EEB 122: Principles of Evolution, Ecology and Behavior

Lecture 9

 - The Evolution of Sex


There are several explanations for the evolution of sex and its continued prevalence. One is facilitating the spread of helpful mutations while hastening the removal of harmful ones. Another is expediting resistance against pathogens. Sex does have several costs compared to asex, such as only giving half your genome to offspring, having to find mates, and the risk of predation and STDs. Overall, the benefits outweigh the costs and sex has a firm hold on the majority of the recent branches of the tree of life.

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Principles of Evolution, Ecology and Behavior

E&EB 122 - Lecture 9 - The Evolution of Sex

Chapter 1. Introduction [00:00:00]

Professor Stephen Stearns: Now before I get going on today’s lecture, which is about the evolution of sex, I thought that I would just share this picture with you, which I took at ten o’clock on Saturday morning. These are the Hamden Golf Course turkeys, and they sometimes show up in my backyard, and they’re absolutely remarkable creatures.

If you look at them, probably the first thing that strikes you is how do they make those iridescent colors, and is there a different way perhaps that they make the color in their neck, or perhaps on their face? Their neck is red and their face is blue. Is that biomechanically different? In fact, these colors are a diffraction gradient. There’s no dye in them at all, and the colors in the head, the blue color, is actually made by kind of a fractal matrix of bubbles. The red color I think is a dye. So there’s some weird stuff going on in the way that turkeys make colors.

Why the heck do these turkeys look like this? Well the standard explanation for that, which may or may not be true–it hasn’t been tested too explicitly in turkeys, although it has in pheasants and in peacocks, which are both related to turkeys; they’re all in the family gallinaceae–is this is the product of sexual selection, and that what you’re looking at is what the female brain of the turkey finds attractive. Well there’s a deep mystery in that. Why should something that a female turkey thinks is beautiful also elicit the sensation of beauty in my brain? I last shared a common ancestor with a female turkey about 150 million years ago. Has the perception of beauty persisted unaltered in both lineages for 150 million years? So you see the contemplation of turkeys in the snow can take you a long way.

Now today I want to talk about the evolution of sex, which will eventually get us to sexual selection in a bit over a week. And in so doing the messages that I want to get across are that this is first a fundamental question in biology, because it shapes almost everything that we study in biology. Sex, in the sense that I’m going to use it today, in terms of organized diploid sex, has been around probably for about one and a half billion years, and it’s had many, many consequences.

There is a puzzle about sex, and we will see that it is complicated and costly, and therefore it needs an explanation. I think it was the Marquis of Chesterfield, or someone like that, who on advising his son on the con–on the issue of sex said, “It doesn’t last very long and it’s extremely expensive.” [Laughter] And we will look at some of the consequences of sexual reproduction for large-scale patterns in the plant and animal kingdoms.

Now I need to set this up by distinguishing between recombination, reproduction and gender, because the word sexoften elicits in the minds of non-biologists a composite of all three things. Recombination is the process that causes offspring to differ genetically from their parents and from each other. Now there are some exceptions to this.

For example, armadillos always have identical quadruplets, which makes them convenient for some things. Identical twins in humans, of course, are an exception, where the recombination has made them different from their parents, but they’re still identical to each other, and that is because they derive from an early mitotic event in development; so they were originally the same zygote. And then we have the extravagance of polyembryonic wasps where a parasitic wasp lays a single egg into a caterpillar; the egg starts to develop into a blastula; the blastula fragments into hundreds or even thousands of pieces, each one of which then develops into an embryonic wasp.

Some of those sister wasps differentiate into warrior castes and go cruising around the caterpillar, wiping out other wasps that may have laid their eggs into the caterpillar. They don’t make it, they die, but they clear the way for the others, that then eat up the caterpillar and hatch as wasps, out of the caterpillar. So there are always fascinating biological exceptions to the idea that recombination makes siblings different from each other. In some cases they are not, but normally they are.

