028 - Sperm wars, sneaky sheep, substandard stallions and more
Kat: Hello, and welcome to Genetics Unzipped - the Genetics Society podcast with me, Dr Kat Arney. In this episode we’re bringing you highlights from the Society’s Centenary Conference, held up in Edinburgh last month.
We’ve got stories of sneaky sheep, substandard racing stallions, the Vikings of the Scottish Isles and a ceilidh with a scientific spin. Plus, news from the front lines of the sperm wars.
Hopefully you can’t have failed to notice that The Genetics Society is celebrating its centenary this year, recognising 100 years since the first meeting in the summer of 1919. The final event of the year was a scientific conference up in Edinburgh, bringing together hundreds of geneticists across a range of fields to hear the latest discoveries and reflect on a century of progress.
There’s an extra Edinburgh centenary connection, as the Animal Breeding Research Station of the government’s Board of Agriculture and Fisheries was established in the city in 1919 and evolved over the next 10 years to become The University of Edinburgh’s Institute of Animal Genetics.
Sadly, I can’t bring you interviews with every speaker, but here are a few highlights to give you a flavour of the event. Huge thanks to Kay Boulton and the organising committee for a fantastic event, from which I’m sure my liver and my dancing feet will eventually recover.
Sneaky Soay Sheep
Take a boat 40 miles out into the choppy Atlantic off the north west coast of Scotland and you’ll get to St Kilda – a collection of islands that makes up the westernmost of the Outer Hebrides. St Kilda is home to a large flock of Soay sheep, which have lived wild in their windswept home for 4,000 years. They’re rather attractive animals, with rugged brown fleeces, large horns and distinctive eyebrows.
Susan Johnston and her colleagues at the University of Edinburgh have been following these isolated animals since the 1980s, carefully documenting the population rises and crashes over the years and more recently using sophisticated analytical tools to take a closer look at the genes of individual animals in the larger population.
But in order to genotype a Soay Sheep, you’ve first got to catch it - and, as I found out when Susan and I sat down to chat about her work, that involves a lot of leg work.
Susan: We go out for several expeditions each year. The first is for lambing which is around April time. We're not allowed to use anything like sheepdogs on the islands, we have to do it all by hand. We basically stock the lambs quite soon after they're born.
We get in really quickly and we take a small blood sample and we give them a tag which allows us to identify them for the rest of their lives, just through binoculars or whatever.
Once we've caught them, weighed them, then we just let them get on with their lives. Then every August we go back to try and do a large scale catch of as many individuals in the population as possible.
Kat: So you're just running around, sheep chasing?
Susan: Yes, exactly. So we build these corral traps, but we have to hide them behind some of the old ruins on the island. Then we basically have to use sheep psychology to trick them into running into the corrals. So they think that they're escaping from us but we're actually capturing them. So it's a bit of manpower involved, it's really good fun.
When we catch them as adults we do all sorts of body measurements, take blood samples. We take faecal samples so that we can look at parasites, blood samples so that we can look at things like their immune responses and their antibodies and so on.
It's an amazing project because we have so much data on these individuals. Also, because we take blood samples we can also take DNA. So we can do things like paternity testing to work out how successful different rams are. We can also use it for all sorts of genetic studies without manipulating the animals in any way.
Kat: So, tell me about some of the things you're studying at the genetic level. What are you particularly interested in?
Susan: The Soay sheep are interesting because we see a lot of variation and traits where we wouldn't necessarily expect to see variation. At a very simple level there's things like their horn development.
The vast majority of male Soay sheep have these large horns that they use for mating but there's a really small proportion of the males that have no horns at all. So this is weird, because you expect big horned males to be more successful --
Kat: Big, horny males, yes.
Susan: Yes. They pass on their big horned genes, so why on earth do we still have these small horned genes in the population? So that's one example. That was from my PhD work that I did, quite a while ago now. We were able to kind of map the gene that controlled the horns.
When we found the gene we were able to actually explain this evolutionary puzzle because we found that males that have two copies of this big horned gene have very large horns, and they have high reproductive success but they die very young.
