Principles of Evolution, Ecology and Behavior

E&EB 122 - Lecture 8 - The Expression of Variation: Reaction Norms

Chapter 1. Introduction [00:00:00]

Professor Stephen Stearns: Today we’re going to talk about developmental plasticity and reaction norms, and in the process we are going to complete our assemblage of all of the tools we need to understand microevolution, at least as a first sketch.

You’ll recall that last time we were discussing developmental control genes and the way they lay down basic patterns in body plans. They provide insight into the deep history of developmental constraint and phylogenetic constraint, and they also set up patterns that then interact, during the course of development of individual organisms, interact with the environment to determine what the phenotype actually looks like.

The main thing that I’ll be talking about today is the concept of a reaction norm, and in so doing I would like to fundamentally alter the way that you probably think about organisms. I want you to think about organisms, or about genomes at least, as having the potential to produce many different things. The actual thing that is realized depends upon the particular environments encountered, the particular history of that individual organism, and this can have profound effects on the way it looks, the way it behaves, and how long it lives.

So this completes our basic understanding of all of the fundamental processes that are operating in microevolution. And after this point we’re going to go on to discuss major features of phenotypes, and on Monday we’ll discuss the evolution of sex, and we’ll go on to discuss things like life history evolution, sex allocation, and genetic conflict: all of those sorts of things.

So today I’m going to define a reaction norm. I’ll tell you where it fits in the evolutionary process; where it came from; how it interacts with genetics; how you can actually visualize the simultaneous effects of genes and environment by making reaction norm plots. That’s an important thing. There’s been a long controversy in our general culture about Nature versus Nurture. Today I’m giving you the tool to take that issue apart and understand it rigorously. You will end up seeing that all aspects of all organisms are determined both by genes and by environment, and there are clear ways to think about it.

Then I’ll show you how this kind of immediate, short-term phenotypic plasticity interacts with developmental control genes and phylogenetic constraints, and I’ll do that with the butterfly wing, and we will see at the end that in fact biology is–heh, it’s not surprising–biology is complexly organic, in a very deep way, and we can see that in the butterfly wing example.

Chapter 2. Reaction Norms [00:03:22]

So, this is what a reaction norm is. Okay? It’s a property of a genotype. One can also define reaction norms for larger collections of things. You can define a reaction norm for a family, for example. All the sibs in a family might share a certain component of their reaction to the environment. But strictly speaking, a reaction norm is just the property of a single genotype.

So what it does is describe the set of phenotypes into which one genotype can be mapped, as the environment varies. So in the simplest case you have one trait and you have one environmental variable, and this is the way that that genotype, one genotype, would react to this one environmental variable.

Now, organisms have lots of traits, and there are lots of environmental variables, and so you can immediately see that this simple picture can be generalized into an N-dimensional reaction surface. It can get very complex if we’re not just dealing about temperature, but say food, population density, presence or absence of members of the other sex, many things. And we think about that happening over the whole course of the organism’s life; you can generate quite a complex reaction surface. So each genotype has the potential to end up anywhere along this reaction surface, depending upon the environmental history. So the study of reaction norms is intended to make that process explicit.

Now where’s it fit? In the last lecture I gave you one slide that had on it, “This is what ecology and behavior do; this is what genetics does; this is what development does, in evolution.” I am now repeating that slide, that basic message, in a diagrammatic context. Okay? So we can think of the evolutionary process basically as being a cycle that moves between genotype space and phenotype space. So this is one generation, this is another generation. And reaction norms develop at the stage where the genotypes that are present in the just fertilized zygote are being translated into the phenotypes of the adults.

When the gametes are then mapped into genotypes, to produce this array here–so when the zygotes are formed–this is the Hardy-Weinberg Law; this is basically population genetics up here. Down here, when the phenotypes that are being produced by the reaction norms then undergo behavior and ecology to determine a surviving set of organisms that can mate and reproduce and have babies, that’s natural selection, down here.