Reproduction is not the same as recombination, and we can see comparatively, through these contrasting examples, why it is that recombination and reproduction are not always necessarily coupled. In us they are, but if we look at bacteria and clonal plants, we can see that they can reproduce without recombining. And bacteria can actually arrange to have sex and not divide at all. They can undergo a recombination event and simply change themselves genetically, and then wait for awhile and divide later.

And, of course, in plants, clonal plants have the option, many of them have the option of either producing asexually or sexually. Often they produce sexually in the parts of them that will then disperse to another place, and asexually in the parts of them that will stay here; here being more predictable than there.

Gender is something that is really not at all the same as recombination or reproduction. Gender is maleness and femaleness. So it’s all of the secondary sexual characteristics of the two genders. And that is something that originated with the production of gametes of different sizes.

That didn’t happen until after meiosis originated in evolution, and it then created a situation in which sexual selection could occur; where there was one kind of selection on things that made lots of small gametes–sperm–and another kind of selection that operated on things that made a few large gametes–eggs. So those are three different things.

I also need a few words, and I’ll refresh your memory or introduce them to, depending on where you’re coming from. Isogamy means that we’re dealing with a species in which all of the gametes are the same size. That happens often in the protists, in unicellular algae and protozoa, that they produce gametes of the same size. Anisogamy comes where there are gametes in two different sizes, the big ones being eggs and the small ones being sperm. So anisogamy is the condition with which most of you are familiar. Syngamy means fusion of gametes to form a zygote; that is one step in the process of sexual reproduction. Karyogamy is fusion of the two gametic haploid nuclei. So the gametes come together, and then after that happens their nuclei fuse. And these things take time. We will see that those actually are some of the–the time they take is some of the cost of sex.

Now mating types occur at this stage, with isogamous organisms, and they reduce inbreeding. Mating types are common in many unicellular algae and in many ciliates, like Paramecium. They are basically a situation where the organisms of one type can only mate with organisms of another type. So if you are mating Type 1, you can mate with mating Type 2 but not with mating Type 1. This, in some sense, is genetically analogous to having a large number of sexes in the population, but with a rather interesting pairing rule, that you can only not mate with people like yourself. The population then differentiates and evolution produces a huge number of mating types.

Chapter 2. The Traditional View on Sex’s Existence [00:08:54]

Now the traditional view on why sex exists was formulated by August Weismann and then elaborated by Mueller, and clarified by Crow and Kimura, and it goes like this: recombination is there in nature basically because it increases the rate of evolution, and it does so in two ways. It increases the rate at which two advantageous mutations can be brought together, and it increases the rate at which disadvantageous mutations can be discarded; and I’ll illustrate that with a few diagrams in a minute. A consequence of this is that it decreases the probability of extinction. All of that is true, but it may not be why sex exists.

So here is the traditional view. In a large population, if we contrast a large asexual population with a large sexual population, you should think of the vertical axis as being the frequency of a mutation in the population and the horizontal axis as being time, and A, B and C are beneficial mutations that are arising at different places in the genome. They’re not alleles with a single locus. They are three different genes whose combination it would be really cool to have, because it’s going to improve reproductive success, defend you against diseases and so forth.

In the asexual population, first A pops up and it takes over the population because it’s advantageous. Then C, which had occurred once before but not in combination with A, happens sequentially in the same organism that’s already gotten A. So in the asexual population the advantageous mutations have to happen one after another, in a descendant lineage, because there’s no sex to bring them together. AC dies out because shortly after it arose, AB came along and AB was preferential to AC, and then eventually C arises in an organism that already has A and B, and ABC takes over. That’s a process of clonal interference.

In the sexual population these mutations can be conceived of as occurring at just about the same time as they did in the asexual population, but they are rapidly brought together by sex and recombination, and the combination ABC spreads through the population much earlier, achieving fixation here rather than here.

