ELENA KRAMER: All right.
Well, thank you so much for coming out here today.
It's a thrill to be here with you.
So, as you just heard, I'm a plant biologist.
I study the evolution of genetic programs that control the development,
particularly of flowers.
Now, I have to admit, I've sat next to a lot of people on planes
and told them that I was a plant biologist.
And often, their reaction is, help me find out why my fern is dying,
or something like that.
I don't keep things alive.
This is the problem.
I like to grind them up in little test tubes and things like that,
so don't ask me how to keep something alive.
But we talk in plant biology about plant blindness.
People often don't appreciate the importance
of plants in our everyday life, but I think
we can all agree that flowers are very compelling and charismatic.
As a human civilization, we've had a fascination with flowers, really,
from the beginning.
And what we're really trying to understand in our lab
is how we have, over the course of evolution,
generated this enormous diversity of floral morphology,
and then, particularly, how changes in the genetic programs that
control these developmental processes has generated the change in morphology.
And in order to do that, we work at the intersection
of sort of three different fields.
We ask different types of questions.
So for instance, we're very interested in development.
Very specifically, what are the patterns of cell division and cell
expansion, the duration, their localization,
and how do these different patterns generate the morphology
that we're interested in?
So we ask very specific questions about how morphology changes over time.
And then we overlay this information with information about the genes.
How do different genes interact with each other on a local scale,
on a global scale, on the genomic scale?
And ask how these genetic programs control the developmental processes.
And then we take all of those questions and we
put them in an evolutionary context, and say,
well, when we ask all these questions in one species then
we compare them to a different species, what aspects of these processes
are the same, what aspects are different,
and can we understand how those differences arise?
So when we put all those things together,
that's a field called evo-devo, or evolutionary developmental biology.
So we're essentially asking how morphological diversity is generated
over time at a molecular level.
So, why don't we use plants as a model system?
So if you'll let me proselytize for a moment about why plants
are such a wonderful model system.
I'm a developmental biologist.
If I was an animal developmental biologist,
I would only be focused on a very narrow window of that organism's life-- what
we typically call embryogenesis, from fertilization to some type of hatching.
But in plants, the fantastic thing about plants is that if they are alive,
they are undergoing development.
If we look at this plant embryo, you can immediately
recognize that while, yes, there was a developmental process that took this
from a single cell to this embryo, this is not
the entirety of the body of a plant.
So this enormous oak tree started out as this tiny embryo,
and it is in a constant state of organogenesis
and producing new organs in order to generate its body.
And all around us--
I mean, we finally got to go outside today
and enjoy a little bit of nice weather--
you can see trees all over campus, things coming up from the ground,
these are plants that are undergoing organogenesis even
in what we would consider their adult body.
And plants can do that because all throughout their body,
they have reservoirs of undifferentiated cells--
stem cells.
Now, my animal colleagues get really excited about stem cells.
Stem cells are nothing for plants.
They've got stem cells to spare, and their stem cells
are arranged in these specific regions called meristems.
They're domes of undifferentiated cells.
So when I tell you that I want to understand floral development,
this is where we start.
We start with a dome of undifferentiated cells,
and we look at how that set of cells changes over time
to generate floral morphology.
So, this is our big problem.
We have about 350,000 species of flowering plants
that have arisen over the past 150 million years.
That's a big problem.
I don't try-- I'm not looking at that scale, right?
You have to start with something tractable, and what we work with
is a model system called Aquilegia-- that you may know as Columbine.
A lot of you may have this in your yards at home.
It is what we call a recently radiated species flock.
So let me explain to you what that is.
Why is Aquilegia a good model system?
So obviously, it's very pretty, but it's also
very tractable from a molecular standpoint.
It has a relatively small genome, about 300 million base pairs,
and you'll take my word for it that that's manageable.
We have a fully sequenced genome.
We also have a lot of functional tools that
allow us to trick the plant into doing things that we want it to do.
It also has a wonderful array of morphological novelty.
So, I mentioned that this is a radiated species flock.
What am I talking about?
I'm talking about that when we study the evolutionary history of this genus,
when we reconstruct its phylogeny, and understand how the species are related
to each other, we see that these species have radiated over a period of one
to six million years, which is relatively recent.
And in fact, the North American radiation that's pictured here
is less than a million years.
So these are very closely related species.
That means that they're also interfertile,
and that's something that makes the geneticists sit up and take notice
because we can cross these species.
Even species that look quite different from one another, we can hybridize them
and then look at how their traits segregate in later generations,
and map the molecular changes that are responsible for the differences
in morphology.
So this means that we have traditional developmental genetic tools,
and we also have a lot of evolutionary genetic tools
that make it a good model system.
OK, so let's step back a second.
I'm going to tell you a little bit about floral morphology
and floral development.
So, this is what you usually think of when you think about a flower.
You may have a little bit of plant biology, maybe in elementary school,
and they told you that there are four different kinds of floral organs,
right?
So you have sepals that are the productive organs,
the attractive petals that are involved in manipulating pollinators,
the male stamens, and the female carpels.
And these organs are arranged in what we call whorls--
they're concentric circles.
So moving, you get sepals, petals, stamens and carpels.
And about 30 years ago, molecular biologists
working in a number of different model systems
defined a genetic program called the ABC Model,
and this is a model that tells us how each of these floral organs
figures out during development what flavor of origin it wants to be.
So for instance, there are three different classes
of genes, the a, b, and c-class genes.
