The story is about, I don't have a laser pointer,
so you have to, about this tree.
It's a so-called Linden tree of innocence.
It's growing there since beginning of 16th century,
and there is a story connected with this tree.
And the story says that at that time,
the lord of the castle was going hunting into the woods
and was found murdered, slain by a dagger.
And the local boy was accused of this murder,
put into jail.
And as the justice at that time did torture
and all these modern type of interrogations,
however, he was claiming that he's innocent,
and no torture helped.
So they brought him in front of the tribunal,
which was at his castle terrace.
And the tribunal condemned him to death.
And when he heard he's going to die,
he pulled out the small tree growing there
and put it back, inverted in the soil,
and said, if the tree will grow next spring,
it will be the sign of the god that I'm innocent.
And so the judges said, you know, god is an authority,
so they put him back to jail and they waited till spring.
And then in the spring, there were these nice green leaves
coming out of the roots,
and you can still see the tree there even today.
And so they set him free, apparently.
I can't guarantee that, but the tree is there,
and you can see there are these root-like main branches.
I like the story very much.
I heard it from my mother when I was around eight,
nine years old, and I don't want to say
that it was the moment when I got fascinated by plants,
but I definitely got fascinated
because that demonstrates very well
how differently plants can deal with the changes
in environment, to put it mildly, right?
I mean, plants cannot fight, plants cannot run away,
so they evolved all these mechanisms
how to adapt their growth and development,
and like that survive in the put environment.
And they can go that far
that they can even completely re-specify the growth.
And I didn't know at that time that at some point
I will be studying this problem.
So plant and animals, they live different lives.
They start with a zygote as,
would it be possible to dim the light somehow, please?
Because there will be a lot of pictures
that you will not enjoy as much as if they're,
I know it doesn't count that with the sun in Hamburg so much,
but okay, so please.
Well, so both plants and animals start with a zygote
and they have a period of embryogenesis.
And at the moment of the birth,
basically the animals exemplified by human here,
they have all the organs they will have later on.
And basically the postembryonic development
is mainly the elaborating
on the already pre-existing structures.
With plants is very much different.
They also start as a zygote.
They have a period of embryogenesis.
And at the moment when they are born,
so that is equivalent when the seeds start to germinate,
they have only very simple structure.
So they have an apical basal axis.
So they know where is up and where is down.
And they start to make the first leaves.
And if you look at the grownup plant later,
basically all these organs, all these leaves,
flowers, silics, fruits,
all that is the result of postembryonic development.
So that is something what we can't really do.
I mean, the plants have an ability
to keep the cells totipotent.
So they can reinitiate the cell division.
They can start to differentiate and specify
into the different types and into the different organs.
And that is something what we really can't do so well.
So that's the one good reason to study plants.
I mean, they do things differently.
And they can do many things related to development
better than the animals can.
OK?
So there is also other reason to study plants.
In Europe, we don't feel it so much.
But there is a shortage of food on the Earth.
And here you see the regions where, for example,
the water is scarce.
And so with genetically manipulated plants,
I know it sounds terrible, because some politicians made
it sound terrible.
But with these, we can easily increase the yield
by 30% at least.
We can use less pesticides and herbicides.
And well, we will have to do it at some point
if we want to sustain our population.
And the more we know about how the plant development
functions, the better and in a more fine and precise way
we can manipulate the development to our needs.
So definitely, there is plenty of options.
Like we can manipulate the root development
to make roots either longer to reach to the water
or make them more branch to be able to take up
more nutrients from the nutrient-armed soils.
And definitely, well, maybe the ecologists
don't like the fields more that they like desert.
But at least for the vine drinkers,
there is certainly a potential to develop in the world.
So that's a second reason.
And there is also, I would say, maybe the most important
reason.
When you do fundamental research,
whether it's on plants, on flies, on animals,
or on bacteria, I mean fundamental biological
knowledge or fundamental knowledge in any discipline,
never get lost.
And you will never know how you can use it
and from which angle you will come to make it useful.
So blindly going for only applied research
will certainly not bring us far away.
If the galvanic wouldn't start to play
with the stupid frogs hanging from the copper stick,
we would probably not have the batteries
and we would not do the electricity.
And I mean, hanging the frogs on the copper stick
doesn't sound like a very applied research
at the beginning, right?
And therefore, I just want to say the plants
can activate the cell division.
And they can, during the postembryonic lives,
make, in a very regulated way, very organized structures
like primordia for the lateral roots, like here you see.
And of course, they can also have tumors
like the humans or animals have.
But I mean, still they maintain many more mechanisms
how to control the differentiation
and specification to the different cell types.
And it would be certainly of advantage also to medicine
to understand these type of mechanisms.