Now if we look in small populations, the advantage of sex is not nearly as great. Can anybody tell me why? You can see a picture there, but can you interpret it in an English sentence? Why is it that in the small population the advantage of sex is not so great? It still can be advantageous, but it’s not as great as it is in the large population.

Student: You have less animals.

Professor Stephen Stearns: Population’s smaller, yes.

Student: You have less animals for [inaudible].

Professor Stephen Stearns: Somebody want to help Brett out? He’s looking for a word. Yes?

Student: Small population, less genetic variation.

Professor Stephen Stearns: There is less genetic variation in the small population. Yes. Why?

Student: It’s a lower population count, [inaudible].

Professor Stephen Stearns: Where does variation come from?

Student: Mutations.

Professor Stephen Stearns: Mutations. Yes. You can think of the population size, all those genomes out there, as being a net that catches mutations. The smaller population is catching fewer of them, and therefore there are fewer things that it could bring together, and therefore it takes a longer time in the small population for sex to become advantageous, because it has to wait for that mutation to come along. In the large population, it’s there very quickly, relatively quickly.

Chapter 3. The Costs of Sex [00:13:38]

Okay, now about the costs of sex. In an isogamous organism the costs are genome dilution, the amount of time it takes to have sex, and the risk of predation, of sexually transmitted diseases and of the difficulty of finding mates. So let’s step through those.

The cost of genome dilution basically is that by engaging in sex you’ve made a decision that your offspring will only have 50% of your genes, and it’s going to have 50% of somebody else’s genes; whereas if you were asexual it would be 100% your genes. Okay? So that’s what we mean by the cost of genome dilution. And I think that you can see, if you work through it, that this is indirectly also the cost of having males.

You don’t really need to have males at all, if you’re asexual, do you? As a matter of fact, we usually think of asexual species as consisting only of females, and the reason for that is that they make eggs. Okay?

Now you can look at yeast, which can reproduce either sexually or asexually, and experimentally measure this difference between one hour for asexual reproduction and eight hours for sexual reproduction. So let’s do a little mental experiment here.

We start off a vat of beer, and we seed it with one asexual and one sexual yeast organism, and they happily go to work starting to make beer for us. After one hour, we have two of the asexual, and we still just have one of the sexual, don’t we? After two hours, we have four of the asexual; we still only have one sexual. After three hours, we have eight of the asexual; we still only have one of the sexual. You get the idea.

That timing difference has an enormous impact on the relative fitness of the two types. Just because it can reproduce faster, the asexual type is going to sweep through that population and competitively exclude the sexual type; all other things being equal. So we essentially end up with a glass of beer that’s produced almost 99.999% by asexual yeast.

The other cost, of course, is that if you have to go find a mate and take time to mate, you expose yourself to being eaten by a predator. In the process of mating, any kind of disease that mate has could jump into your body or into your offspring. It could be a selfish genetic element that got into your offspring, coming in through the genome of your mate. And it’s pretty hard to find mates at low population density, which is why we find that asexuality, for example, increases in frequency as we go into the deep ocean. And if you look at the organisms that are specialized on eating the carcasses of dead whales, which drop onto the ocean floor infrequently and at great distances from each other, you discover that they have a higher rate of being asexual, or being simultaneous hermaphrodites, than do things that say live on tropical reefs near the surface at high population density.

Then if you have anisogamy, in its simplest form, the cost of males is a twofold cost. So if you’re a female and you have the option of being asexual, and you’re wondering, “Should I be sexual?” and you ask yourself, “What’s it’s going to cost me?”, basically if you count through to the number of grandchildren you have, you’ll have twice as many grandchildren, if you don’t make any males–if you only make daughters you’ll get twice as many–through your female line, bringing–and this is because also the genome dilution effect is coming in. Okay? So anisogamy, plus genome dilution, gives you a twofold cost of sex.