Whereas the males who have two copies of this no horn gene - so they don't have any horns - they live quite long and they're able to have these sneaky matings as well. They're able to find females that haven't been --
Kat: They're just persistent.
Susan: Yes, so you know, hats off to them. But if you're somewhere in the middle, if you have one copy of each, you have medium sized horns. You still have big horns, they're not quite as big but you live longer, so you can compete with the younger big horned males.
So there's almost like a good strategy to be not quite the best. You want to be able to have offspring but also survive.
So, we weren't able to get to this by looking at the horns alone, but by getting to the genetic basis of it, we were able to solve this puzzle. Now that we have more sophisticated methods of typing many mutations through the genome, we're able to use this information to map genes that underly other interesting phenotypes; things like their colour but also things like their body size.
My current research is even looking at how often they have crossovers during meiosis so it's a very specific and dry topic, but with the wealth of information that we have, we can investigate that quite easily, actually. So it's a really nice system.
Kat: So, looking in a bit more detail at your work because I find it interesting. You say it's not very interesting, it's meiotic crossovers, but this is kind of the genetic shuffling of the deck that happens with every generation. That mixes up what you've got, it helps to create variation, which is then what evolution acts upon.
So presumably, that's quite important, to know how much each individual sheep can shuffle?
Susan: Yes. I guess just to give a bit more detail about what the process is; this meiotic combination is like the exchange of DNA between the chromosomes that you've inherited from your parents. This happens when you're creating egg and sperm cells. What it does is it takes the chromosomes that you inherited, shuffles them and then these are then what is transmitted to your offspring.
It's really important in evolution because it creates new combinations of genes that can be acted upon by selection, and it creates genetic diversity in populations, so it's a really important process. It's also quite risky because this process of shuffling requires breaking the DNA, which can increase genetic mutations and so on.
So it's really this process that goes on in nearly every multi-celled animal and plant. It's really on a knife edge of getting a good level of shuffling and trying not to have too many mutations. So this is a question I'm really interested in.
The sheep are quite an interesting population to look at this because we have so much genetic information but we also know how individuals are related. So we can track how these genes progress through generations and we can actually use statistical methods to work out how much shuffling has gone on.
We can work out if individuals that show more of this shuffling are actually increasing their success in the population, by having more offspring for example, or if perhaps having less shuffling is a bit better because you're less likely to have mutations, and so on.
So, even though it's a very cellular process, we can actually use data from these long-term populations to look at this process in more detail.
Kat: So what does the future hold for these Soay sheep and their genetics and their evolution because they are an island population in a changing world?
Susan: It's hard to know. We are seeing interesting patterns because we've studied them for more than 30 years. We can see a lot of these changes happening in real time. The population is actually increasing on St Kilda in general and the sheep are getting smaller.
We can't directly correlate this with things like climate change, but we can see that this is a trait that we've seen over time. The work that some of us are doing at the genetic level - we're really interested to see if any of the genetic variation in the population has also changed over this time.
Could it be due to things like their changing environment or changing selection pressures on the population? This is still a very open question.
I think to understand the future of the sheep is hard to predict. If we can look at more populations, similar populations of for example; the red deer, but also long-term studies of birds and fish and so on, we can start to get a much broader picture of how these changes are affecting the phenotypes, and also how they are affecting the genotypes of individuals.
Kat: Susan Johnston from the University of Edinburgh, who was awarded the Genetics Society’s Balfour medal at the centenary meeting. And if you’re interested in life on St Kilda, you can follow the adventures of the Soay sheep through their delightful twitter account - they’re @soaysheep.
Sperm Wars
Kat: Another speaker at the centenary conference whose caught my attention was Peter Ellis - a man who is very interested in mouse sex (genetic sex, that is, which is primarily determined by X and Y sex chromosomes).
Male mice have X and Y sex chromosomes and produce sperm through a process called meiosis - half of which have an X chromosome while the other half have a Y. Females with two X chromosomes use meiosis to produce eggs with only X chromosomes. There’s a 50:50 chance of an X or Y sperm meeting with an X-bearing egg, so you’d expect a 50:50 ratio of males to females, right?
