Synopsis: Special Evolutionary Episode! The Debate Rages Between Justin and Kirsten (Or, Was It Lamarck and Darwin?), Refereed By Dr. Tim Coulson and His Shrinking Sheep
Justin: Disclaimer! Disclaimer! Disclaimer!
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One of the wonderful things about science is that it is the only motive thinking that seeks to ignore that personal world to reject our illusions and force the mind to look at information each time as if the real world were brand new and in need of introduction.
This way of saying without assumption of knowing can make visible in a glance that which would have remained invisible to the filtered eye — a glance of Hubble’s data plot revealing an expanding universe; a glance like Fleming’s bacterial dish ushering in the age of antibiotics, a glance that patterns across a flickering screen signaling that a cosmic discovery; a genetic breakthrough or needed cure is on the way, one step closer or at least within our reach.
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Yet, we will continue with wide-eyed introductions to reality, continue glancing over steady strings of data that flows past our radio vision seeking that data plot that oddly dotted dish, that flickering signal from an illusion free world of This Week in Science, coming up next.
Good morning, Kirsten!
Kirsten: Good morning, Justin! We have a great show ahead. This is This Week in Science. And it’s a very special episode of me kicking buckets under the table.
Justin: Yeah. That’s normally where my shins are. I’ve got – today I’ve got bucket guard.
Kirsten: Bucket.
Justin: Large plastic bucket between me and Kirsten just in case I get kicked.
Kirsten: That’s great. Well, no, we actually are going to be talking about evolution the entire hour. That’s what the show is going to be dedicated to. We’re dedicating it to understanding what is understood about the wily ways of evolution.
And our guest for the entire hour is Dr. Tim Coulson from University College London who just last week published a paper in the journal Science on the environmental selection of shrinking sheep in Scotland. And so, hopefully, he’s going to set us straight.
According to his website, Dr. Coulson is a population biologist who studies how demographic rates vary across groups of individuals and environments, and identifies the ecological and evolutionary consequences of this variation.
Hopefully today, we will be able to elucidate some of the evolutionary details about which Justin and I have been debating for the last two weeks. And so, without any further ado, let’s bring him on the line. You want to hit the button – hit that little green button.
Dr. Coulson, are you here with us?
Tim: Hello.
Kirsten: Hello.
Justin: Welcome to This Week in Science.
Kirsten: Welcome.
Tim: Thank you.
Kirsten: Yeah. Thank you for joining us. We’re very excited to have you here or at least on the phone and kind of – we’re going to talk about the newsy aspects of your sheep publication in Science and we’re going to then dig deep into the details of evolution with your assistance. I guess – let’s see, we can start with the news of the week which is your story.
Justin: Yeah.
Kirsten: And to make the story short, you’re blaming climate change for shrinking some sheep, like put the sheep in the dryer too long.
Justin: Yeah, it’s that they added heat to the moist Scottish tundra that’s shrinking them. What’s happening here?
Tim: So, what we found is over the course of our study, winters have got shorter as our measure of the climate, the North Atlantic oscillation has changed with time. And what this has meant is that spring as is occurring through much of Northern hemisphere is actually arriving a little bit earlier than it used to.
And a consequence of this means that many of the smaller – slower growing sheep that in the past, when winter is sort of a bit longer and little bit harsher, these animals would have used to keeled over and died by the end of the winter. Many of these are now surviving. And this has had two consequences.
This has brought the average size of the sheep in the population down a little bit. So, the average sheep is now smaller than it was about quarter of a century ago by that 5%. But also the population has actually increased as conditions on the island have actually got a little bit better.
Justin: So yeah, the shorter winter is longer feeding time. There’s more stuff growing, right?
Tim: That’s right. There’s a slightly longer period when the grass is growing. But there’s also a – the period when the grass isn’t growing as is consequently also a little bit shorter.
Now, a lot of people immediately say, “Well, wait a second, there’s more grass, wouldn’t you expect larger sheep?” But now more grass has actually meant more sheep but also has meant that some of the smaller slowing growing ones is surviving.
Justin: And this is on an island. But this isn’t where – we weren’t – wouldn’t call this like an island dwarfism effect at this point?
Tim: Not at this point now. So this is on an island. It’s a group at St. Kilda archipelago; it’s a group of islands about 18 miles off the West Coast of Scotland.
And we’ve studied them on the largest islands – an island called Hirta. The sheep has been on the archipelago of islands from between 3,000 and 4,000 years. And they’re thought to be very closely domesticated to – a very closely related to their sheep. They’re initially domesticated by mankind.
And as far as we are aware, certainly for, since historical records were written down whilst people lived on the island, people left in 1930, these sheep have essentially been managed.
Now, we don’t believe this is a sort of classic case of island dwarfism that is being seen and things like elephants and rhinos in some of the Mediterranean islands.
And then (unintelligible) that dwarfism to many much, much longer than we’re talking about now. For example the decline of the majority of the decline in things like elephants on the Mediterranean islands took well over 100,000 years.
Kirsten: Mm hmm. And what do you think the factors are – what the people think the factors for this the island dwarfism that would not or not necessarily be the same as what you’re witnessing in Scotland.
Tim: Since highly possible what their processes that we’ve actually been able to describe, identifying to our account their contributions are, are the same sorts of processes that leads to change and body size on islands especially when you arrive in a simple system where there is little competition for food from other species and there’s no predation.
Since highly possible that, that the changes in the way that competition of food occurs as we’ve actually been report– as I’ve been describing there, in this case, it’s been caused by shortening winters.
Kirsten: Mm hmm.