This word Acarophenax is going to come up several times, because it’s a spectacularly perverse mite, and we all are interested in spectacular perversion. So Acarophenax is a mite that has an extreme example of local mate competition. And has anybody already run into this example? Can you tell me what it is? Mites, many mites, not just Acarophenax, lay their eggs into their abdomen, where the eggs hatch out inside the mother, and the brothers then impregnate their sisters, inside the mother, and the brothers die and the sisters eat the mother. That’s pretty spectacularly perverse.

The question is, if you are the mother, how many sons should you make and how many daughters should you make, in order to get the maximum number of grandchildren? Okay? And we will run through this when we have the Sex Allocation lecture next week, but I just wonder if any of you can anticipate that. Here you are, you’re the mother mite. You want to maximize the number of your grandchildren. You’re not worried about getting eaten, because your kind have always had that, that’s just a normal part of life. The only issue that occupies you is how many sons should you make and how many daughters should you make? You’re a little bit worried about the lady next door and what she might be doing. Any idea?

Student: Only one son.

Professor Stephen Stearns: You only make one son, and that’s because that one son can make enough sperm to inseminate all of his sisters. And if you made two sons, you would have some sperm that was going to waste, and you could’ve used that egg to make another daughter that got inseminated. That is, in fact, the solution chosen by Acarophenax and all such similar mites; one son, many daughters.

Now to go back to this slide, just to remind you. I’ve been telling you lots of interesting natural history, but the point of it that sex is costly. It takes time, it dilutes your genome, and if you are anisogamous it costs you everything that’s involved in making sons, who otherwise might be irrelevant if it weren’t for whatever advantage they might bring in with sex.

So the paradox of sex is basically that’s it regular, complicated and costly. And, as I indicated with the example of the yeast in the brewer’s vat, asex should rapidly take over sexual populations. Nevertheless, when we look at the Tree of Life, we see that the majority of organisms are sexual, and even the ones that we think of as being asexual, like bacteria and viruses, in fact have evolved something like sex. So it seems to be a good thing.

We’ve got this traditional explanation that sex speeds up evolution and reduces extinction probability. But it has a problem. It is couched at the level of the species or the group. Okay? And it’s not strong enough to maintain sex against the invasion of asexual mutants. The reason is that if you think of it in terms of being good for the species because it causes the species to last a longer time before it goes extinct, well the generation times of species are orders of magnitude longer than the generation times of individuals.

Vertebrate species last usually one to ten million years. Individuals last months to years. So about 10difference in how fast things happen at the individual and the species level. So any individual advantage–for example, asex–could be multiplied thousands or millions of times before the group or the species advantage of not going extinct so frequently could take effect.

The individual advantage of asex seems to be roughly twofold each generation, and that adds up to a big difference over a lot of generations. So asexual mutants should always be taking over. But they don’t.

Now before I go into the solution to that problem, I want to give you a little bit of what we think is the evolutionary sequence in matters sexual. In prokaryotes, bacteria and archaea, probably the repair of ultraviolet damage to DNA was very important. Then mitosis originated and eukaryotic cell division. So once the eukaryote ancestor formed, with the proper cytoplasm and nucleus, and we had multiple chromosomes, mitosis originated. We’re back about probably 1.5 to 2 billion years here.

Then meiosis, which is really a very, very complicated symphonic arrangement, originated by a duplication and modification of mitosis. Then only after we had mitosis did we get isogamous mating types, and then we had the evolution of anisogamy. Now the evolution of anisogamy is actually a big deal because it is what eventually led to the differences between males and females. So sexual selection only starts to happen after we have things that make gametes of different sizes. So the ideas about why that happened are kind of interesting, because they’re right at the origin of male/female difference.

One of the ideas is that a bigger egg would improve offspring survival. So some of the individuals in the population, in the isogamous population, might be under selection to produce bigger eggs, because they could then have babies that survive better. They could also produce more pheromones. So they could advertise, so those eggs could advertise their presence better. A bigger egg is a better perfume factory. So you should think of eggs as being big, fat perfume factories. Okay?