Well, for one family of mice in Peter’s lab at the University of Kent, that isn’t the case. So what’s going on?
Peter: In the mice I'm looking at, for some reason, that ratio, even though it's the most fundamental first law of Mendelian genetics, was broken. They actually produced 60 percent female pups and 40 percent male pups. We're looking to understand why that is and whether we can apply it to something that is economically a bit more important than a mouse.
The world does not need more female mice but it could well do with more female dairy cattle or even more female pigs. Because in the pig industry, almost every sausage, every bit of bacon you have eaten, has come from a female pig. Because male pigs tend to develop an off flavour called boar taint. So they either get slaughtered before puberty, which is an economic loss, or they are castrated.
Kat: Which is presumably a bit of a pain in the pig.
Peter: A pain in the pig, yes. A pain in the everything. It's an animal welfare issue and an economic issue for the farmers.
Kat: So what have you found out so far about these mice that seems to skew more female than male? What's going on there?
Peter: Well, it turns out that what's actually going on is a kind of internal war inside their own genomes. I said we have the X and Y chromosomes, where the male passes on the X, then you have a female pup. If you pass on the Y then you have a male pup. But there are genes on these chromosomes and so you can get genes on the X that fight to get into the next generation.
So the genes on the X chromosome will be selected to try and produce more female offspring, and the genes on the Y chromosome will be selected to try and produce more male offspring. I say, "try", it's the processes of natural selection.
This leads them into an arms race with each other. So what we find on the mouse is there are huge complexes of what we call ampliconic genes, genes that are present in many, many copies. There might be 600 copies of a given gene on the Y chromosome, or several tens or dozens of copies of the corresponding gene on the X chromosome.
If you get an imbalance in the copy number between the X and Y chromosomes, then it skews the sex ratio either towards females or towards males.
With transgenic techniques in the mice we can push that thermostat a little bit either way. We've worked out that these are the genes regulating sex ratio. We don't yet know quite how they then cause the sex ratio to be different but we do now know that it's down to the morphology and the shape of the sperm, and how well they swim.
Kat: So you've discovered that there can be this genetic difference that drives the sex ratio difference. But obviously, genetics then have to make an animal. So what do we know about how those genetic differences are actually driving this in the living animals?
Peter: Well, these are genes that are expressed in the germ cells while they're forming sperm. To make sperm, you have to start with a cell that has two copies of every chromosome. Then you go through the meiotic division and it goes down to one that has one copy of each chromosome. So; one copy of chromosome one in each cell, then you'll either get the X chromosome or the Y chromosome.
So, after they've undergone the meiotic divisions, the X and Y are now in separate cells. So if you like, they no longer have each other's interests at heart and they are able to fight with each other.
The genes on the X chromosome are producing something - we don't exactly know what - that seems to poison the morphology of the sperm. It will make the sperm be hyper condensed and an abnormal shape and it will affect the Y-bearing sperm worse than the X-bearing sperm. So the X-bearing sperm are making something that crosses over to the Y-bearing sperm and prevents them functioning properly. It's almost like a war between them.
Kat: Sperm wars!
Peter: Yes, sperm wars, literally. The X chromosome produces things that prevent the Y sperm swimming properly and prevent them developing the correct shape. Thereby it means they are less effective at fertilising.
Kat: How did you find this out? How do you tell whether something is a stronger sperm or a weaker sperm, in the sperm wars?
Peter: Well the person I was working with when I was a post-doc called Paul Burgoyne, he noticed that there was a particular strain of mice in his colony that was producing excess females, so we worked out that there was something going on there. In terms of how we analysed the sperm function, we did actually, almost the simplest experiment possible.
We just took the sperm from an adult mouse with one of these deletions, put it at the bottom of the tube and let it swim upwards through the tube. Then you can collect from the top of the tube where you've got the fastest swimming sperm, the middle, where you've got the middling sperm and the bottom, where you've got the ones that are lazy, can't be bothered to get out of bed. Then we just count how many X-bearing cells or Y-bearing cells there are in each fraction.