Tim: But it’s entirely impossible that that change is due to animals being isolated away from competitor species so into specific competition and some (catalyst) could result in similar effects. We just don’t know at the moment.
But the reason we studied the sheep on this island in the middle of nowhere, way of Scotland…
Kirsten: Yeah.
Tim: …is because it’s almost like a natural laboratory. It’s a very, very simple system. Sheep are the only large vertebrates from the island. They are the only large herbivore on the island.
So, we have a remarkably simple system consisting of sheep and vegetation. So, if we can understand the ecological and the evolutionary dynamics on this island in this very simple system, we can have a little chance in more complicated cases where there are many species co-existing, predators, et cetera.
Kirsten: Right.
Tim: The good news is we’ve actually made recently good progress in understanding what’s going on in the system, not just in terms of the body size but also in terms of animal behavior, in terms of the population dynamics, et cetera.
Kirsten: Yeah. So, what are some of the animal behaviors and dynamics that are going on there that could potentially lead into this difference in what you’ve been seeing over the last quarter of century?
Tim: So, in terms of the population dynamics that we see, one of the reasons this island started is the dynamics are relatively unusual for a large mammal. The population fluctuates quite substantially over time. And between three and five or six years, there’s quite a large population crash went up to 60% or 70% of individuals die.
Now, the severity of these crashes does change from time to time. And so, we haven’t seen a large die off in the last few years. We keep predicting one but one hasn’t occurred recently.
So, one of the things that has happened dynamically over the course of time is – as I kind of alluded to this a little bit earlier, as the winter length is shortened and conditions during the winter have actually improved. This has meant that more smaller slower growing individuals are surviving which actually corresponds to a decrease in selection pressure.
So, natural selection has actually decreased over time in this study. And this selection typically favors big sheep. But the selection for the bigger sheep has actually declined a little bit over time.
Now, one of the other things that we did on this paper, rather than explain why the sheep is shrinking, we also were able to explain why this positive selection which one would traditionally have expected to lead to an increase in body size wasn’t realized.
Kirsten: I think that’s really interesting, the – just the language that’s use to describe, you talk about this positive selection pressure or having it be removed. Whereas, the way I was envisioning it is that it’s all natural selection. It’s just a change in, you know – a change in the environment has just shifted the emphasis of the selection pressure.
I mean, is that just a difference in the way of interpretation or is it, or what am I thinking wrong?
Justin: Yeah.
Tim: So, the way that ecologists and evolutionary biologists can report the strength of selection is using something called the selection differential. And what this really just tells you is a difference between – if we’re looking at survival selection so, in this case, whether a large or small animals are more or less likely to survive.
As well, what is selection differential does? It tells you the difference in the trait value between surviving individuals and the entire population before selection occurs.
So, something is actually quite easy to measure if you’ve got enough data and data are good. And one of the things we were able to do is actually characterized. So, in our breakdown of all the factors that contribute to a change in body size, we were actually able to measure accurately and in an unbiased manner the strength of the selection differential.
And it’s very clear that these selection differentials have declined over time. So, an environmental change has just altered the way that the strength of the selection differential. It’s still there.
Kirsten: Mm hmm.
Tim: Selection is still occurring. But it’s just taking place in a slightly different way and slightly less strongly than it was before. And there’s also, as you say, had a shift in the growth rates.
It’s entirely possible that the shift in the growth rates with more smaller, slower growing animals surviving have a genetic underpinning in which case, is subject to evolutionary change itself.
We haven’t actually done the quantitative genetic methods on the growth rate per se. However, we have done it on total body size, it’s actually body size. We find that absolute body size is partially determined by genes.
Kirsten: Mm hmm.
Tim: So given the fact that we have seen a change in the selection pressure on a trait that we know is influenced partly on genes, what we’ve found is that climate change or the changing environment is actually influencing the way that evolution is occurring.
Kirsten: So, it is having an effect on the allele, the gene frequency in the population. Is that what…
Tim: That’s right.
Kirsten: Yeah.
Tim: It will be having effect on the allele frequencies. Now, we don’t – we’re starting together with colleagues at Sheffield and Edinburgh – we’re starting to get an understanding, a little bit of how the actual genes, so that actual growth size, genetic growth size associated with body size.
However, we don’t know – body size is really quite a complicated character, quite a complicated trait. And there are many, many genes involved. And what biologists tend to do in the case like this, when the many genes involved is you try and make an inference about how important genes are overall without actually identifying the specific (loci).
And the way you do this is you look to see whether related individuals, with our parents, with our offspring or cousins are more similar for the character or the trait you are looking at than non-related individuals.
So, although we haven’t been able to specifically prove there’s been a change in gene frequency…
Kirsten: Mm hmm.
Tim: …what we are able to do is to workout that there is what’s known as the heritability of the trait which we identified by compelling where the body size is more similar amongst related individuals than it is amongst individuals that are not so closely related.
We are able to then come up with the number between 0 and 1, which tells us how much or what proportion of the trait is due to genes. And a value of 0, heritability of 0 tells us the trait, a body size in this case, is entirely determined by the environment. While a value of one would tell us it’s entirely determined by genes.
What we find in the case of body size is a value of between 0.1 and 0.2. It depends how you do the calculations which tell us that 10% to 20% of your body size and how big you grow to is determined by genes.
Whilst the rest is determined by environmental conditions be those environmental conditions in utero and you’re developing as a lamb or once you’d been born and as you’re growing – is growing the juvenile stage.
