The Naked Scientists explore the discovery of a gene that triggers nerve repair; research showing that 'fake' acupuncture has the same pain relief effect as real acupuncture; how the analysis of brown clouds over East Asia shows the main culprit to be burning biomass; how the discovery of an 18 million-year-old fossil challenges the theory of when New Zealand was undersea; why DNA previously thought to be "junk" isn't; how the study of the genetic variations in stomach bacteria describe human migration.
Plus in 'Stuff and Non-Science', does watching TV really make you short-sighted?
Chris Smith: In this week’s show, the truth about acupuncture. Can it really knock a migraine on the head?
Kat Arney: Some trials have actually shown that acupuncture does have benefits for relieving pain, and now a review by the Cochrane Researchers, this is a group that analysed the body of scientific evidence about different medical treatments, they’ve shown that acupuncture can actually be an effective treatment for preventing headaches and migraines, but there is an interesting twist.
Chris Smith: And we’ll be revealing the point about that twist in just a moment. And talking of twists, a surprising secret has emerged from the double helix that’s our DNA this week. It turns out that what we’d dismissed as junk isn’t.
David Tollervey: What was thought was that the genes which were used to synthesise RNAs were isolated by very long stretches of DNA that did nothing, they were often referred to as junk DNA. And it turns out that this is simply wrong. The human genome is almost entirely used to make RNA, and the question then was what on earth was all this other RNA doing.
Chris Smith: David Tollervey, and he’ll be explaining what the DNA formerly known as junk actually does. Plus, in this week’s ‘Stuff and Non-Science’ we take a square look at watching telly and reading in low light. Can it really leave you short-sighted?
Hello, I’m Chris Smith, welcome to Breaking Science, which is produced in association with the Open University. First, let’s take a look at some of this week’s top science news stories from around the world, and on the trail this time is Kat Arney, so Kat, scientists are making progress in making nerves repair themselves.
Kat Arney: Yes, and it’s good news for sufferers of nerve damage, or at least tiny nematode worms with nerve damage. This is work from researchers in Utah who’ve discovered the molecular signals that cause regeneration of damaged nerves. Now the team led by Marc Hammarlund was studying these little worms that are known as C. elegans, and they published their results this week online in the Journal of Science Express, and what’s exciting and intriguing about their finding is that the signals required to regenerate nerves are different from those that are needed to grow nerves in the first place, which could shed light on why attempts to regrow nerves in mammals such as humans so far haven’t really worked so well.
Chris Smith: Now presumably there’s a reason why they’re using worms for this?
Kat Arney: Worms are just a great model system for looking at the nervous system. They’re transparent, you can mark the nerve cells really easily. They were studying these worms that had genetic faults in a gene called beta-spectrin, and this means that their nerve cells, their neurons break very easily, and the worms attempt to repair this damage. They don’t do it terribly well but they give it a go. But the scientists found out that when they removed another gene called DLK1 the worms just couldn’t fix their damaged nerves at all. And then the team also went on to use precision lasers to cut the nerves in healthy worms and compared their regeneration with worms lacking DLK1, and again they found that DLK1 was really important for nerve regrowth.
Chris Smith: So the inference of course being that because this particular protein, if you take it away, this gene DLK1, nerves regenerate a bit worse, it might have some kind of role involved in that. So what actually is the gene, what do we know about it?
Kat Arney: Well we know that it’s something called a MAP kinase kinase kinase. That sounds a bit complicated, but put simply it’s just a type of protein known as a kinase that sticks molecular flags on other proteins which then activates them, and this tells the cell, the nerve cell in this case, to regrow. And as well as helping to fix damaged nerves, the team also found that adding extra DLK1 could actually stave off the slowdown of nerve repair in normal worms as they get older.
Chris Smith: Fine for worms but what about humans, do we have this gene?