Now the important thing is that all of these things go on in every generation. You can’t get away from any of them. In every generation there’s genetics, in every generation there’s development, and in every generation there’s ecology and behavior. So they’re all necessary components of understanding the microevolutionary process.

This is the first picture ever made of a reaction norm. It was done by a German guy named Woltereck, working in lakes near Munich, and so he called them reaktionsnormen, not reaction norms. And what you see here are the morphological changes that are going on between generations–so this is a mother, this is her offspring, this is the offspring of this one, and so forth–within a single clone.

These are water fleas that are reproducing asexually. So what you’re looking at is a series of different phenotypes that are all produced by the same genotype, the genotype is being copied exactly, and in the middle of the summer they are producing these helmets and spines.

There are a number of cases that are pretty well studied where this happens. There are spines, helmets and neck teeth in these water fleas, which are called Daphnia, and they are induced by dissolved molecules that are associated with predators, and the predator’s efficiency in eating those Daphnia is affected by the production of those spines and helmets, on the Daphnia.

Making a spine or a helmet has a reproductive cost. So if the predator’s not around, you don’t want to make the spine, because it’s costing you babies. So it is a contingent plastic reaction. You get a signal from the environment that says, “Oh, oh, danger. What do I do?” Well basically what you do is you modify the development of your offspring so that they’re safer, but your offspring won’t be able to have as many babies because they’re better at not being eaten. There are bent shells in barnacles that do the same thing; they make them resistant to snail predators, but they reduce the barnacle’s fecundity.

This cost is important. If the cost were not there, then the organisms would make the defensive structure all the time. If it was cost-free, why not do it all the time? Okay? But it’s not, it cost them something, and so they’re forced to compromise, and they try to minimize the cost of the defensive structures by not producing them unless they get a signal that there’s danger.

Snails parasitized by castrating digenetic trematodes reproduce earlier. By the way, this digenetic trematode is also called schistosomiasis. So this snail is an intermediate host for a serious human disease. Let’s take a look at these.

When Daphnia smell midge larvae, in the water–a midge larva is a little invertebrate predator that swims around and it catches Daphnia with its fore legs, like this, and if Daphnia makes a little neck tooth, it makes it harder for the midge larvae to handle it. Evidently this neck tooth actually, although it looks very small, cost Daphnia something, because they only make it when they smell midge larvae in the water.

This is a modern photograph of the helmet and the tail spine on Daphnia. You can see they’re really quite dramatic. And this is where the cost is borne, here. You can see the number of eggs being produced, and there are fewer eggs in the body of this Daphnia than there would be in a mature member of this one. This one has actually just given birth, so its eggs are all out of its body.

In barnacles this is what it looks like. If the barnacle smells the snails, when it’s growing up, it grows up in a clumped-over form. It bends as it grows, and instead of feeding freely out of the top of its body, it feeds very inefficiently, and it pays a price in not being able to make more babies. Barnacles, by the way, are essentially shrimp that swim around as larvae and glue themselves to the substrate and spend their lives stuck to the basement, kicking food into their mouth with their feet. So the feet of the barnacle would be sticking out here. Charles Darwin spent seven years working on barnacles, figuring out that they were actually crustaceans.

This is the data on schistosomiasis, and the neat thing about this experiment is that the reaction in the snail is induced just by water in which there have been parasites, not by the parasites themselves. In other words, you just give the snail a whiff, a little bit of scent that a parasite is likely to get into its body, and its reaction is, “Oh gosh, I am going to die from a parasite, so I better start reproducing.” So it shifts its reproduction earlier in life; and you can see the extent of that shift right here. These are the ones that have been exposed to water with parasites in it; these are the unexposed controls.

So these things that I’m describing are all induced responses, they are all plastic reactions to signals in the environment, and they all shape the reaction norms of these organisms. So those are some concrete cases. Now let’s look at sort of the abstract, visual, analytic framework a little bit.