Kirsten: So, there was somebody in the – there was a popular science write-up in Science Magazine on their ScienceNOW website and they found an Ecologist Malcolm Gordon from the University of California, Los Angeles who praised your study but…
Tim: That’s very nice of him.
Kirsten: That’s very nice of him. But he says, “Other mechanisms maybe at work.” And the quote that they have from him is that he says, “Changing environmental conditions on the island may have led to changes in the chemical composition and nutritional value of the plant foods the sheep eat. And that may have shrunk the sheep.” But, he says, “At the end of the day, climate change could still be the root cause.”
I mean, is he on track or, how do you respond to that kind of a critique?
Tim: So, in order to answer that, I’ll just take a sort of a small step back. So, the approach that we did was we essentially started by saying, “Well, the sheep have been getting a little bit smaller. But there is selection. And, even though it’s supposed to be weak, there is selection to sheep to get bigger. So, why isn’t this occurring?
So technically, what we did was the following: we sat down. And we said, “What are the processes that could actually lead to a change in the size of the average sheep over time, over from one year to the next, over the time spent?” And it turns out that this thing called viability selection which is selection due to larger animals having a better survival chance than small animals.
Kirsten: Mm hmm.
Tim: There is fertility selection which means bigger animals might be able to produce small offspring or might be more likely to reproduce small animals? Does then, growth rates of individual animals that survived so, the average growth rate amongst survivors.
There’s a difference between offspring and their parents in terms of their body size and then there’s just changes in the population structure which, again, is almost like a nuisance that we need to tease apart.
That we are able to find is already mentioned this selection has weakened so, that the strength of natural selection is a little less strong than it used to be.
However, (though) we’re still pushing for sheep to get a little bit bigger. Now, the reason they weren’t getting bigger in this first instance was because when we looked to see the difference between the traits of offspring and their mothers, we found that there was a process that there were always small sheep being born into the population. And this process of small sheep being born into population is caused by young mothers that are breeding for the first time are just incapable of producing large, heavy lambs themselves.
Kirsten: Mm hmm.
Tim: This is probably because the mothers haven’t bred before. They’re not necessarily – well, they’re not fully grown. They haven’t reached their body size. But those effects weren’t enough to explain the decrease in size. They were enough to explain spaces in size.
Kirsten: Right.
Tim: So, where the sheep haven’t been getting bigger. They have been getting smaller because of this growth rate effect that have decided before…
Kirsten: Mm hmm.
Tim: …that I’ve described before. Now, each of these processes that I’ve just described adds up perfectly to tell you the change of average body size. And what we did is we described, we applied this equation for each year of our study. So, each of the 25 years, we’ve been studying these animals. And then we found there was a decline in growth rate.
So, then what we did was a statistical analysis of the growth rate from year to year. And we were able to find that population density for the number of animals on the island and winter weather as I’ve already described influenced this growth rate.
Now, we could have fairly, you know – statistically, we then used to have a little bit more and came to the conclusions that this effect as the winter is getting a little bit shorter and sheep growing a little bit more slowly.
Now because this part of the analysis is a statistical analysis and we haven’t – it’s not an exact description there. There are potentially other factors that could be involved in this process that we haven’t been able to measure and we haven’t been able to characterize.
And of course, it’s entirely possible that, we have missed some things and one of those things we could have missed may well have been the fact that change in growth and pressures have lead to a change in the secondary plant compounds.
Kirsten: Mm hmm.
Tim: And some plants are a little bit harder to digest given the changes in the growing season. As we’re already ingesting and, and insightful comment, it is something that hopefully we’ll be able to address in the future.
But certainly from the analysis that we have done now, we’re fairly confident that one of the roles that’s coming out as important is that the change in the length for the growing season means that small animals are actually able – slower growing animals are able to survive.
And we’re fairly confident that’s true but we’re not in the position to actually rule out the other processes as being important. So, I think it’s a great comment and one that we almost certainly going to follow up on in the future.
Justin: And you mentioned the population density and how people are – they have been sort of predicting the crash.
Kirsten: Yeah.
Justin: Is the population really high right now for the sheep on the island? Are they…
Tim: Yeah. The population is probably as high as it’s ever been.
Justin: Awesome.
Tim: As I said, as the sheep has got smaller, the total numbers on average, it just jumped around a lot have been already said, the total number has been going up.
And in fact, we are predicting at the moment that this year, we are probably going to see more sheep on the island than we have since we’ve been studying them.
Justin: So, are the sheep overall getting less grass to eat even though there is more being grown?
Tim: Overall, we have suspect that each sheep – because there is these two processes going on. The growing season that has increased in length, sheep has got a little bit smaller but the total number of sheep has increased.
I suspect the amount of grass per kilogram of sheep has remained approximately constant. But it’s the timing that’s changed and the strength of selection.
Kirsten: It’s fascinating. If you just tuned in, you’re listening to This Week in Science with Dr. Kirsten Sanford and Justin Jackson.
And so, this story is, I think, really interesting. And listening to all of the different pressures, the different selection, environmental, natural, growth rate, all these various pressures that go into determining the population and traits of the population have kind of go back to the crux of this debate that Justin and I have been having for the last couple of weeks about how evolution works.
And in the last couple of weeks, Justin has been arguing for what seems to be a very Lamarckian view of evolution.
Justin: Not Lamarckian. It’s not.
Kirsten: And at one point, you almost came across it as supporting like some kind of intelligence behind evolution. I don’t know what we’re going out there.
Justin: Yeah. I think it is. And I think life is a very intelligent system.
Kirsten: It’s a (smart).
Justin: Not intelligently designed.
Kirsten: Evolution is – right though. I know.