Kat Arney: Humans do have versions of DLK1, but it’s not really quite the miracle anti-aging nerve repair serum that we might hope just yet, and it’s really just the first step in a long road towards understanding these molecular signalling pathways that tell damaged nerves to regrow.
Chris Smith: Indeed, certainly an important medical consideration. Now sticking with nerves, is acupuncture all in the mind, that’s a big question isn’t it?
Kat Arney: Yes, and especially this week when we saw the announcement there’s going to be a regulator for alternative and complementary therapies to try and crack down on cowboy therapists. And the debate about complementary and alternative treatments does rage, some people say it works, some people say, you know, it’s all rubbish, and there’s definitely a lack of solid scientific evidence really to show this.
Chris Smith: I was just going to say, is there actually anything that’s been done to prove that acupuncture and treatments like it do have a clinical effect, they do benefits patients?
Kat Arney: Well there has been some research in clinical trials of acupuncture. This is a treatment where needles are put into specific points in the body. These correspond to so-called lines along which energy, or chi, flows. There’s actually very, very little anatomical basis to acupuncture, these lines don’t correspond to nerves, they don’t correspond to anything anatomically, but some trials have actually shown that acupuncture does have benefits for relieving pain. And now a review by the Cochrane Researchers, this as a group that analysed the body of scientific evidence about different medical treatments, they’ve shown that acupuncture can actually be an effective treatment for preventing headaches and migraines, but there is an interesting twist.
Chris Smith: Which is?
Kat Arney: Well, the scientists have found that fake acupuncture, where they put the needles in in the wrong place and don’t put them in right, is just as effective as real acupuncture. So this suggests that actually the benefits of acupuncture are likely not to be down to specific lines of chi and all these kind of things but a powerful placebo effect.
Chris Smith: I was going to say, it’s probably more likely a sort of ritualistic thing isn’t it, people expect there to be a good outcome, a placebo benefit, so they get one. And also when you’re concentrating on having needles stuck into you, you’re less stressed and lots of headaches are caused by tension anyway. But how did this Cochrane Review itself come to this conclusion that you could stick the needles just about anywhere?
Kat Arney: Well, they did two studies. One was looking at research that had been done into acupuncture for frequent tension headaches, these are sort of mild to moderate headaches, and they found that overall eight weeks of acupuncture left patients with fewer migraines than those that had been given preventative drugs, so that’s good, but the fake acupuncture procedures were pretty much just as effective as real acupuncture. So really acupuncture could be an alternative for people who suffer from tension headaches and migraines who don’t want to take these drugs.
Chris Smith: So the conclusion of that study is you go to the sewing box, you grab a needle, you dip it in some boiling water and just shove it anywhere and your headache will go away?
Kat Arney: Well, it seems to be, yes.
Chris Smith: Did you endorse that? No, hopefully not.
Kat Arney: No.
Chris Smith: Well look, let’s make the journey away from acupuncture to East Asia and this whole question about brown clouds, because you’ve heard of living under a dark cloud but brown clouds are a major issue there.
Kat Arney: Yes. This is not so much a pea-souper as more a mushroom-coloured souper, and this is a huge brown cloud of pollution that you can see hanging over South Asia and the Indian Ocean during the winter. It doesn’t just block out the light and look unpleasant, it can actually be deadly. The pollution causes deaths from heart disease and lung disease, and it can actually cause cancer, and this has been shown in countries like China and India.
It’s also, and this is bad news as well, thought to cause global warming and climate change in the area. And although scientists have known about this cloud for some time, you can’t miss it, it’s in the sky, its origins have been a bit of a mystery. Is it caused by soot from burning wood and burning dung, which people used to cook and heat their homes, or is it due to fossil fuels, things like coal-fired power stations or the emissions from cars.
Chris Smith: Yes, because most people say those parts of Asia, very heavily industrialised, lots of manufacturing, it’s just man-made pollution.
Kat Arney: Exactly. But writing in the Journal of Science this week, Orjan Gustafsson and his colleagues in Sweden, the Maldives and India have analysed the cloud from a mountaintop in Western India and from the Honeymoon Island of the Maldives using radio carbon techniques to answer this question.