Chapter 3. Reaction Norms in Populations [00:12:10]

Here is one reaction norm. I have sketched a common one for many poikilothermic organisms; many things that are–you would think of them as cold-blooded; they don’t regulate their body temperature. The higher the temperature, the smaller they are at maturity. That would work–this general relationship describes how tadpoles grow, how many fish grow.

If you look at a population, it can be conceived of as a bundle of reaction norms. So there are many genotypes out there. So if we have a very small population with just about five or six genotypes in it–the green dotted lines are the individual reaction norms for the different genotypes, and there could be a population mean reaction norm. You just calculate the mean value across all the environments and all the genotypes, and that describes how that population responds.

This is important when you’re trying to summarize this kind of complexity in ecology. You want to know how one population might react as the environment changes, so that you can analyze its impact on another one: a predator acting on a prey; a parasite acting on a host; a grazer acting on a plant. This is a good picture to have in your mind of what that population looks like.

Now traits can have very different expression patterns; it’s not as though all traits have very dramatic reaction norms. And I just chose the example of five digits in many tetrapods, including ourselves, to indicate that you could have three different genotypes, and you could change population density a lot, and the number of digits on the hand wouldn’t change. Everybody would have five fingers. There are some things that are just not sensitive to the environment. Okay? So think of the individual organism as a mosaic of sensitivities. Some of it is not sensitive at all to changes in the environment, or almost insensitive, and other parts of it are quite sensitive.

For example, fecundity. If you increase population density, fecundity will go down in individual organisms, because they’re having to compete harder to get food. So if you restrict food, by any mechanism, fecundity will drop–and an increase in population density is one way to do it–and the genotypes in the population can react differently to that increase. In all three cases fecundity decreased, but genotype 1 was quite sensitive, and genotype 3 was much less sensitive to the shift in population density; and that makes a difference.

As a matter of fact, if you think about it, right here, if you have a fluctuating population, and this population is going between low density and high density, you have a method of maintaining genetic variation right there, because the reaction norms cross, and the guys that were good at one density are lousy at the other. So if the population cycles back and forth between them, one time G1 is favored, the next time G3 is favored, and so forth. Okay? So I’m trying to develop the notion that by sketching reaction norms, you can come up, very quickly, with a useful analytical picture of what’s going on in a population.

For example, if you have this sort of a reaction norm pattern for four genotypes, and you select upward here, you’re going to lead to no response over here at all, because they all happen to converge at this point. So selection here doesn’t make any difference to what you observe in this part of the environment. But in this case, the crossing reaction norm case that we had in the last picture with fecundity, if you select upward in this environment, you’re going to have a downward response here.

If we select at low population density, and population density is low for a long time, it’s going to produce a shift in the population over here, because G1 will be favored, and it has low fecundity at high density. Okay? That’s this situation.

We can just look at a sketch of a reaction norm and we get a sense for how sensitive that trait is to changes in the environment. This is not a very plastic trait, it’s pretty insensitive, and we can see that because it has a shallow slope. This trait’s very sensitive. You change the environment a little, it changes a lot.

Now it’s not just spines and helmets that have reaction norms. This is a picture of an Affymetrix GeneChip for Drosophila melanogaster–it’s got 13,500 genes–and what the chip is doing is it’s picking up the messenger RNA, which is being expressed in the organism; and the intensity of light that you see at a given spot is a measure of the concentration of messenger RNA for that particular gene. So in one picture you have a summary view of the output of the entire genome. Okay?

These things have reaction norms. I put this in for Andrea. Okay? Andrea just wrote a paper about this. So these things have reaction norms. If I gave you Drosophila and I exposed them to high temperature and low temperature and you extracted their mRNA and you ran them out on a GeneChip and you compared the two patterns, you would see big differences in the patterns of all of those light spots. And if you did that carefully, you would be able to draw the reactions of the expression patterns for all the 13,500 genes in the genome. So these concepts are general. They’re not limited to morphology. They apply to any aspect of the phenotype, and this is now a very popular way to measure phenotypes. Okay?