And one shouldn't forget that these unimportant things
like cells or genes or transposons or interfering RNA,
they all were originally discovered in plants.
And without these terms, you can hardly
imagine to have any type of biological research nowadays.
So therefore, don't despise plants, please.
That's mainly for the grant agencies
that are not sitting here.
But just be aware that working on plants has its merits.
OK, let's be more specific.
So the story of oxen, the plant hormone
that we are mainly interested in, started with Darwin.
That was the Darwin when we had his period of doubts.
And he didn't want to come out with an evolutionary theory
because of the opposition of the church.
At that time, he amused himself studying
the movements of plants.
He realized that the canary grass seeds,
he was feeding his canary, were always
growing to the light in the cage.
And he started to study this phenomenon and similar phenomenon
where the plants are changing the direction of growth
according to the environment.
And so he did this serious, very simple experiment.
He found out that the tip of the young grass
is the place which is important for the bending.
Because if you cut off the tip or if you
cover the tip with something that is not transparent,
the grass will not grow anymore towards the light.
And so like that, he actually found out
that he postulated that there must be a signal moving
from the tip where the perception of light
happens to this place where actually the cells are
responding and elongating more on one side
and therefore bending the whole organ is bending.
So he postulated existence of the influence that
is regulating plant growth.
And later that influence was captured in the gelatin,
analyzed, and later the people identified
the chemical nature of oxen that is the indoyl acetic acid.
And once the physiologists had a battle of oxen on the shelf,
they could start to play their games,
meaning putting it on the different plant species
at the different times of day and night
and watching what's happening.
And they found out that basically many things
happen.
With oxen only, you can mess up basically almost all aspects
of plant development.
So starting with embryo development,
with formation of all organs, with differentiation
of vasculature, that's the tissue that
is connecting basically the new organs
with the pre-existing vascular network.
The response is to light and gravity.
So no canary grass growing towards the light,
no shoots growing up, no roots growing down
if you mess up with oxen.
And while that's remarkable, you have a simple chemical
structure that cannot contain too much information.
And you have this range of physiological processes
that are regulated by this simple structure.
And that was a good news for some people,
because they said, oh, oxen is important because it's
doing so many things.
And these were mainly the people working with oxen.
And for the rest, it was a sign that oxen is strange.
It cannot be that it will give a specific information
to do so many different things.
And therefore, they thought it's not a signaling molecule,
but simply something what is required for a growth,
like glucose.
If you wouldn't have a sugar, also not much would happen.
But that doesn't mean that sugar in that context
is a signaling molecule.
And so there was this confusion for decades,
where the people were quarreling what oxen is about.
And in the last 10 years, there was one very important discovery
that started to shed a bit of light on this confusion.
And the discovery was that the oxen
is distributed within plant tissues in a very defined way.
So meaning you have these.
Here you can see by the activity of the reporter,
either by the green fluorescence protein like here,
or by a gas protein doesn't matter simply.
These green or blue spots, they indicate
the places of high oxen activity.
And it was not really predicted that we
will have this very localized oxen activity.
And that was quite a surprise.
And within several years, it was clear
that basically these oxen gradients,
how we started to call them, you can
see during all the developmental processes that
are regulated by oxen.
So here you see a shoot apical meristem.
So that's the part of the plant up which
makes leaves and flowers.
And here, basically, you see a one single cell
with a high oxen activity.
And this will be the cell that will make a new flower.
From all these cells around, that
will be the one cell that will make the flower.
Here you see the embryo.
So the cell which will, sorry, it's very difficult.
The cell which will make the root
is the cell which accumulates oxen.
Here you see the flower organs, all these beautiful, colorful
things.
Originally, they start as a spot of oxen activity.
The lateral root, before the primordium
starts to develop, you have a high oxen activity
in the cell which will make the lateral root.
And the mentioned gravistimulated root.
So this is a root which is supposed to grow down.
And photostimulated shoot.
So that's light coming from that side.
And it makes the asymmetric oxen accumulation
on the shaded side, basically.
So these were, as I said, unexpected and visually
appealing.
You see these nice pattern.
And the question is, are these nice localized patterns
meaningful?
So does the accumulation in the given cells
give the instruction for the change
of the developmental program that we then
see happening, like bending, like formation of new organs?
And so there was a number of nice experiments done.
I picked up one which is very visual,
done by our collaborators in Switzerland.
So they took a tomato meristem.
So the part, the dividing, growing part of the stem.
And they put a droplet of oxen on the side.
Here the oxen paste is being colored.
And so that was sufficient to make
the initiation of the new leaf.
And at the end, you've got a fairly normal tomato leaf.
So you put from outside a droplet of oxen.