Justin: Or, not intelligent creator but life is smart. I’m going to (unintelligible) for that.
Kirsten: I’m giving you a hard time.
Justin: Life is clever. How about that?
Kirsten: It is.
Justin: It’s a clever setup.
Kirsten: It’s clever. So anyway, Lamarck historically – okay, historical background. Lamarck proposed sometime before Darwin that gradual change during an organism’s life time might be passed on to their offspring.
Justin: Mm hmm.
Kirsten: But he was never able to propose a mechanism that was suitable for that process to actually explain it and it kind of fell out of favor. And it’s been out of favor for a really long time.
Darwin came around to propose this process of natural selection, the gradual change on kind of a generational time scale that was supported later by Mendel and the discovery of DNA.
And since we have elucidated more aspects of evolutionary theory, the crux of the concept remains that evolution is based on the genetic information that’s available and it’s driven by mutations.
Natural selection acts on the phenotype or kind of what the organisms look like. And, it’s kind of like the phenotype is like the user interface for a piece of software.
Justin: Interesting.
Kirsten: And then a code is like the DNA. So, the phenotype is like the output of the genes. And so, if a mutation in the genes doesn’t make the user interface unusable, things work fine and you’re able to still make things work.
But when a mutation breaks that interface between the organism and the environment, the organism is not going to survive to be able to pass on that broken gene and then the environment chooses the winter, survival of the fittest.
And so, I’d like to argue that it’s possible for there to be other instructions present that can be passed on to the next generation that alter the way the genes are read and turned into output.
Justin: But that’s my argument.
Kirsten: But the bottom line…
Justin: You can’t take my argument and your argument. That’s not fair.
Kirsten: The bottom line to what is possible is always going to be the genes. It’s always going to be the genes.
Justin: No, it’s not always going to be the genes.
Kirsten: And when you start using epigenetics as like this, catch all explanation, it’s a just so story and it just losses…
Justin: What’s a “just so” story?
Kirsten: Well, it’s just so. It’s just so.
Justin: No, no. I think it’s – I think we have to go back to the Marx Brothers movie “A Day at the Races” and we have to go to the “Tutti Fruitti” ice cream scene. You have no idea what I’m talking about. You’re completely blank.
Kirsten: I have no idea what you’re talking about. I don’t watch things that are in black and white.
Justin: Basically, Groucho Marx goes to bet on a horse. And he gets a, “Psst! Hey, you want to know who’s going to win? I got the book.” And so, he gets the book on who’s going to win.
And he looks at it and it’s encode. It looks like DNA code effect. It’s just the series of letters. “What’s this?” “Oh, you need the code book to go with that book.” And so, he gets the code book. And he’s got the code book but then he needs the breeder’s book to go with the code book.
That’s kind of where I think we are with DNA. DNA has turned out not to be the blueprint. It’s turned out to be much too simple to explain everything that’s going on and we thought we – okay, we thought we will get this code and we would be able to troubleshoot.
We would be able to pinpoint diseases and just see where the things are going wrong and know what needs to be monkeyed with, but we don’t. We’re looking at it and we’re finding that the same gene discrepancies in different individuals can show up – manifest these different – completely different diseases.
We’re seeing that creatures that have — what was the example recently, they did that — they cloned cats. They cloned a cat. And the cloned cat had a different coat than the original.
Or they’ve had flies that they found that if they incubate at different temperatures, the flies’ eyes color changes. And the eye color change from having been incubated at a different temperature is passed on to later generations.
So, there is something beyond simply the genes. The genes are not enough to explain. There’s a way of – there’s certainly ways of turning them on and off. But I think there are also effects of the genes that are translated differently based on the environment. I think the environment is a much bigger factor than it’s been giving credit for.
Kirsten: All right. Dr. Coulson, after listening to our two disparate – well, kind of, I guess yeah, mostly desperate points of view.
Justin: You hedged yours. I didn’t. I stuck to my guns. We like, “Oh, maybe everybody’s right. We can all be friends.”
Kirsten: Do you have any comments about the points of view that we both brought up?
Tim: Well so, I guess my take on this would be first, we need to have a good definition of what we mean by evolution. And I think they’re working definition that most our population geneticists or evolutionary biologists would be is that evolution has occurred.
Evolution is measured by a change in allele frequencies. So you see a shift in allele frequencies over time. Now, that change in allele frequencies is caused by selection and of course new alleles have brought in to the population through mutation.
Now, a little of what you guys have been arguing about there is how you go from those genes to the phenotype. And that’s a really difficult question. And this question – a lot of works have been done at the moment.
And one thing that is really clear is that we don’t have this really simple map that goes from your genotype through to your phenotype. So, the set of map, how you get from the genotype to the phenotype is really rather difficult and it’s really rather hard. And there are all sorts of additional drivers that can come in there and influence that mapping.
So that’s going to be things like the environment. But when you say the environment, we – it’s kind of a catch all for huge number of different things so that environment could be the environment that you have experienced when you are growing. It might be the environment you experienced now. It might even be the environment that you experienced when you are in gestation in the womb, et cetera.
And that environment may well be influenced by what your mother did and what your mother experienced. And we all said that some of these inter actions are remarkably complicated because some genes can then be switch on or switch off as a function of that environment. So, you can get these epigenetic effects going from one generation to the next.
And really in order to understand, so you spot on selection to operate from the phenotype, that’s what selection sees. So, it sees your body size. It sees how good you are at fighting disease. It sees all of these sorts of things. And selection operates there whether you survive or whether you reproduce, determines whether you pass on your genes, et cetera.