There are lots of things like GeneChips out there. How many people in the audience know, or have heard of GeneChips, or other methods of measuring outputs? You’re not quite densely scattered enough to have you turn to everyone around you and explain what they are. [Laughs] If I had about twice the density, I could just stop talking and have you all explain to each other what a GeneChip is. Okay. We can leave that for a later date. Suffice it to say that in modern molecular technology these things, which are now just about ten years old, a little over ten years old, are methods of looking at the expression of all the genes in the genome all at once; and they too have reaction norms.

So to sum up on reaction norms. A reaction norm is a description of how genes are mapped into the phenotype as a function of the environment. They are properties of genotypes. So if you really want a proper, rigorous way of measuring a reaction norm, you have to be able to clone the organism, so you can get the same genotype replicated and then test it in different environments. If you wanted to do that for humans, what kind of data would you use?

Student: Twins.

Professor Stephen Stearns: Twins. What kind?

Student: Identical.

Professor Stephen Stearns: Identical twins. Identical twins are probably the only–I suppose there might rarely be, these days, identical triplets. I suppose there might even be, somewhere in California, identical octuplets. But most of the time we deal with identical twins, and that’s about as far as you can go, in humans, with this sort of thing. But in Daphnia, or in plants, it’s possible to get genotypes replicated, up to a hundred individuals sometimes, and then you can make a very accurate measure of a reaction norm.

You can think of a population as a bundle of individual reaction norms; and that’s an important concept because when we come to ecology we’re going to be thinking about how predators interact with prey, and about how competitors interact with each other. And when we do that, normally the way that biologists have done it in the past is they’ve chunked those things as species, where they have a species typical property. Okay? So all the species 1 are supposed to behave one way, and all of species 2 are supposed to behave another way.

But the differences between the individuals in those species are really important, and when the two species are interacting, it’s not like they’re all identical individuals interacting. They are different, and when the species interact it’s bundles of reaction norms interacting with bundles of reaction norms. And this produces important effects. For example, it tends to stabilize ecological interactions. So remember that for say about six or eight weeks down the line, when we get to ecology. This property of populations has important consequences.

There’s a real easy way to talk about the sensitivity of phenotypes to the environment. You just make a reaction norm plot and look at the slope. If the slope is steep, those organisms are very sensitive to changes in environment; if it’s flat, they are not.

And in terms of the kinds of intellectual tools that one might pick up in the course of a liberal arts education, in order to deal in later life with the claims of people who want to talk about the evolution of IQ, or racial differences, or lots of stuff that involves assumptions about genetic determination, reaction norms are useful because they visually describe the contributions of genes and environment to the phenotype. And, for example, I will put up a speculative plot, just to illustrate the potential social significance of what I’m talking about.

If, for example, I put IQ up here and I put Family Annual Income down here–already we’re in trouble, right; we’re not being politically correct anymore–and then I do this, basically what I’m saying is that if I took human identical twins and I raised one here and the other one here, I could get that. Okay? And what that shows you–by the way, I don’t know that that is true; I’m just trying to give you something to remember, that will convince you that this sort of analysis can potentially be significant–what that shows you basically is that people might appear to be real smart in one environment and stupid in another, compared to the other ones in the populations, and that these things are context dependent. So, that’s just an illustration of this point down here on the bottom.

Chapter 4. Developmental Constraints on Reaction Norms [00:23:42]

Okay, so I’ve been talking a lot about phenotypic plasticity, and I’ve shown you these wonderful examples of Daphnia reacting sensitively to predators and so forth. Does that mean that organisms are really plastic? Can I just pick up a bunch of clay and mold it into anything that I want, depending on the environment that I expose it to? No I can’t.

And that’s because, as we learned last time, the large-scale structure is determined by things that are hard to change, and those are developmental patterns that have a deep evolutionary history, and they set up a rigid framework within which the plasticity is expressed. So the things that change slowly–those are the developmental control genes–are constraining the things that change rapidly. I just lost a little bit of text off the bottom.