Once this–and this is now frequency dependent selection–once some of the organisms started to make bigger eggs, the others, some of the others, could decide, “Oh, I don’t need to make a big egg and invest a lot of energy in it because somebody else is doing that for me; instead I’ll try to inseminate lots of eggs.” And they got selected to make sperm. Okay? So they made many small gametes that could swim fast and were good at detecting perfume. That’s one idea.

Another idea on anisogamy is that those big eggs have got cytoplasmic organelles, and those cytoplasmic organelles have got their own independent genome in them, that they had when they came in as mitochondria or as chloroplasts or as spindle apparatus. And you don’t want to generate a situation in which you have competing cytoplasmic genomes, because if you do, you get an uncontrollable evolution, microevolutionary process going on in the cytoplasm that can cause the takeover of the cytoplasm by a basically selfish mitochondrion or a selfish chloroplast.

There are, in fact, mitochondrial cancers. There are cases in which mitochondria get out of hand and you end up with cells that are just packed wall to wall with mitochondria. You don’t want that. You want to have the cell to be a relatively well regulated, well biochemically balanced environment. So one of the consequences of biparental inheritance, where you are only getting your organelles from one of the parents, normally the female, is that you avoid conflicts. Okay? This may or may not have been important at the origin of anisogamy, but it is certainly one of the reasons for its maintenance.

And before I go into mutations and parasites, let’s recall something that August Weismann said back in 1892: “Sex has a huge number of consequences.” It’s been around for a long time, and so when we try to detect why sex originally evolved, we’re dealing with a situation in which the original reasons are concealed by lots of layers of adaptations that have built up since then.

So we have to clearly distinguish between causes and consequences of sex. But this is now very hard to do because the original causes are now covered up with so many of the secondary consequences. People have been repeatedly fooled by confusing consequences for causes. In a sense I suppose the bottom line on that slide is we actually are in a position were we can talk intelligently and we can do science on the reasons for the maintenance of sex, but we have difficulty–and may always have difficulty–in identifying the real reasons why sex originated, because that happened a long time ago, in a different situation, and it’s had all kinds of consequences.

Chapter 4. Recombination [00:28:02]

Okay, so what kinds of forces maintain recombination? When Alex Kondrashov wrote a paper about this about, oh gosh, it’s fifteen years ago now, he came up with forty-three, and I’m only going to list a few. I’m only going to list the ones that I think remain plausible and can be demonstrated experimentally or comparatively. However, I want you to be aware that if you decide to write a paper on this, and you want to know what are all the reasons that people have given for the origin and maintenance of sex, that the list is on the order of forty or fifty hypotheses.

There are two important genetic hypotheses. One is repair and the other is mutations, and in a sense mutations really are an issue of repair at the level of the population. And there are ecological hypotheses. Parasites and pathogens, and the co-evolutionary problem that they pose, are accepted by many now as a major reason why sex is maintained in populations. And it is also true that recombination spreads risks and hedges bets in ways that go beyond the issue of whether your children are going to be infected by a particular pathogen. You can deal with all sorts of ecological situations. So you can think of the reasons as falling into two general categories: genetic and ecological.

So back in prokaryotes, a lot of repair mechanisms were evolved, and they are sophisticated. They’re still in operation; they’re readily studied in microbiology laboratories. DNA polymerase itself does proofreading. If a nucleotide has been excised and is missing from the sequence, then you can use the complementary strand to patch it in. So that happens, and that needs a double-stranded DNA, not a single-stranded RNA. So if you’re just dealing with a single-stranded RNA virus, it may very well have difficulty doing this kind of repair, and has a very, very high mutation rate. I want you to remember whenever I say mutation, that it is often a problem of inadequate repair. So the repair mechanisms actually control the mutation rates.

In eukaryotes we have this kind of proofreading, and we’ve got a lot more. There are some repair mechanisms that actually need diploidy. So you have a whole extra chromosome. You have two double-stranded DNA molecules, and you can go to the alternate as a backup. So you can use that to repair any mutational damage.