We found that in the fastest swimming population, we can see there are more X-bearing cells than Y-bearing cells. We can then correlate this with the fact that the Y-bearing cells are a worse shape than the X-bearing cells.
Kat: So, what next? Where do you go with all of this information that you now have? You've got the genetic information, you've got a bit of information about what might be going on in the sperm, what do you still need to discover?
Peter: We need to find that last piece of the jigsaw, the bit in the middle: How does this genetic regulation actually translate into causing the difference in sperm morphology? We have some ideas about how to do that and that's our next project over the next few years.
But ideally, once we've found that link in the middle, we can then look to see how this translates to other species. Can we use this to develop a way of sorting sperm in pigs or in cattle? Unlikely to be in humans, because we don’t have the same kind of ampliconic genes to the same extent that we see in many other species. But ideally, we can do something to reduce waste in the animal industry with this kind of information.
Kat: Peter Ellis from the University of Kent.
Horses for Courses
Kat: Moving from mice to larger mammals, Edinburgh has a rich tradition of animal genetics, particularly focused around the Roslin Institute - the birthplace of Dolly the Sheep. But while most breeding programmes and genetic research focus on farmyard animals, there’s been a lot less attention paid to the fleet-footed beasts of the field.
Patrick Sharman, a PhD student at the University of Exeter, is taking a closer look at the genetics of race horses, and started by telling me the story of one of the most infamous racehorses in history.
Patrick: Ah, Snaafi Dancer. So, Snaafi Dancer was sold at auction in 1983. He cost over $10 million. This was a new record I think, for a yearling. I think the previous highest was about $5 million. $10 million for a racehorse might not sound a lot, until you consider he had never set foot on a racehorse.
He was only 18 months old at the time, he'd never even been sat on by a jockey. He was considered to have a great pedigree and he probably looked as though he could run quite fast.
Kat: It was a nice photo; he looks like a good-looking horse.
Patrick: Yes, I mean I'm sure the people who bought him knew what they were looking at, knew what they were talking about, knew far more than me about what a racehorse should look like. But unfortunately it didn't turn out that way, he was particularly slow, apparently. So much so that I don't think he ever made it to the racecourse.
But given he had this great pedigree; he was sent to be a breeding stallion to see if he could be producing the next load of champions. He went to stud and it turned out he was infertile.
Kat: That's ten million quid basically down the tubes.
Patrick: Funny story to us but I'm sure not to them, at the time.
Kat: Let's look into this idea of racehorses having a pedigree. Obviously as people who are interested in genetics, pedigrees are all about genetics. They're looking at how things follow down the generations. I would assume that racehorses have pedigrees and we must know a lot about their genetics?
Patrick: Well, we do have a pedigree record of racehorses going back somewhere to the 1500s, 1600s. So in terms of a pedigree record, a genealogical record, there's an incredible record. Not 100 percent accurate, I think, they found a few mismatches along the way.
Kat: Naughty horses!
Patrick: Well, I think more naughty owners, actually, claiming their horse is by a particular stallion and then it turned out it wasn't. Obviously, these days you can't get away with that because everything is tested; blood samples are taken and parents are tested. But yes, we have a great record of the thoroughbred pedigrees.
Racehorse breeders have been trying to produce champions for hundreds of years. Long before Darwin came up with his theory of evolution by natural selection, racehorse breeders were already using genetics. It wasn't called genetics at the time but they were using their knowledge of pedigrees, they were selecting the best horses to breed and they were succeeding in improving the breed. They still are.
Kat: Obviously we have all the pedigrees of racehorses and we also have the records of how fast these horses have done. So what do we know about how this matches up to genetics?
You mentioned that they will take blood samples to prove that mummy horse and daddy horse are who we think they are, so; can we use that genetic information to work out, is this actually going to be a fast horse?
Patrick: Theoretically it's possible. There is at least one company I know of which collects blood samples and is capable of doing genomic testing. To what extent they've found genes responsible for performance, I'm not sure.