So let’s do this with the example of Distal-less. Distal-less is a developmental control gene. The pictures here basically are showing you how the Drosophila larva gets set up very early in development. The first thing that happens is that an anterior/posterior axis gets laid down. That’s done by the Hox genes. Then the dorsoventral axis is determined by Sog and Chordin and Decapentaplegic and things like that.

Then, after the basic axes of the organisms are laid down and segments are formed, other things turn on that determine whether you’ll be dealing with a head, a gut or a tail. Interestingly, the name for the gene that induces heart formation is Tinman, from the Wizard of Oz, who didn’t have a heart. Okay? So they give neat names to some of these things.

And what we’re worried about today is this gene here, Distal-less, which determines body wall outgrowth. Remember last time I also showed you that picture of Pax6; that’s the gene that induces eye formation. But today we’re going to talk about Distal-less. And if you look at the body of a fly, this is where the action of certain mutations takes place. If you get mutations in Distal-less, these are the parts of the body which are going to be affected. They are all extremities, all out-pocketings of the body wall, which are then being developed into antennae or mouth parts or legs. Vestigial is working on wings and haltiers, and Eyeless is working on the presence of eyes. Okay?

Now in order to tell you about this deep developmental constraint in butterfly wings, I first want you to notice that there’s something that’s called a Nymphalid groundplan. The Nymphalidae are a large family of butterflies, and in the nineteenth century German biologists, with German thoroughness, out to eight decimal places, did an exhaustive study of thousands of butterfly wings, and they were able to take that whole family of Nymphalidae, with its hundreds of species, and reduce them all to variations on these themes.

So they found that in the middle of the wing you could have stripes; in the outer part of the wing you could have what they called border eyespots, or border ocelli; right on the edge of the wing you could have bands, and so forth. So that this would describe all of the different kinds of things that you could do with butterflies. And we’re going to focus on the eyespots.

Now this is the diversity of butterfly wing patterns that you can get in about ten minutes in the Peabody Museum collections. They are beautiful, they’re just amazing. I remember the first time I saw a birdwing butterfly in the collections at the Bishop Museum in Honolulu. The birdwings come from New Guinea and other parts of Southeast Asia. They’re about that big. They’re the largest butterflies on the planet. And actually their form is a bit like this guy, except they’re about four times bigger.

And you can see that simply by varying the location where colors are expressed, and by varying the size of the different elements, you generate a huge number of patterns. You can even use them to write numbers on wings. Evolution has written numbers on the back wing of this particular butterfly; this is an ‘89 butterfly.

The model system in which this is best studied is in a butterfly called Bicyclus, and it has been worked on by Paul Brakefield in Leiden, and Sean Carroll in Madison, Wisconsin, and Antonia Monteiro in our department, and a number of other people, Vern French in Edinburgh. And Bicyclus has a number of neat features. One of them is that it is developmentally plastic.

In the wet season it looks like this, and in the dry season it looks like this. And, in fact, these are two brothers who have been produced in the laboratory, with this one being raised under wet season conditions and this one being raised under dry season conditions. So one genotype can elicit a range of phenotypes, and you can see that in the process the eyespots change considerably in their size and intensity.

Now it turns out that you can fish the Distal-less gene out of Drosophila, and you can use that segment of DNA to recognize the homolog gene in the butterfly, and you can then put a reporter onto the homolog, and you can ask that gene to express its reporter when it’s being expressed, so that you can see visually where the gene’s being expressed. When that’s done, you can see that every place that an eyespot is going to form in the adult wing, you can see the gene being expressed in the wing disc, in the developing pupa.

The way that butterflies and flies and other holometabolous insects develop is that after the caterpillar or the larva has fed for awhile, and it’s starting to form its pupa, the cells reorganize in the pupa, into structures that are going to be parts of the adult, and the wing disc, that’s going to be the wing in the adult, looks like this in the pupa, and it’s sitting right on the surface of the pupa.