But the most interesting kind is recombinational repair; well let’s put it this way, to somebody who thinks at the population level, the most interesting kind is recombinational repair, and that is because it isolates the defects on a subset of gametes. You can have mutations in five or six genes. Recombination could put them all into one set of gametes, and if those gametes die, those mutations are gone. So recombinational repair isolates and throws away, through natural selection, the defects in the genome.

There is a concept here that I want you all to absorb and understand, and it has to do with the way that mutations will accumulate in small populations that are asexual. And it’s important because it can be shown that this idea is at least theoretically true–it can be demonstrated experimentally in small populations–and it is a serious, long-term problem for anything that’s asexual. Works like this.

In a small population, the class of organisms that has the fewest mutations is eventually lost by drift. Okay? So you should think of this starting off with a perfectly clean population of let’s say bacteria. It’s a small one, there are only ten or twenty of them. None of them have any mutations. Then the first mutation arises, and eventually it drifts through the population and it is fixed. That will eventually happen. At that point all the organisms in the small population have one mutation.

Because they all have one, they can’t get rid of it. The process happens again. Then they have two, and so forth. So that leads to an inexorable increase in the number of mutations in the class of organisms that has the fewest. It goes–the fewest goes from zero to one to two to three, and so forth. And the kinds of organisms that are afflicted by this would be mitochondria and chloroplast in the germ line, and ancient asexuals like bdelloid rotifers.

What’s going on basically is that this correlation between reproductive success and trait or genetic state gets wiped out by the Law of Small Numbers. As you decrease the size of the population, it becomes less- natural selection becomes less and less powerful. You just get more noise, simply due to sampling issues; you just have a smaller number of organisms, so the tightness of the correlation goes away, it gets noisy.

So the smaller the population, the more important random events are. When it’s very small, natural selection has very little opportunity to operate, and the reason it loses its force is that the correlation of trait variation with reproductive success is lost in the noise of a small number of arbitrary events.

So that’s what’s going to go on when say you start off an oocyte with two or three mitochondria; that’s a very small number of mitochondria to go into an oocyte, and that’s a genetic bottleneck through which mitochondria will go in every generation. There might be 10,000 of them in your liver cells, but if they’re a small number in oocytes, then they are going to experience drift.

So you can think of this as stochasticity driving a wheel around, and there is a lever here that allows it to go forward but won’t allow it to go back. The capital letters are beneficial genes, and the small letters are mutations, and Muller’s ratchet will take this population and at first one of these genes will get replaced, through drift, by a deleterious mutation; then two; then three; then four; then five; and so forth. And if you plot here, from few at the top to many on the bottom, the number of deleterious mutations that are carried by the least loaded genotype–that is, the type in the population that has the fewest deleterious mutations–it’s increasing, and fitness is going down.

This won’t happen in a sexual population, and it won’t happen in an infinite asexual population. The infinite asexual population is big enough always to have some individuals in it that don’t have any mutation, and they will keep taking over. But in a finite asexual population, Muller’s ratchet operates.

So it’s important in organelle DNA, and this problem of Muller’s ratchet in organelle DNA could be solved, for example, if mitochondria had sex. There has been a controversy over whether mitochondria have sex, and if you would like to read a paper that was written for this course on that issue, it’s up on the website–it’s called Example Paper–and it reviews the status of that issue about two years ago.

In mammals, mutations in organelle DNA may be solved with gamete selection through oocytic atresia. One of the reasons why female mammals may make 7,000,000 oocytes, when they’re embryos, and then kill most of them before they start menstruating, is that they are getting rid of mutations that may have built up in the mitochondria.

What about the ancient asexuals, those bdelloid rotifers? Well they have really two possibilities. One is that they could try and arrange their physiology so that they could make the effects of any mutation more serious. And that has been suggested as a hypothesis, and I find it implausible; but it’s a hypothesis which is out there.