Kat: It surprises me - with an industry that's as wealthy as horseracing, that's got these incredible records not only of horses performances but also of their pedigrees - it really surprises me that there hasn't been more interest in understanding which genes, which variations are related to horseracing performance.
Patrick: There hasn't been much implementation of what we would call quantitative genetics. Not that I know of. Of course, any organisation could be doing it behind closed doors and why would they tell the rest of the world if they had been successful? So it could be happening without us knowing.
But telling the racing world that there's another way of doing it, that they could use quantitative genetics - it's just another theory. They've already got bookshelves of race breeding theories out there.
Kat: We don't need your stinking genetics!
Patrick: Well, exactly. It's just another one.
Kat: Maybe they don't want to know?
Patrick: There's beauty in the mystery, I guess, of breeding racehorses. It certainly has a romantic aspect to it. Whereas pig breeding and cattle breeding don't.
Kat: It's not romantic, pig breeding.
Patrick: So I've heard. I'm not sure racehorse breeding is, if you've actually been in a breeding shed.
Kat: I find there's an interesting parallel with the genetics of humans doing sport. Because I know there are some tests you can do, you can look at specific genetic variations and say, well, maybe you're a sprinter, maybe you're more of a distance runner, that kind of thing.
I'm always a bit skeptical about that, because there's so many variations that must add up to sporting ability, not just muscle strength but your mindset and how anxious you get.
So would something similar be the case with a horse? Can you not just say, well, you need to have long legs and big muscles, that's going to be a fast horse? Is there probably going to be more to it than that?
Patrick: Well yes, sure. In terms of distance preference, I think that's been found to be fairly heritable, but in terms of how good a horse is going to be, like you say, they need the right mindset. So even if they've got big lungs, a big heart, fast twitch muscles, when it comes to the final 100 yards of the race, you need the mentality as well.
We know that personality traits are heritable as well, so there's no reason you couldn't breed horses to be more competitive. That happens anyway. When breeders select stallions to use for their mares, they are looking for stallions who produce winners, who produce offspring who want to race.
I've known a few stallions who produce offspring who are a bit shy when it comes to the final 100 yards and they don't put in 100 percent effort, and those stallions tend not to persist.
Kat: And presumably there must be ones who just get the killer instinct for the finish line?
Patrick: Yes, for sure. Certainly offspring of certain stallions which are strong enough for the finish, you would say.
Kat: And finally, do you like a flutter? Do you watch the horses and do you bet on them?
Patrick: Yes. I grew up watching racing. I shouldn't say it, but I grew up betting as well. Not in a serious way. I blame my mother.
Kat: And do you still bet now that you know all this information?
Patrick: The more I know, the worse I do and the less I try to bet.
Kat: Sound advice - that’s Patrick Sharman from the University of Exeter.
The Vikings of the Northern Isles
Now it’s time to switch from animals to humans. The Medical Research Council’s Human Genetics Unit in Edinburgh was originally set up in 1956, initially to study the impact of radiation on human health in the wake of the atomic bombs dropped at the end of the Second World War.
At the time, the structure of DNA had only just been discovered, and while geneticists were busy crossing animals and plants to understand heredity and health, there were relatively few techniques for studying genes in human cells, and DNA sequencing wouldn’t be invented for another twenty years.
In fact, there was just one - cytogenetics, literally looking at chromosomes down a microscope to spot any patterns or abnormalities.
And, as the Unit’s current director Wendy Bickmore explained to me, with that simple tool they set out to study the genomes of the world.
Wendy: So one thing the Unit did in the early days, after it was the MRC Group on Radiation Biology it became the MRC Clinical and Population Cited Genetics Unit, a real mouthful to say, I have to say. But they went out and they started doing population genetics.
They went out to a Hebridean island in the Outer Hebrides, a very small one called Barra. And they decided to just ask the question; how variable is the human genome? Just by looking at it. Indeed they did find that it was what we call polymorphic, there are many forms of it.
Kat: Just by looking down a microscope you can see differences?
Wendy: Absolutely. So that laid down the idea that it would be worthwhile going out and looking at diverse human populations to see how much variation there is. So then when you fast-forward into the molecular era where you can clone and sequence DNA, people then started trying to ask; can we link changes in the human genome to disease? Of course, many diseases have a genetic origin.