So that if you want to do developmental biology experiments on it, you can go through the wall of the pupal case and you can pick out a few cells and you can move them around. So, in fact, you can go in and cut one of these things out and put it down somewhere else; if you do, it will make an eyespot there.

So this is actually an exceedingly neat system to work in because you can actually do cell manipulations, as well as genetic manipulations. You can manipulate both the developmental biology and the underlying genetic structure, in butterfly wings.

This is another species; it just has two eyespots, and when you look at its wing disc, it just has two places that Distal-less is being expressed; and those are going to be right in the center, right where that white spot is.

So Distal-less is actually telling the wing disc where to make eyespots, and the Nymphalid groundplan says you can only make those eyespots in certain places. And the Nymphalid groundplan, the butterfly wing groundplan, is arguably about 100,000,000 years old; it’s ancient. So does that mean that you can’t change the eyespots? No it doesn’t.

Almost everything about the eyespots has a reaction norm, except their location and number. Within a given species you’re always going to get the same number, and they’re always going to be in the same place, but whether they’re big or so small that you can’t even see them depends on the environment in which they’re expressed.

So if you raise a whole bunch of families, and you compare the siblings across families, to make reaction norms, you can see that the diameter of the white part of the spot and the diameter of the black part of the spot changes as you go from low to high temperature. You have low temperatures in the dry season and high temperatures in the wet season, and that shifts the reaction norms on the butterfly wing.

Well I’m a sucker for analogies, and analogies are dangerous. You might think that the eyespot was a vase, and into that vase you’re going to stick a bundle of reaction norms. And you can think of the vase as being the phylogenetic history of the developmental constraint on the butterfly wing, and it’s holding those reaction norms within a certain range, but that the environment then is allowing them to vary, to the degree that a bundle of flowers could flop out of a flower vase.

Well it turns out–I’m sorry for this; this is something that I checked this morning and it wasn’t going on. At any rate, I’ll read this out for you. Can we think of macroevolution as having constructed a vase, within which the reaction norms sit? And the answer is no.

And the answer is no because some of the genes that are controlling the shape and the position of the eyespots–so things like Distal-less–are also involved in determining the slopes and the shapes of the reaction norms. These two things are genetically entangled, and their entanglement is a case of the same gene having two different functions at different times in development, and natural selection will operate on it throughout the lifecycle.

So it’s not as though there are some things that are constraints, that are not being changed, and there are other things that are genes that are sort of tweaking the constraints a little bit. In fact, the same genes are involved in producing both things. So if we want to shift the slope of the reaction norm by selecting on phenotypic plasticity in Bicyclus, we are going to be selecting on genes that are also determining the location and number of eyespots.

If you think this kind of stuff is nice, you can go and look on the Web, on these sorts of websites. Antonia works on butterfly wing patterns. Gunter works on the tetrapod limb, and with Vinny Lynch he has recently been looking into the origin of the mammalian female reproductive tract. So they have been comparing things like duckbilled platypuses and spiny echidnas–which are mammals that lay eggs–with kangaroos and eutherians–which are mice and lions and things like us–and discovering where it is that the mammalian female reproductive tract actually came from. It turns out that the HOX genes are involved in that, and that it’s another one of these stories of gene duplication making the development of new structures possible.

Rick Prum, who’s our department chair and works in the Peabody Museum, is one of the world experts on feathers and on the fact that dinosaurs had feathers, and if you’re interested in working with Rick, you can certainly drop in, and he’s a very friendly guy and would be happy to show you what he knows about feathers. So this is an active area and it produces a lot of fascinating research.

Chapter 5. Benefits and Limitations of Studying Reaction Norms [00:36:23]

To summarize my overview of it, what I want to emphasize is that the phenotype, the whole organism that you see, and the whole lifecycle of that organism that you see, is a mosaic of parts, and their pattern of determination varies tremendously in evolutionary age. So if you just look at my own body, the parts of me that are extremely old are the fact that I have four limbs and five fingers, and the parts of me that are evolutionarily relatively young are the size of my cerebral cortex and some other aspects of me.