But because the map between the genotype and the phenotype is so complicated, it’s often really rather difficult to actually just look at the phenotype and look at selection and to be able to say how that’s going to change allele frequencies.
And then of course, on top of that, we’ve got the whole process of mutations and how mutations occur, whether they occur in some parts of the genotype more preferentially than other parts, in terms of how the DNA is actually repaired by DNA repair mechanisms.
So, I hate to sound as I’m coming down in the middle there but I suspect you’re both right. But most of your point would be that’s kind of start from a sensible definition of evolution. I think changes in allele frequency is good. Adapt to the evolution, so adaptive change is caused by selection. Yes, you can get evolution by a drift, just demographic chance effects and what have you.
But then, actually going from selection on the phenotype to the changes in genetic level is really quite hard because the map between genotype and phenotype can be very complicated. It can be influenced by the environment. And the environment with this multi-dimensional many faceted and hard to measure thing that’s out there.
Kirsten: All right. Well, on that note knowing that I’m right and Justin’s right, we are going to take a very short break. We will be back in just a couple of moments. This is This Week in Science. Dr. Coulson, please stay on the line because we have much more to discuss with you when we come back after the break.
Tim: We’ll do.
Kirsten: Thank you.
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Justin: So, I said yeah. I say Lamarck is definitely the father of evolution. And the guy turns to me and he start swinging and – oh, we’re back. Oh, wait.
Kirsten: Welcome back. This is This Week in Science. And we are on the phone with Dr. Tim Coulson from the University College of London.
Tim: Imperial College London, (unintelligible).
Kirsten: Imperial College of London. I’m sorry. I’m wrong. Yes. And we are back and we’ve been having just a wonderful discussion. If you just joined us, Justin and I are both right in our own ways. Hopefully, we will find a way to meet in the middle knowing that we both have some aspect of correctness.
So if – let’s kind of get back to the nuts and the bolts of evolutionary theory. We mentioned Lamarck and – I mentioned Lamarck and Mendel and Darwin, I mean is there anything that you think historically is important to the understanding of how we’ve gotten to where we are in our understanding of evolutionary theory?
Tim: Well, I think there’s a huge amount. I mean, you’ve started with obviously the right names there.
Kirsten: Right.
Tim: But I think one of the most important things that has happened over the years is as the verbal theories of, Darwin have actually been, expanded and we’ve been able to write down equations to describe what’s going on. We’ve been able to measure that, the force of adaptive evolution, as I mentioned before, that selection. We can measure of that occurring.
We’ve also been able to have the huge advances that have occurred in terms of gene affecting individuals and being able to work out levels of genetic, how individuals differ. So, you need – for evolution to occur, you need genetic differences between individuals and you need selection.
We’ve been able to prove both of those things. So, even if we’ve got to a point now as you know where evolution is proven. It’s not theory. It’s approved. It’s actually out there.
And now we’re already starting to be able to get to grip with putting the nuts and bolts from the serious complexities that arise behind it. And at the moment, many of those complexities are going from genotype to phenotype.
So, I believe there’s been a huge body of evidence that is built up over that past few decades that really helps us get a much, much clearer understanding of how evolution works, how it’s led to the diversity of life we see at the moment.
And we’re starting to get an idea of how our actions on a natural world may well be influencing the way evolution may occur in the future. What I expect will happen over the coming decades is we’ll get to a point where we’re able to make evolution to a more predictable science than it is currently.
But in order to do that there, we are going to need to understand this link between the genotype and the phenotype which is what we were discussing before the break.
Kirsten: Right. And it is that mapping that’s currently the point of complexity.
Tim: Absolutely. It’s understanding. So, we know that genes may well play a part in many aspects of the phenotypic – the phenotypes. So, may well play a part in many of the things you can measure individuals be that, those thing’s behavior, be their, personality, be their body size and body shape, be their ability to fight diseases.
You name it; people now are identifying genes associated with these traits. The question now is how do you go from the gene to the phenotype?
Justin: Yeah. It’s actually one of my favorite studies is the Trut Fox study, where they were breeding over I think 50 years or so, breeding foxes based on temperament. They were sort of doing an experiment to see if they could domesticate a wild fox.
Tim: Right.
Justin: And as they were doing this – just based on a temperament, just based on which ones could be friendlier towards the humans over successive generations. They noticed the coats were lightning on the ones that they have been selecting out.
And it turns out they discovered that the link between temperament between stress levels hormones and the expression in the coat and even in skull shape. There’s even skull and some tail and ear shape differences that have been taking place over the generations, which is really an expression of stress in utero of the fox mothers. Right? But, yeah, I think it’s very interesting that we’re finally now making these connections between them.
Tim: I think that’s right. So, I think one of the points for you bringing out that is an interesting one, is that often as, correlations between different traits. In the case of the fox, it appears that temperament is genetically correlated or in some way or in some way linked to coat color.
Now, whether that’s actually through genes that are linked together, genes that determine temperament and genes that determine coat color are closed together on a chromosome or whether it’s through a hormone level switching themselves may be influenced by genes that then go through – their hormone levels influence temperament and coat color.
I’m not sure, but I think it’s a sensitive level of complexity that we’re now starting to get a grip of. We’re now starting to understand.
Kirsten: That gets into the question of these kind of maternal effects and how things like what happens, what the mothers eat, what the hormone levels are like how that affects the offspring. Is there any recognized paternal effect that, anything that happens to the sperm before it gets to the point of conception and gestation?
Justin: Yes.
Tim: Most of the maternal effects where you can expect maternal effects into kind of two classes is what then as maternal environment effects…
Kirsten: Mm hmm.