Chris Smith: Why radio carbon?
Kat Arney: Well it’s just the best way they could find of analysing the cloud and working out what proportion of it had come from burning wood, this biomass, burning wood and dung and what had actually come from much older fossil fuels.
Chris Smith: And what was the result?
Kat Arney: Well they discovered that the main culprit in the cloud, which makes up about two-thirds of it, is actually soot from burning organic matter, this biomass. So that’s wood, dung, the sort of things that are used for cooking and heating homes all the way across Asia.
Chris Smith: So we’ve been blaming the wrong thing all along, it’s not cars and industry, it’s just people heating their houses and cooking their food.
Kat Arney: Well it’s partly to do with fossil fuels and cars, but the researchers do suggest that if we can cut down on using biomass for cooking and heating it will have a very big impact on air quality and climate change, and potentially health in the region as well.
Chris Smith: And one other worry that people have raised about this is that because that cloud traps heat beneath it it’s actually accelerating the retreat of some of the glaciers in the Himalayas and this could make floods, because you melt glaciers very fast you get lots of water coming off and it could flood things. But look, from fossil fuels to how a fossil could be triggering a row in New Zealand about how long New Zealand has actually been in existence, because some people argue about how old New Zealand really is, so what is this fossil telling us?
Kat Arney: Yeah, when you think about New Zealand you probably think about rolling mountains and ‘The Lord of the Rings’, or maybe ‘Flight of the Conchords’. But actually you may not imagine that the islands were once completely submerged by the sea. Or were they? Because there’s evidence to suggest that New Zealand was in fact buried in the ocean around 25 million years ago, but a new discovery from scientists at University College London and the University of Adelaide and the Museum of New Zealand have now found something that challenges that idea.
Chris Smith: Which is what?
Kat Arney: Well the scientists led by Mark Jones have discovered an 18 million year old fossil of a lizard-like reptile known as a Sphenodon, and back in the time of the dinosaurs Sphenodons were found all over the place, over the whole globe. But today they exist only in the form of a distant ancestor, and this is the New Zealand Tuatara lizard. This is a highly endangered species that’s found on islands around the country’s coastline. Now previously the oldest known Sphenodon fossil was around sort of 34,000 years old, but this new specimen is much more ancient, dating back to around 19 to 16 million years, that puts it back in the early Miocene era.
Chris Smith: So how does this fit with what we thought was going on with New Zealand coming out of the waves like Poseidon fairly recently then?
Kat Arney: Well New Zealand’s thought to have broken off from this huge land mass called Gondwanaland, this was the enormous super continent that broke up to make most of the continents that are now in the Southern Hemisphere, that’s Antarctica, Australasia, Africa and South America. And that split off about 82 million years ago carrying animals and plants with it, so this would have included the Sphenodon ancestors of the Tuatara lizards.
Now, some scientists think that New Zealand, or Zealandii as it was then, was completely submerged underwater around 22 to 25 million years ago, but the discovery of this new fossil and others beside it suggests that at least enough land did remain above sea level to support their survival. And the other quite sweet thing about these results is that it shows that the ancestors of the Tuatara were a pretty hardy bunch as they managed to survive an eight degree drop in temperature around 40 million years ago, which sounds pretty chilly to me.
Chris Smith: Which proves what New Zealanders have been telling us all along, that they’re born survivors. Thank you, Kat. That was Kat Arney from the Naked Scientists with a round up 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, that’s at open2.net/breakingscience.
In just a moment we’ll be heading back to the Antipodes to find out how the first humans arrived there. Researchers have solved the mystery by studying bacteria that are carried in people’s stomachs. But first to the biochemical recipe book that is the human genome, and the question that scientists have been grappling with for a long time, which is why does most of our DNA appear to be junk and doesn’t code for any genes? To find out, David Tollervey has been studying yeast cells, which are very similar to our own cells, and what he’s found is that what we’ve been calling junk DNA isn’t junk at all. In fact, it plays a very important role in switching genes on and off by producing a specialised family of molecules called RNAs.