People started with the simple Mendelian disorders that are inheritable. Cystic Fibrosis is a good example, Huntingdon's career was one of the early wins in this area. People took very simple linkage approaches. You needed to assemble huge families and then be able to follow alleles.
Kat: Is that the family tree, kind of thing?
Wendy: Yes, all pedigree based. That was very successful and identified many genes causing Mendelian disorders. Of course that's limited. You needed to have big pedigrees; you can only find Mendelian disorders this way.
Kat: So, these are the really obvious diseases where basically, if you've inherited either one copy of the duff gene or two copies of the duff gene, you're going to have the disease? It's fairly obvious to spot it.
Wendy: Yes, it is if you've got the numbers. But people are actually going out now specifically picking interesting groups of individuals, particularly those that are geographically isolated, to study their genetics.
Because these are usually populations on islands or in small, mountain-bound regions which were founded by relatively small numbers of individuals - so called founder populations - and their descendants have largely stayed in that region and there hasn't been a huge influx of other people from outside. So that's a really interesting genetic structure.
In that situation, rare genetic variants that are rare in the whole population of a country or continent can rise to quite high frequency just by chance. It's called the Jackpot Effect, in these small bottlenecked populations.
Of course, now we can move beyond that and really start to look in nuclear families - trios; mother, father, one child, with no other pedigree information than that - to try and see if there are genetic variants associated for example with a major developmental problem in a new-born baby. New mutations, what we call de novo mutations that neither of the parents had, because each of us acquires about 15 new mutations in our genome that our parents never had.
So copying the genome is very, very good but it's so big, errors creep in. Every generation accumulates new mutations.
Kat: I call this the Philip Larkin effect. You know, they muck you up, your mum and dad, they throw in all the things they had and just a few just for you.
Wendy: Yes, they do try very hard not to, but it's not perfect.
Kat: Tell me about one of the populations that you've been studying, the Northern Isles. What is this area and who are these people?
Wendy: The Northern Isles are Orkney and Shetland. They are off the North coast of Scotland. Actually, if you look on the map for Shetland, it's closer to Norway than it is to Scotland and the UK. So, it turns out that these individuals, these islands were founded by people from the Scottish mainland, but also from Norway with Norse ancestry.
Kat: Vikings?
Wendy: Essentially, yes. And the study is actually called the Viking Health Study. So they are Vikings. Actually, in the study we have only chosen to study people in the population now who can show that they have had at least two grandparents - preferably all four grandparents - originating from the Northern Isles as well. So we know that we're looking at the genotypes of that ancient founding population.
Kat: What have you started to find?
Wendy: First of all we're understanding the architecture of the whole population. We are indeed starting to be able to link lots and lots of different traits to genetic markers in the population, that affect the health of the population - what we call common disease. We're also finding those rare alleles --
Kat: The Jackpots.
Wendy: -- the Jackpots that cause much more severe monogenic disease. We've actually been able to recently publish a case where a damaging variant in a gene - which can give rise to something called long QT syndrome which affects heart rhythm and can result in really catastrophic cardiac failure - and being able to find that actually, within that isolated population we can trace that allele back to distant members in the same population.
People that don't know they're related to each other, but they share that ancient genetic variant, and be able to identify it to their health practitioners, their GPs, that they may have a genetic change that may put them at risk.
Kat: Looking into the future, now we're gathering hundreds of thousands, even millions of DNA sequences from people all over the world, how should we start to think about this concept of the human genome? What is the human genome of the future?
Wendy: Well of course, there isn't a human genome. There are billions of human genomes, tens of billions of human genomes. In genetics we often talk about things like wild type and mutant. Well, there's no such thing in the human population. There's no wild type. We are all mutants.
Kat: We're all wild, we're all mutants, I guess.
Wendy: Yes, so studying that diversity is really interesting from the point of view of biology and medicine. I think it's also really fascinating from the point of view of human history; being able to understand the history of human migrations and social changes.