Tim: …which comes in the environment and utero and this maternal genetic effects that come from the genetic composition of the egg. That will also be paternal – there will be paternal genetic effects that has been much less work on paternal genetic effects than has been on maternal genetic effects that I’m aware of. But I’m sure that indeed some work has been going on there.
But certainly on those species like mammals where it’s the mother that obviously bears the young in utero, we would expect maternal effects to be – maternal environments effect to probably be stronger than any paternal genetic effects for most traits that we look at. I suspect that was the case.
However, obviously in other species where parental care is a little bit different and males can actually contribute substantially to racing offsprings like seahorses would be a good case to look.
Kirsten: Mm hmm.
Tim: One might expect to see very strong paternal effects.
Kirsten: Right. So depending on how – who is carrying the burden of that gestation.. yeah.
Tim: Of the developing young, absolutely.
Kirsten: Yeah, right.
Justin: Mm hmm. There has been some evidence of paternal effects, the (pembri) study. This strange village in Sweden like that had taken records in the 19th century over like 150 years and took very meticulous records of levels of – amount of food that they had to eat in this village and the death, death reasons, and death rates of its people.
And they found that there are correlations between famine – times of famine and the grandfathers when the grandfathers are just pre-puberty, right?
Kirsten: Mm hmm.
Justin: And later medical affects diseases in their grandchildren so that if you are the young man who had – living in the time of famine, your grandchild would be more likely to get diabetes perhaps but – or no, would have less of a chance. So, I think it was heart attacks but if you were living in the time of feast, that they would have a higher risk of diabetes.
Kirsten: Right.
Justin: And it was correlated pretty well because they had very good records over 100 of years in an area where diet wasn’t a factor or they were eating the same poor, awful that taste gruel.
Tim: (Unintelligible).
So, I wasn’t aware of that study but I mean that makes good sense. As I said, there’s nothing to rule them out. It’s just I think more focus is being – has (set) in humans, in mammals has been invested and tried to identify maternal effects.
Kirsten: Right, which is interesting. I think that’s the bias, you know.
Justin: Mm hmm.
Kirsten: Who’s in-charge of rearing the young in humans and so, we’re going to go to our maternal effects whereas, having things that…
Justin: Right. It’s also I think easier to track because maternal effects are going to happen while pregnant. And then you know that’s the time to be watching.
Kirsten: Mm hmm.
Justin: The paternal effects from Lamarck’s (pembri) study were…
Kirsten: But that – skipping generations so that’s…
Justin: They were skipping generations but is also in the weird spot because the area in which the effects were taking place on their fathers was when they were just going to that stage of pre-puberty.
Kirsten: Yup.
Justin: So, it was a very odd time to really be tracking ahead of to watch for our future generation versus…
Kirsten: Yeah. And I think…
Justin: …when you got somebody pregnant, it’s easier to know. It’s time to pay attention, maybe a little too late.
Kirsten: And this definitely gets into that that area of epigenetics and like what are the controls that are possibly getting, what are the changes that are happening during someone’s lifetime that could potentially affect what genes are turned on or off.
Justin: Right.
Kirsten: …down the road in your offspring or your offspring’s offspring.
Tim: Absolutely, absolutely.
Kirsten: I’m just…
Tim: And that scenario of burgeoning research at the moment and, we still have a huge amount to learn in that area. But you’re absolutely right that it appears that all sorts of genes can be turned on and off as a function of behavior in environment you experienced.
And there’s been some quite nice research in mice for example that share cross generational effect, the amounts of grooming. Let’s say, individuals have – when they were young that appears to then, influenced gene expression in themselves and then passing on phenotypic consequences to bear offspring.
Justin: Wow!
Tim: So, absolutely, there are these epigenetic effects with different genes being turned on as a function of all sorts of aspects of your environment. But it’s – as I said, it’s kind of – it’s an emerging area. It’s a very exciting area. And over the coming years, I’m sure, we’re going to hear many more exciting stories as we gain insight into how these effects actually occur.
Kirsten: Yeah. Someone on Twitter – I’m looking at the Twitter feed right now, Mike Chelen is asking, what fruit fly eye color study you’re referring to and what that had to do with the conversation? No, I added that.
Justin: Oh, you added that. I have to look that up. But it was…
Kirsten: I’m just giving you a hard time. What else is new?
Justin: I pulled that out off of the NOVA’s website. So, if actually, if you go to NOVA’s website and looked at epigenetics, it will be able to link you over to that one.
I don’t have it right in front of me here. But it was an interesting study because, it was white-eyed fruit flies that they’d incubated at a different temperature I believe and it resulted in a red-eye.
But what was more interesting is that the success of generations of breeding with that fly also had the red-eye tint to them. So, it wasn’t just something that it affected that one generation and it was a multi-generational thing.
And it didn’t actually ended up being removed, I think after successive– like, five generations or something the red sort of went away again, which is also interesting. But I think…
Kirsten: Fascinating.
Justin: Yeah. Like – I would make my Galapagos Islands, I would make that the Arctic. I think, there’s something – I think we could find at least one of these effects of the environment, of hormones, certainly in epigenetics taking place and the fact that there are so many white animals in the Arctic.
And I know, it’s one that – every time I brought this up, people go, “No, that’s the most obvious example of natural selection. All the white ones survived.”
But I think, if you look at the Arctic, which is a very lonely, very non-competitive place, you can go – you can walk for days and not see a soul. And then, you look at the foxes who with less stress, hormones had less pigment being put into their fur, you could sort of see where any animals that had wandered out and were making a living in the Arctic were having probably a less stressful time.