David Tollervey: Well there have been several classes of RNA that either do things in the cell, they make things called ribosomes which synthesise all the proteins in the cell, or transfer RNAs which carry information and allow the proteins to be made in a specific way, or they’re messenger RNAs, and messenger RNAs carry the information from your genes. And the genes in principal have all the information you need to make a human, but you can’t use it in that form. It’s a bit like a computer hard disk, your computer hard disk has all the information on it to run the computer, the operating system’s on there but it can’t be used when it’s in the hard disk. To use it you have to first copy it and then use that copy to do things.
Chris Smith: So to continue your computer analogy, that’s a bit like taking the program off the hard disk and actually executing it in the computer’s memory, it’s just putting it into a different form, in this case it would be RNA, to then do something useful with that information?
David Tollervey: That’s correct, yes. The DNA is copied into RNA, which is a closely related molecule, and then you use the RNA to do stuff.
Chris Smith: But what you’re saying is there are more of these RNAs than you would expect on the basis of just doing that job, and I guess the key question is why?
David Tollervey: Right, so what was thought was that the genes which were used to synthesise RNAs in the human genome were isolated by very long stretches of DNA that did nothing, they were often referred to as junk DNA. And it turns out that this is simply wrong. The human genome is almost entirely used to make RNA. And then question then was what on earth was all this other RNA doing, and it’s actually a very intractable problem in humans, and so that’s the problem we’ve been trying to work out in yeast.
Chris Smith: Because for a long time people have said well if we’ve got all this junk DNA, and that’s costing us energy for cells to make that junk DNA, why do we have it, why haven’t we got rid of it. And now you’re saying that actually it does have a very useful purpose, it’s making these RNA molecules, but that still leaves the question well what are they for?
David Tollervey: That’s correct, yes. So in the budding yeast there’s a similar class of RNA also of enigmatic function, and what we did is we took one of these RNAs, so we made a specific mutation that prevented it being synthesised and then we looked for changes in other genes in the yeast cell.
Chris Smith: So what you’re arguing is that these RNA molecules, far more having no function actually may be tweaking the activity of other genes coming off the DNA?
David Tollervey: That, when we first did the experiment we didn’t know that but that’s what we found, that’s right. So in the genes there are two strands of DNA, and one strand of DNA carries the information that’s used to make the protein, and these other RNAs are made from the opposite strand, so they run through the gene in the opposite orientation to the RNA that’s going to make the proteins.
Chris Smith: So they’re kind of like the genetic mirror image, so does that mean that they can if needs be cancel out the expression of the gene and effectively turn it down, turn it off like a genetic dimmer switch?
David Tollervey: That was a possibility that we considered, but that turns out not to be how they work exactly. To understand how they work I have to tell you a little bit more about how genes are organised in humans. Each human cell, and you have billions of cells, has about two metres of DNA in it. If you stretched it out it would stretch two metres. Obviously to get it into the cell you have to really, really squash it up, you have to pack it very closely. But, and here’s the tricky thing, you have to pack it in such a way that you can still get at it if you need it.
And there’s a special mechanism for folding up the DNA, a special set of molecules, and these form a structure which is called chromatin, and this chromatin packs up the DNA, folds it maybe half a million times smaller than it would be if you stretched it out, and they control the ability of the DNA to be unfolded and then used to make RNAs. And so the RNAs that we’re looking at turn out to regulate the structure of this chromatin such as to regulate the expression of the protein coding chains.
Chris Smith: So this adds a whole new layer of complexity to how genes get turned on and turned off, because people used to think that they were just the genetic equivalent of switches at various places in genetic material, you could turn genes on and turn it off. One would think that this is how you get the complexity that we do, given that there are so few genes in the human genome, and also when a human is developing you can get the same gene having multiple effects in different tissues.