I had a conversation recently with a colleague from India where they also have isolate populations but are isolated - not geographically because they're stuck on an island, but they are isolated socially by the caste system in India. That creates these rare Jackpot alleles in communities that are living side by side but with other communities, but really the genetic information doesn't mix.
So uncovering all that is going to be so interesting for understanding the history of countries, nations and populations, I think.
Kat: Wendy Bickmore, the director of the MRC Human Genetics Unit in Edinburgh.
Stripping the Helix
Kat: Finally, the centenary conference was rounded off by fiddle player and former neuroscientist Lewis Hou and his ceilidh band. I caught up with him after a riotous round of ‘Strip-the-Helix’ to find out more about his blend of science communication and folk dancing.
Lewis: So, my background is an interest in music as well as in neuroscience originally and in public engagement. I was really interested in how to work with everybody, not just people who were already engaged in science.
The nice thing about ceilidh, if you've ever done a ceilidh, is it's not about how good a dancer you are, as we've found out at the conference.
Kat: Yes, I've just finished, I'm very sweaty, my feet hurt, I'm covered in bruises. Look at that! I can confirm that pretty much no one was a good dancer by that point.
Lewis: But the spirit of it is all about the participation. Everyone gets up and gives it a wee go and that's exactly the spirit that we want to bring into science. You don't have to be an expert; everyone can feel welcome.
We have two genetics dances that we developed with the Wellcome Trust and researchers here in Edinburgh. We have the Meiosis Waltz which we developed with some community groups. That explains the different stages of meiosis in a very beautiful dance, very similar to a St Bernard's but it's quite a new dance.
Kat: So meiosis is the process of DNA being copied and cells dividing, so how do you work out what steps you show that with?
Lewis: So we've worked with dancers and community groups and researchers. We did it as a kind of co-production. There's a stage in meiosis where all the chromosomes come into the middle of the room, for example.
So we film that in the video, with dancers coming into the middle and then they kind of break apart from their partners, into two halves. So meiosis is the forming of new cells, so we represent that in dance form.
Kat: And then what about the Stripping the Helix? That's what we've just done, very, very fun, very, very chaotic. What are you trying to show there?
Lewis: Stripping the Helix, okay, the video version which is much more controlled than the one in practise, shows dancers in different colours. So they're paired with a partner based on their colour or their adenine and thymine as cytosine and guanine, for example.
Then what happens is that they split into two groups and then they do what looks a little bit like the traditional Strip the Willow, which consists of a partner, a couple at the very top, going down to each of their partners or bases, for want of a better word, and they represent pulmonarias. I think it's just trying to approximate it.
On the video we do it in a slightly more controlled manner. We show how mutations happen, we throw away the wrong dancers and they get replaced.
Kat: Well I will say I know a little bit about genetics and there was definitely some replication slippage. Because the first time up and down the strands I was dancing with one person and then the second time around I was like, you aren't the base I started with, but we'll do it anyway.
Lewis: Absolutely. So when we're working with schools that would be a great opportunity for us to talk about different types of mutations, point mutations or is it a whole slip. We can talk about these as proper dance models and criticise them but also use them just for fun.
Kat: It certainly was a lot of fun. Less so the following morning… That’s science ceilidh founder Lewis Hou, and you can find out more and book your own event at https://www.scienceceilidh.com/
That’s all for now. We’re taking a break for Christmas and will be back with a new show on the 2nd of January. But don’t go anywhere, because just like a scientific Santa Claus, we’ll be bringing you a few treats over the festive season.
You can find us on Twitter @geneticsunzip and please do take a moment to rate and review us on Apple podcasts - it really makes a difference and helps more people discover the show.
Genetics Unzipped is presented by me, Kat Arney, and produced by First Create the Media for The Genetics Society - one of the oldest learned societies in the world dedicated to supporting and promoting the research, teaching and application of genetics.
You can find out more and apply to join at genetics.org.uk Our theme music was composed by Dan Pollard, and the logo was designed by James Mayall, transcription is by Viv Andrews and production was by Hannah Varrall. Thanks for listening, and until next time, goodbye.