And if you were to look into the plasticity of my cerebral cortex, you would discover that it is incredibly plastic, and that when I am a little baby and I’m just born, I have billions more connections in my nerve cells than I do when I’m seven-years-old, and that a great deal of my mental development, between birth and the age of seven, has essentially been the remodeling of my cortex by plastic interactions with the environment. And in fact that’s what a lot of learning is about; it’s about plastic response to environment. So I am myself, as are you, a mosaic of things, of very different evolutionary ages.

The basic developmental patterns that we see in animals are mostly about 500,000,000 years old. In plants they’re a bit younger. The HOX control of body symmetry and body pattern in animals is arguably about 600,000,000 years old; maybe a little less, maybe 550,000,000. The ABC pattern of flower development in flowering plants is probably somewhere between about 95 and 135,000,000 years old; that’s something that happened in the Cretaceous.

Now let’s shift timescale and go down to one generation, one organism, encountering a specific environment. Its plastic reaction to the environment has evolved relatively recently, and it implements specific contingency plans. Daphnia that come from lakes that do not have fish in them and haven’t had fish in them for a long time, don’t react when you put the smell of a fish into the water. The Daphnia that come from lakes that have had fish in them for along time react, and react strongly and quickly. So the plastic reaction is something that can evolve.

I want to caution you though, it is not as though all the fine details of the plastic response are adaptive; they are not necessarily all adaptive. For example, think about temperature. If we are studying the plastic reactions of organisms to temperature, it may very well be that things that live in the Arctic have a different reaction norm than things that live in the tropics, because they’ve encountered a different temperature regime, and that that’s an evolved reaction. But it’s also quite possible that it’s just biophysically impossible to do something when it gets colder; that doesn’t have to evolve.

So I want you also to be able to think of the necessity of taking something like a plastic reaction norm and dissecting it analytically so that you can figure out what part of it’s adaptive and what part of it is just there because that’s the kind of stuff that organisms are built out of. They are biochemical systems, and biochemistry, we know, has reaction rates that change with temperature and with a lot of other things. Okay? So it’s not–this is not all adaptive.

The thing you actually see, the organism you analyze, is just one point on a multidimensional reaction surface. It could have been a lot of other things, and all those other things that it could have been are important when we think about evolutionary ecology, when we think about population dynamics, when we think about interactions between hosts and parasites, because they represent all those other potential interactions that could be going on in other circumstances. Okay?

So by thinking about reaction norms, we can both express the genetic variation in the population; we can express the developmental reaction to the environment, the way all of those different genetic combinations will react to the environment; and we have the potential to visualize the dynamic over generations, as both the gene frequencies and the environmental circumstances change. So there’s a potential here for a lot of interesting analysis. I think the basic take-home point though is this one.

Every phenotype is the product of both genetic and environmental influences, and the way they interact to produce the phenotype is extremely important. So it is almost never the case that you can claim that only Nature, or only Nurture, accounts for what you see in organisms.

So that basically completes what I want you to know about microevolutionary principles, before we now go into the analysis of how natural selection shapes phenotypes for reproductive success. I’m going to use all these concepts. For example, when we get to the evolution of age of maturity, I’m going to talk about reaction norms for age of maturity in human females, and in fish, and in mammoths. So I want you to remember these elements.

I also want you to remember, as we go forward, that everything that you see in organisms has an evolutionary history. It doesn’t have to be an adaptive history. It might be drift. Things might happen in phenotypes that are byproducts of stuff that’s going on somewhere else in the organism. There are all kinds of alternatives that you should be continually prepared to compare, when you’re trying to analyze what you see, but everything that you see has evolved. All you have to do to see that is remember at one point your ancestors were bacteria, and everything else has come since then. So next time we’re going to start talking about how organisms are designed for reproductive success; and our first step is why do they reproduce sexually?

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