David Tollervey: That’s correct. So one of the surprises of course when the human genome was sequenced was that humans only had about 24,000 genes, something like that. Yeast has more than 6,000 genes. This is a mystery because humans have, of course, hundreds of different cell types, a complex body plan, not to mention however many genes you need to make a human brain. And so there had to be more complexity somewhere, and yeah, so all these RNAs add an additional level of complexity which helps fine tune the genome, fine tune expression and coordinate probably the expression of different genes.
Chris Smith: So that’s how we get away with having fewer genes than a banana. That was David Tollervey from the University of Edinburgh. He’s published those findings in this week’s edition of the journal Molecular Cell.
To an even older question now, which is how did the first humans reach Papua New Guinea, Australia, New Zealand and the South Pacific Islands. Archaeological findings suggest that this colonisation was occurring at least 50,000 years ago, but it’s very difficult to track human movements when so little remains of those early people. But what they have left behind is their genetic legacy, not so much in their own DNA but in the DNA of a bacterial parasite called Helicobacter pylori that lives in the stomach. And what scientists have found is that as the first modern humans spread out across the world they took their own forms of this bacteria with them, and although the people have gone the bacteria are still living on in the stomachs of their descendants today.
And by studying samples collected from native populations in Taiwan, Melanesia, which includes Papua New Guinea, Australia and Polynesia, which includes New Zealand, researchers have now been able to piece back together the movements of those first humans, and what the data suggests is that there were two migrations. Here’s Mark Achtman.
Mark Achtman: There were many indications from different areas about different groups of people in the Pacific about when people first arrived there and where they may have come from but it was not particularly coherent, and it was coming from many disciplines at once. So I was hoping to look for a coherent picture of how people migrated, originally migrated to the Pacific.
Chris Smith: One way to solve those kind of puzzles is an approach that’s already been taken, that’s do archaeology and look at the remains, but you’ve taken a slightly different approach?
Mark Achtman: We took advantage of a bacterium that infects the stomachs of most of the world’s population called Helicobacter pylori and whose genetic diversity mimics that of humans very strongly, and isolated these bacteria from the inhabitants of a number of different places in the Pacific and looked at genetic diversity.
Chris Smith: Oh I see, so you’re relying on the fact that populations of humans have been carrying Helicobacter pylori with them wherever they’ve gone, and because the bug evolves and changes genetically then you can use the genetics of the bug as a proxy of where people came from?
Mark Achtman: Exactly. In the past we would use information on known human migrations to interpret genetic diversity within the bacteria, and it’s shown that it accompanied humans out of Africa 60,000 years ago, and looks very much like human genetics did.
Chris Smith: So once you’d got the Helicobacter pylori samples and you began to analyse them genetically, what patterns began to emerge?
Mark Achtman: That was very simple. The moment we looked at the sequences it was very clear that we had something new among the Australian Aboriginals and found exactly the same pattern in the New Guinea highlanders. And it was the same thing, the moment we had the samples from the Taiwanese Aboriginals it was very clear that they were closely related to the isolates from Polynesians and Melanesians.
Chris Smith: So what is the implication of that association, the fact that you’ve got these populations that are now linked together, and what does that tell you about how people must have moved to get there?
Mark Achtman: What we’re seeing is extremely striking signs of two totally independent migrations that happened according to our estimates about 30,000 years apart, which is a very long time. This is not all that obvious when you’re there in place, when you talk to people in Papua New Guinea, they don’t really distinguish between the highlanders and the Melanesians from the islands, it’s all one group of people now. But the bacteria are telling us that there are two totally different sources of where these people came from and when they came there.
Chris Smith: And if you put that together with climate models and geographical and geological models, do you have any idea why people discovered, invaded, visited these people twice in the past so far apart?