They weren’t problem worried being devoured, at least the young, probably won’t worried about being devoured or the mothers won’t be worried being devoured.
So that, with less stress, you can end up with the lighter fur and then, because that’s the pull you have, these lighter-furred animals, the natural selection starts taking over to where you have. The very lighter ones perhaps are having better odds at survival.
Maybe, but over all, the thing that gets the things moving because I don’t think I’ve argued against natural selection at any point.
Kirsten: No, you haven’t.
Justin: But I would argue against random mutation. I think, unless I’m missing the definition, I don’t mean intentional, I don’t think there’s an intentional mutation. But I’m saying, there’s a reason for the mutation, right? It’s not – we don’t – it’s a mechanism…
Kirsten: I was going to answer that.
Justin: Yeah.
Kirsten: But I’ll let Dr. Coulson, the expert to answer that point.
Tim: Again, there’s quite a lot of work being done on what causes mutation and whether there are some areas of the genome where mutations occur a little bit more frequently or less frequently than other areas. As well as research on a DNA or your DNA repair enzymes.
So, there are enzymes out there that are being selected that will go along and check your DNA and would repair. Repair it may seem to be a little bit more covering some parts of the genome than on other parts.
Now, my understanding is that, mutation – whether a mutation occurs at a specific point or not is random, just a chance event. It’s something, something that goes wrong in terms of the DNA there.
However, I do think, there is mounting evidence that mutation rates to actually increase when stress, environmental stress increases. And that maybe because less resources have put towards DNA repair mechanisms.
So, the DNA is not being repaired as fast as it used to on the good condition, or it maybe – it may mean that there are more anti-oxidants have to have that increase mutation rate.
So, I think, mutation rates can certainly vary as a function of the environment that an individual finds itself in. But I think the positioning of each mutation is essentially random. Although there are areas in the genome where mutations do occur at a higher rate and elsewhere.
Kirsten: Mm hmm.
Tim: That’s my understanding. Although I haven’t research myself mutation rates in a huge amount of detail.
Kirsten: Right. And then, getting into the point that Justin was making about the possible hormonal effects leading to the changing coat color that allowed certain individuals to survive better in the Arctic, do you think that kind of, I guess, evolutionary mechanism could be – have been in place?
Tim: That strikes me as, actually that would be my first hypothesis. It strikes as probably quite as slightly labored argument, I think. I suspect that the Arctics are pretty stressful place. there’s not a huge amount of food there. It’s cold. life is at – certainly vertebrate life is that relatively low density. So, it’s probably quite hard to find something to eat.
So, I’m not – I don’t think, I’d probably think about moving up to the Arctic for a nice, easy, stress-free (unintelligible).
Justin: You’d have to – yeah, you’d have to get used to mouse meat and Narwhale which is actually surprisingly good.
Tim: I would take your word for it. But of course, it’s something, it perhaps it’s actually spot on, that’s the way it’s working. But I’m just – I suspect, that wouldn’t be the first hypothesis I’ve got in (trying) task.
Justin: I take perhaps spot on, that sounds – it’s (unintelligible).
Kirsten: Nice. So, thinking about the idea of epigenetics more, do you think that there are, in the growth rates, I mean, can you imagine or postulate any places where epigenetics might be impacting your shrinking sheep that that might, the climate change effects might be leading, through epigenetics somehow to this change?
Tim: It’s entirely possible. What we have already – all we’ve been already to say so far is that we have seen that the decline in both in growth rates and so our statistical analysis of that declining growth rate, we’ve found that we’ve been able to explain a reasonable amount of variation with, climatic drivers and what have you.
You know what, pinning to – and this appears to be driven primarily to the shortening winters and more individual surviving there maybe – as I said before, there maybe all sorts of all the factors out there that we haven’t measured and some of them could well be epigenetic factors. Some of them maybe purely environmental…
Kirsten: Mm hmm.
Tim: …as well. And, I’m not going to speculate on what other processes might be operating, it could be – as we discussed that, it could be changes in the levels of plant secondary compounds. The, potentially many of the factors that one could try and bring in here. Certainly whatever the processes that’s going on, it does appear to be driven or whatever the mechanisms are that have lead to, the changes we have observed. It does appear to be the case.
And, this is what we, I’m happy to state that it does appear to be the case that it is the changing climate that’s causing changes in the growth rates and the fact that smaller sheep are now surviving better than they used to exactly what the mechanism is that’s causing that we haven’t been able to pin down but hopefully in the future, we’re be able to pick up there.
Justin: And then, hopefully, we can recreate the effect in people because if there was just smaller people everywhere, again, we’d have more resources to go around.
Tim: But then we might end up with even more people, other than that, as you asked me before about the food per sheep…
Justin: Yeah.
Tim: …and I say, in fact the food per kilogram per sheep is — are remained about constant. The problem of course, that we have got is we’re just using more and more and getting bigger and bigger. Well, that’s what I hear they’ve got in California any way.
Justin: Oh, my goodness. All we need is – no, all we need is one earthquake, and it’s like a reset button. It’s like…
Kirsten: I know.
Tim: I’m not (unintelligible) on that one.
Justin: No, no. The freeways are full of people like getting out – getting the heck out of this, what on Earth moves, really, it’s like that. I heard about it, I thought it was a myth.
Kirsten: Back to the Midwest.
Justin: Back to the Midwestern, back to the East Coast, they go.
Kirsten: We’re getting towards the end of our show. This has been so fabulous. I guess, one final question from the perspective of a population biologist, a life scientist, studying evolutionary processes.