If you can make any mutation really serious, so that it kills anything that it occurs in, it has no chance to accumulate. It’s only the deleterious but not fatal mutations that can accumulate. So that’s a logical possibility, but biologically I find it implausible. Or they could always maintain a very large population, so that drift is not a problem. And most of the things that are ancient asexuals do have at least large populations; not infinite but certainly large.

So here’s a bdelloid rotifer, and it’s managed to escape these problems. Nobody has ever seen a male bdelloid rotifer. You could go outside OML and take some moss off the side of the building and put it into a cover slip, and some bdelloid rotifers would swim out of it. They’re all over the planet. Even though it’s avoided the problems with mutations, we don’t know how it’s dealt with pathogens and parasites. Okay? And that’s this next issue.

Chapter 5. Pathogens and Parasites [00:38:25]

Parasites are the principle way that the idea of co-evolution is realized in the context of the evolution of sex. What happened to the Red Queen, or what happened to Alice when she met the Red Queen in Lewis Carroll’s book Through the Looking Glass? Did any of you run into that? Alice sits on a chess board and she is–this is kind of in a dream–and she’s trying to march down the eight squares of the chess board so that she can be promoted to a queen. She’s a pawn in the chess game, and she’s trying and trying to get there, and the Red Queen comes up to here and says, “Alice, in this game you have to run as fast as you possibly can, only to stay in place.”

So it’s called the Red Queen Hypothesis, and the idea is that in evolution organisms are evolving as fast as they can, but they’re in fact not increasing their fitness, and they are not decreasing their long-term extinction probability because the parasites and pathogens in their environment are coevolving with them and keeping up with them. So it’s called the Red Queen, basically to communicate the idea that if you are in a co-evolutionary arms race, then you may have to run as fast as you possibly can, just to stay in the same place.

So what it requires is genetic variation for resistance in the host; genetic variation for virulence in the pathogen. We can see that in Daphnia and its parasites, and in crop plants and their pathogens. So the assumptions appear to be fulfilled in some well studied systems, and you can see some of the data here. Okay?

So this is a case–this is a complex table. I’d like you to be able to interpret things like this. Basically what’s gone on here is that ten clones of Daphnia–or is it nine?–nine clones of Daphnia have been isolated from a lake, and out of each of those clones a strain of a parasite has been isolated. This parasite is Pasteuria ramosa, and it infects the body cavity of Daphnia and castrates it. Okay? Often parasites castrate their hosts.

The numbers are the percentage infected. Okay? If you look at that you can see, for example, that this strain of Pasteuria is really good at infecting the host that it came out of, and really lousy at infecting this other clone of Daphnia here; does pretty well in E and G; and very, very poorly in B, C, F and H. So one way to look at it is to ask, “Where do the parasites do well?” And the answer is, only in some of the clones.

Now if you ask, “How about the Daphnia, how are they doing against the parasites?” Well you can just go down a column and you can see that this Type D here is actually pretty resistant to almost everything out there, and at the worst it gets hit by this parasite that came out of clone G, over here. So from these data you can conclude that there is genetic variation for resistance and there is genetic variation for virulence, in a natural population.

The parasites are selecting for host resistance. The hosts are selecting for parasite virulence, but the parasites have to keep hopping around, onto different hosts. The parasite selection is happening on a time scale of days, and prevalence of a particular parasite decreases as resistant host types increase in frequency. So that’s just what you need to maintain sex. Okay? So that one looks pretty plausible.

There’s another example from nature that’s pretty well studied, and that’s worms living in snails and ducks in a beautiful lake on the South Island of New Zealand, and the people who get to go study this stuff go to one of the most beautiful parts of the world, where they then put on wet suits and dive into freezing cold water. [Laughs] Okay? The behavior of scientists is difficult to explain.