Mark Achtman: The simplest explanation for why they first got there about 30-40,000, 50,000 years ago to Australia is because of the ice age that was going on at that time. Sea levels were low, distances to travel were limited, and there was a very strong technological development and they were able to handle boat travel even across reasonably long distances. However, those distances that they could travel were still much, much smaller than what was needed to get out to Melanesia and Polynesia and that simply wasn’t possible for another 20-25,000 years. So the Polynesian migrations are tremendous achievement for humanity, to be able to sail that far and colonise new islands, it simply wasn’t possible until 5,000 years ago.
Chris Smith: That puts a whole new spin on the term travel bug doesn’t it. That was Mark Achtman, he’s from University College Cork, and he’s published that work in this week’s edition of Science. 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 hopefully not sitting too close to her television these days is Diana O’Carroll.
Diana O’Carroll: This week on ‘Stuff and Non-Science’ we have Don Mutti to tell us does watching too much telly and reading in low light really make you short-sighted.
Don Mutti: That would be a myth. I think the short answer is no. There’s a couple of reasons for the myth. One is that short-sighted children tend to score a little bit better on standard IQ tests so there’s a little bit of truth to the stereotype that your near-sighted or short-sighted child is sort of a brainier child, but there’s a lot of variation and a lot of exceptions to that rule. Another reason for that sort of stereotype is that once children become short-sighted they do tend to read a little bit more than children who aren’t near-sighted. But that’s not really saying that it’s a cause, that’s just a difference between what near-sighted children and non-near-sighted children do.
A couple of studies, one in Singapore and one that I was involved in here in the United States looked at children before they became short-sighted and looked at how much reading they did, and that’s really the test of whether it’s a cause or not, and there was no difference in how much television, how much reading the children did who eventually became short-sighted and those who didn’t.
Diana O’Carroll: Don Mutti from the Ohio State University College of Optometry. And it seems that although you can make your eye muscles feel tired, it’s much more likely genetics will make you short-sighted than a small print book. We’ll have more non-science to stuff next week, but until then keep your suggestions coming in, firstname.lastname@example.org.
Chris Smith: So no need to worry about the torch under the bedclothes any more, you won’t go blind. Thank you Diana, that was Diana O’Carroll with this week’s ‘Stuff and Non-Science’. Well that’s it for this time, we’ll be back next week with another round-up 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 to get there from the BBC Radio Five Live Up All Night web pages. The production this week was by Diana O’Carroll from thenakedscientist.com, and I’m Chris Smith. Until next time, goodbye.
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In the news
'Axon Regeneration Requires a Conserved MAP Kinase Pathway'
by Marc Hammarlund, et al
in Science Express (22 January 2009)
'Brown Clouds over South Asia: Biomass or Fossil Fuel Combustion?'
by Örjan Gustafsson, et al
in Science (2009) vol 323, pp495-498
'A sphenodontine (Rhynchocephalia) from the Miocene of New Zealand and palaeobiogeography of the tuatara (Sphenodon)'
by Marc E.H. Jones, et al
in Proceedings of the Royal Society B (2009)
'Acupuncture for tension-type headache'
by Linde K et al
in Cochrane Database of Systematic Reviews (2009, Issue 1)
David Tollervey on 'A ncRNA Modulates Histone Modification and mRNA Induction in the Yeast GAL Gene Cluster' by Jonathan Houseley, Liudmilla Rubbi, Michael Grunstein, David Tollervey and Maria Vogelauer in Molecular Cell
Mark Achtman on 'The Peopling of the Pacific from a Bacterial Perspective' by Yoshan Moodley, Bodo Linz,Yoshio Yamaoka, Helen M. Windsor, Sebastien Breurec, Jeng-Yih Wu, Ayas Maady, Steffie Bernhöft, Jean-Michel Thiberge, Suparat Phuanukoonnon, Gangolf Jobb, Peter Siba, David Y. Graham, Barry J.Marshall, Mark Achtman in Science
Donald Mutti for 'Stuff and Non-Science'