If you are primordium in the first whorl,
you're only exposed to A function, and that tells you to be a sepal.
In the second whorl, you have A and B function that tells you to be a petal.
Stamens are exposed to B and C together and then carpels to C alone.
So this is what we call a combinatorial code.
Each little position in the floral meristem has a different set of genes,
and that tells the organ what kind of organ to be.
And the way that they came up with this program
was by examining mutants, and developmental geneticists,
we love mutants.
We make mutants all the time.
We like to knock out gene function and then infer from the way
the plant looks--
or any other organism--
the way it looks what the function of that gene must be.
And the genes that comprise the ABC program have something in common
that when you knock them out with mutation,
you dramatically change floral morphology.
You transform the identity of one organ into the identity of another.
And so here, for instance, if you eliminate this B-class gene,
then all you have are A and C functions in the floral meristem.
And the petals turn into sepals, and the stamens turn into carpels.
And this is a complete transformation, so this
highlights how minor genetic changes can have really
profound effects on morphology.
So these are the kinds of genetic programs
that we think about when we think about floral evolution.
OK, so how are we applying this kind of model
in the context of our model system, Aquilegia?
So there's a lot of interesting things about Aquilegia flowers.
These guys, up here, those are the sepals.
And usually, you think about sepals as being green and protective,
but these are not just green and protective, they're bright red,
or sometimes blue, or white, or yellow.
They're what we call petaloid, which just means that they're showing.
So this is an interesting question.
Here, we have the ecological function of pollinator attraction
that has been transferred from the inner whorl of the flower
to the outer whorl of the flower.
So how does that happen, and what's going on at the molecular level
in order to make these sepals bright and showy?
Another really interesting aspect of the Aquilegia flower is this nectar spur.
So the true petals in the second whorl have this long, tubular structure
that terminates in a nectary, and you can just imagine all the things
that Aquilegia is doing to manipulate pollinators to make them go all
the way down here and get the nectar.
So there's all kinds of things that we can study here related
to how the spurs first evolved.
They're what we call a key innovation that
were important for the radiation of the genus.
And what is the genetic basis of their diversification in morphology?
They get longer and shorter, and they're curved into different shapes.
So we're studying all these different aspects across species of Aquilegia.
And then one of my favorite things about Aquilegia flower
that I didn't even realize until I started
dissecting them is that they actually have five types of floral organs.
They have this fifth type of organ called the staminodium, which
is a sterile organ positioned between the male stamens
and the female carpels.
So, how the heck does that-- how does that work?
The ABC Model gives us a very elegant mechanism
for giving us four types of floral organs, what
happens when we intercalate a fifth type of floral organ
into that genetic program?
So we've been studying all of these questions.
Another one that I'm going to show you today
is, we've been interested in this question about,
how does the flower know when to stop?
You think about a flower.
Once it makes those carpels, then it stops.
It doesn't make any other floral organs, and that's actually
a very carefully controlled genetic process.
In most of the flowers you might think of,
there may only be one whorl of stamens like in this Snapdragon.
But here, we're looking down on an Aquilegia flower,
you can see that there are many whorls of stamens,
so how does the meristem decide how many whorls it's going to make?
And to investigate this, we started by actually
working with these C-class genes because this
makes sense when you think about it.
It turns out, the C-class genes confer the identity
of the stamens and the carpels, but in conferring identity of the carpels,
they tell the floral meristem to stop.
So, what we want to ask is, what happens when we knock out
the function of these genes?
And in Aquilegia, we use a molecular tool
to trick the plant into silencing our gene of interest.
And when we do that-- here's a wild type Aquilegia flower, and here's
a flower where we have used this trick to silence the C-class gene.
And you can already see it's looking a little weird, but as it develops,
you see that the stamens are completely replaced by petals.
And the staminodium, that novel organ, and the carpels
are both replaced by sepals.
And when we look inside the flower, you may not be able to see this,
but there are actually dozens and dozens of whorls
of organs here, so it's clear that this gene also
controls floral meristem termination.
Now, this was actually just the first step in this project.
We were trying to confirm that this gene functions the same way in Aquilegia
that it functions in other species.
We expected it to be conserved because, in fact, all around you,
you see mutants.
These are all mutant varieties.
So here's a rose, a daffodil, and a peony.
Where on the left, you see the wild type flower
that has a single whorl of petals and many whorls of stamens.
And on the right, you see an Agonis mutant
that has the transformation of stamen identity
into petal identity and the indeterminancy of the floral meristem.
So actually, you're looking at mutants all the time,
you may just not have known it.
So homeotic or transformative mutants have always
been very unpopular in horticulture.
So, I hope I've convinced you that evo-devo is an interesting field.
If you're not totally taken by plant biology as I am,
you might be interested in some of my other colleagues--
Mansi Srivastava, who studies these fascinating little flatworms that
have the capacity to regenerate their entire bodies from just
small fragments of their body.
They're actually thought to be immortal.
My colleague, Cassandra Extavour, who studies
the evolution of the genetic pathways that
control germ line specification, which is incredibly important for evolution
and development.
Cliff Tabin over at the medical school studies
the diversification of vertebrates and particularly the vertebral column
itself.
Why don't snakes have any limbs?
Why do ostriches have such long necks?
My colleague Terry Capellini over in Human Evolutionary Biology
is actually using evo-devo approaches to understand the evolution
of the skeleton in humans.
So he uses mouse models a lot, but what he's ultimately interested in
is actually human skeletal evolution.
So that's everything I want to tell you about evo-devo, so thank you.