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8. Evolution, Ecology and Behavior: The Expression of Variation: Reaction Norms
Poziom:
Temat: Nauka i technologia
Prof: 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.
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.
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.
>
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.
Prof: Twins.
What kind?
Student: Identical.
Prof: 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.
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.
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?