There’s a question that’s been posed by the John Templeton Foundation in the name of Darwin’s year of birth and the Origin of Species Anniversary and also, this year of science. Does evolution explain human nature? Do you have an opinion on that?
Tim: It must certainly contribute, there’s no doubt about that. And, again, there’s a lot of work by human evolutionary biologists investigating this.
Again, I’m going to (unintelligible) on this but I’d be absolutely staggered if the evolution didn’t play a role and I would suspect that that role is relatively important.
Kirsten: Excellent.
Tim: And not a particularly good answer.
Justin: But the thing here…
Kirsten: It’s like you’re hedging a little, that’s all right.
Justin: And this is back to the…
Tim: (Unintelligible) you caught me there on air I don’t really know very much about that.
Kirsten: You don’t know about human nature? What planet are you from?
Justin: The thing that keeps coming to mind is the chicken and the egg. And it’s like one of the oldest, silliest things to talk about in evolution.
Kirsten: Mm hmm.
Justin: But a lot of these does sound like that to me. I mean, whether it was, whether it was our genes or whether it was our selection that created our human behavior or for our human behavior drove our genes in the direction or if it was – if it’s epigenetic creating the change but natural selection propagating it or it’s the other way around.
It’s – which came first? And I guess, what it is is we got to stop worrying about the hierarchy of it. There isn’t necessarily one that came really before the other.
Kirsten: Right. It’s probably a very complex interactive web.
Tim: I’m sure that’s right. And you basically remember – again, it’s really boiling down to that map that’s in the genes and the phenotype and kind of have a feedback on one another.
Justin: Mm hmm.
Kirsten: Mm hmm.
Tim: And then, how selection is operating on the phenotype in changing the underlying genes. It just goes on and on and on.
Justin: I prefer linear. I prefer linear. Linear, just put it one line, like, the…
Kirsten: ABC, take it easy.
Justin: Think about the ape and then, he morphed into the guy with the brief case, the line up there.
Tim: I got to (unintelligible) about simple otherwise I’d be out of a job.
Justin: For your sake, I hope it doesn’t get simplified then.
Kirsten: Thank you very much for joining us this morning. It’s been fabulous speaking with you. Thank you for your opinion.
Justin: Your referee-ring.
Kirsten: You’re referee-ing.
Tim: No, that’s (unintelligible) it’s been all my pleasure.
Kirsten: Yeah. Thank you. And I look forward to hearing much more about the Scottish sheep and, I know that you’ve got what is it, SLAPPED…
Justin: What?
Kirsten: Isn’t that what is it? SLAPPED? It’s your research group looking at…
Tim: Yes, that’s right. That’s a right. It’s a slightly tortured acronym that one of my science folks came up with but…
Kirsten: Right. So, you’re looking…
Tim: It’s kind of stuck.
Kirsten: You’re looking not just at Scottish sheep, you’re looking at animals all over the place and so.
Tim: We have projects all over the world. Yeah, absolutely.
Kirsten: Great. So, I look forward to hearing much more about your work and the work that you’re doing with others. Good luck and we’ll speak with you sometimes in the future, I hope.
Tim: Thank you. Goodbye.
Kirsten: Bye.
Justin: Goodbye, Dr. Coulson.
Tim: Bye.
Kirsten: Yes. That was Dr. Tim Coulson from the Imperial College London not university – I got that one wrong. Next week, we will be talking with our – I think it’s next week. I hope I don’t have the date wrong. But, I think it’s next week. We’re going to be…
Justin: Sometime in the future.
Kirsten: We’re going to be talking with our favorite science and politics author, Chris Mooney.
Justin: Yey!
Kirsten: Yey!
Justin: Mooney, all right.
Kirsten: He wrote, “The Republican War on Science”. He wrote the…
Justin: Storm…
Kirsten: “The Storm…” something, something about hurricanes. I can’t remember. I’m awful. I can’t remember the name of his book. But he’s back with another book and it’s all about the, “Unscientific America”.
Justin: Mm hmm.
Kirsten: Yeah. So, it will be very interesting to talk with him…
Justin: Yeah.
Kirsten: …about the way that Americans perceived science and also, the schism between the intelligencia and the public.
Justin: The intelligence – and you know what? You should write in to us with your opinion on that, ahead of that show. So, we’ll have some of that for those kind of questions or comments or observations that you’ve made about how science is being treated in the news or in your community or anything like that.
Kirsten: Yeah. We’d love that. So, you can email us at kirsten@thisweekinscience.com or justin@thisweekinscience.com.
Justin: Put TWIS somewhere in the subject otherwise it goes right to our very intensive spam-filter which filters out everything that doesn’t have TWIS somewhere in the subject line.
Kirsten: Yeah. You can also go to the Forums on our website. Our website is twis.org. And additionally, there are Show Notes with links to stories that we discuss during the show.
This week, there’s only one show, I mean, one story. So…
Justin: And you can always hit us in the middle of the week, in the middle of the night even, if it so hits you, strikes you @jacksonfly or @drkiki on the Twitter.
Kirsten: On the Twitter. And we thank you so much for listening this week. We hope you enjoyed our special hour long show on evolution and all the nuts and bolts that go – there’s so much to it than what we got to– people spend years talking about this subject and we just spent an hour. But it was lots of fun. It was very enjoyable.
We will be back here on KDVS next Tuesday at 8:30 am Pacific Time. We hope that you will join us again for more great science news.
Justin: And if you’ve learned anything from today’s show, remember…
Kirsten: It’s all in your head.
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