So this is the lifecycle of the worm. The adult worms are in the duck. They make eggs. The snails pick up the eggs. The worms reproduce in the snail’s body. Then they are excreted as cysts. The ducks eat the cysts, and the life cycle goes around like this. Okay? So anytime this loop can be completed, the worms can stay adapted to the snails and to the ducks. If this is broken at any point, then the worms are no longer adapted to the snails, or to the ducks.

This is the kind of situation in this lake in New Zealand. The ducks are in shallow water, and the worms come out of the ducks and infect snails. They only manage to close the loop in shallow water, because the ducks don’t dive very deep to eat the snails. The worms that are coming out of the snails and going into deep water are from a source, and they’re going into a sink, and they become maladapted to the snails; they can’t keep up with the evolution that’s going on, in the snails down here, because just about everybody that’s getting into the snails down here, in fact, is adapted to the ones in shallow water.

So up here there’s more snail sex, and down here there’s less snail sex. And that’s a very short distance. We’re only talking about maybe twenty or thirty meters apart, for these populations. The only difference is the depth of the water, and whether that loop is connected or not. And where the loop is broken, where the parasite cannot complete its sexual life cycle, it loses the arms race with the snails. The snails don’t need sex. Asex takes over and spreads through the population.

Chapter 6. Modern Asexuality and Conclusion [00:44:54]

So asex hardly ever has an exactly twofold advantage. It’s a bit more difficult usually in animals, and sometimes it’s easier in plants than 2:1. There are cyclical parthenogens–Daphnia, some aphids, some beetles, have a series of asexual generations, followed by one sexual generation, and the analysis of these guys has led us to the conclusion that you don’t need very much sex, but you do need a little. You can have sex about once every ten to a hundred generations, and it is almost as effective as having it every generation.

And in mammals and birds, there are no costs of sex, because the asexual alternative is impossible, and that is because early development requires genes from each parent to activate in complementary fashion. So when you were a very, very small embryo, consisting of a few cells, you had to have some genes from your father turn on, and then some genes from your mother, and then some genes from your father, and then some genes from your mother, in sequential fashion, or development would not occur.

That pretty much means that asexuality becomes impossible. Asexuality would only work if that whole developmental sequence could be carried through only by genes from the mother. And apparently there has been a process, an evolutionary arms race, probably involving conflict resolution, that has led to the kind of development that birds and mammals have.

There’s an irony in this. We now have so many advantages of sex that we have a hard time explaining asex. How did those bdelloid rotifers survive? We can easily understand why asexuality would repeatedly originate and spread. It can spread like gangbusters. It has low cost short-term; big cost long-term. The long-term cost basically is pathogens and parasites, even if it can arrange a solution to the mutations that drive Muller’s ratchet. Okay? So if you look at the Tree of Life, what we see is that the asexual types are up on the twigs and they have sexual ancestors.

And most of the asexual types are not too old; they’re usually on the order of somewhere between 50,000 years and 10,000,000 years, and there are very few of them that are older than that. It appears that these forces catch up with them in the long-term, and drive them to extinction more rapidly and more pervasively than they can drive sexual types to extinction.

So we have good individual selection explanations for recombination. You don’t have to invoke group selection or species selection. It has a lot of explanations. The ones that seem to be pretty general are repair – mutations - and parasites. Those are certainly experimentally substantiated. We do not understand how ancient asexuals have survived; that’s an open issue. And sex has had some very important macroevolutionary consequences.

Probably the most striking is the very existence of species. We would not have things in nature that we called species if there were not sex. Instead we would have clones that just kept fragmenting and kept filling in morphospace fairly continuously. What sex does is it integrates populations and causes the co-adaptation of their genomes, so that we get breaks separating the things that we call species. They are things that hang together. The other is this phylogenetic distribution of asex. It’s up on the twigs, it’s not down on the main stems of the Tree of Life. Next time we’re going to discuss genetic conflict. It’s something that happens, and it happens much more easily in sexual than in asexual species.

[end of transcript]

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