyes pop out, here’s Diana O’Carroll.

Diana O’Carroll: This week’s ‘Stuff and Non-Science’ was inspired by an email from Phil, who asked if it's possible to pop an eyeball out and return it to the socket without any damage. Here’s Dr Stephen Juan with the low down on eye popping myths.

Stephen Juan: Now some people can voluntarily propel their eyeballs to go out. Sometimes it's one eyeball, sometimes it's two. The first case where this happened was reported in 1928, in the American journal of Ophthalmology, and it was about a 20-year-old man who worked as a circus performer. And it supposedly caused him no problem and he had normal vision. But it is a myth that people who if they sneeze without their eyelids being closed that their eyeballs will pop out - that doesn’t happen. The eyeballs are locked in with all sorts of connected tissue, and it's only when there’s an abnormality in the connective tissue that people can voluntarily propel their eyeballs outwards.

It is impossible to remove an eye and then put it back in because the optic nerve, which runs from the eye back into the brain, that’s what an ophthalmologist is looking at during an eye examination, the optic nerve is pretty tight and there just isn't the room to take an eyeball out and then put it back in.

Diana O’Carroll: That was Dr Stephen Juan. He’s from the University of Sydney and is author of the Odd Body books. So you can’t pop an eyeball by sneezing all that easily, and if you did your optic nerve wouldn’t let it go very far anyway. But if you do have any more stuff and non-science then send it to me diana@thenakedscientists.com.

Chris Smith: So no excuse for closing your eyes when sneezing in future. I challenge you to try it. Thank you Diana. That was Diana O’Carroll with this week’s ‘Stuff and Non-Science’. That’s it for this time. We’re back next week with another roundup of global science news.

Breaking Science is produced in association with the Open University, and you can follow up on any of the items included in the programme via the OU’s website. That’s at open2.net/breakingscience. Alternatively you can follow the links from the Five Live Up All Night websites to get there.

Production this week was by Diana O’Carroll from thenakedscientists.com, and I'm Chris Smith. Until next time goodbye.

Does it sound good? Why not get the Breaking Science podcast, and receive new episodes as they're released?

Background

These are the sources used by the Naked Scientists in making the show:

In the news

'An overlooked, pink, new species of land iguana in the Galápagos'
by Gabriele Gentile, et al
in PNAS

'Environmentally Sustainable Fibers from Regenerated Protein'
by Andrew J. Poole, Jeffrey S. Church, and Mickey G. Huson
in ACS

'Neuropeptide Y Gene Polymorphisms Confer Risk of Early-Onset Atherosclerosis'
by Shah SH, Freedman NJ, Zhang L, Crosslin DR, Stone DH, et al.
in PLoS Genet 5(1): e1000318. doi:10.1371/journal.pgen.1000318

'HDAC4 Regulates Neuronal Survival in Normal and Diseased Retinas'
by Bo Chen and Constance L. Cepko
in Science

Interviews

Andy Parton on 'Gamma flicker triggers attentional selection without awareness', by Frank Bauer, Samuel Cheadle, Andrew Parton, Hermann J. Müller, and Marius Usher in PNAS

Lauren Cator and Ben Arthur on 'Harmonic Convergence in the Love Songs of the Dengue Vector Mosquito', by Lauren J. Cator, Ben J. Arthur, Laura C. Harrington, Ronald R. Hoy in Science

Stephen Juan for 'Stuff and Non-Science'

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