And the cells that get a lot of oxen get convinced.
Now is the time to make a leaf.
And they initiate organogenesis.
And that's one of the many demonstrations
that these local accumulations of oxen
are triggering the process.
So are kicking off the whole series of events
that will then end up by, well, in that case, reformation.
So OK, we have the gradients.
The gradients are important.
How does it happen that we have these localized distributions?
So there are several conceptual possibilities.
But I will leave the discussion out and come to the right one.
So a very easy experiment.
You treat the plant tissues with the inhibitors
of oxen transport that are chemicals that
will block movement of oxen between the cells.
And then you basically kill the gradients.
So in the lower part here, you see
after the treatment, and you see
that the gradients nicely formed in the upper part are gone.
So if you don't have an oxen transport,
you don't have these accumulations.
And all the development goes wrong.
So that kind of indicated that oxen transport is important.
And that was actually how our work on the gradients
connected with our previos work on transport.
So a bit about oxen transport, because that's
the key process in what I will try to explain to you.
Oxen is the only signaling molecule in plants
that have this highly regulated directional transport
between the cells.
So all other plant hormones, they
get distributed through the tissues.
But they don't have this directionality
and this active regulatory mechanism.
So you know, oxen always goes in a given direction
within the plant tissues.
So how that happens?
In the 70s, there were a few guys
that had the idea that you need specific transporters.
So the proteins that will bring oxen inside the cells,
and then the other guys that will take oxen from the cell
and move it out of the cell.
And like that, oxen can move between cells.
And I mean, imagine if you want to move oxen through the tissue,
it has to cross a membrane inside the cell,
get distributed in the cell, cross another membrane out
of the cell, and again, cross a membrane inside of cell.
And that's a quiet, tedious way how
to move a signaling molecule.
And so one can ask why got or evolutions
were so stupid to make the movement of the signaling
molecule so slow and so energetically demanding.
But there is an important issue.
So if you do it like that, every cell in the path of oxen flow
can contribute to the decision how much oxen will flow
and in which direction.
Because according to this theory,
the subcellular position of the efflux carriers
of these transporters that are pumping out
will basically decide about the directionality of the flow.
So if the cell will have a reason
to put the protein on the other side like this one,
then it will redirect oxen flow accordingly.
And you will signal to the different cells,
and oxen will accumulate somewhere else.
And that will have a profound effect on the plant
architecture.
So that was the theory how oxen moves.
And in the late 90s, there was this few glorious months
that within half a year, there were four groups identifying
the same gene family and gene family
that was predicted to be coding for these transporters.
And so it was a plant-specific family.
So the protein looks like that.
It's a plasma membrane protein with a hydrophilic loop
and a lot of plasma membrane domains.
And the family is called pin, because the major member
of the family, if it's mutated, it
gives this ugly pin-like structure.
I'm really sorry that I can't do it in a different way.
But yeah, so this pin-like structure.
No organs, no flowers, just the pin going up.
And because you can get the same type of phenotype,
so same-looking plant, if you treat normal wild-type,
non-mutated plant with the inhibitors of oxen transport,
then it was clear that the genes had something
to do with this process of oxen movement.
And then when you localize the proteins,
they will be only on one side of the cell.
So here in yellow, you see the localization
of the pin protein.
And that's in the longitudinal section of the stem.
So the oxen flows down.
And that's exactly as predicted by the hypothesis
25 years before that.
You know, completely hypothetical protein,
hypothetical prediction, it will be on one side of the cell
to drive the directionality of the flow.
And then, well, a quarter of a century later,
you get the proteins, and they are localized like this.
So that was a glorious time for plant hormone research.
Well, it took another eight years
to demonstrate that pin proteins are indeed
transporting oxen across the plasma membrane.
Don't ask me why it took so long.
I don't know why the others were so slow.
But definitely, we used several approaches how to show that.
So we put the pin proteins in the cultured cells.
So these are simply cells floating in the solution.
And the advantage is that you can do transport assays.
You can put radioactively labeled oxen.
And you can measure how much oxen you have in the medium,
how much oxen you have inside the cell.
And from that, you can measure transport activity
across the plasma membrane.
And so when we put the different pin proteins
into these cultures, we got much less oxen accumulation
inside the cell, which was consistent with having
higher oxen efflux from the cells.
And when we use the mammalian cells,
Gila, or the yeast cells, that was working as well.
So if you put a plant-specific protein
that during the evolution never saw anything
like yeast or animal, you put it into the system,
it will be still able to transport oxen.
And that's for most of the critics,
that's sufficient evidence that these guys are
transporters of this molecule.
So they are transporters.
That was kind of, well, easy to convince people
after these set of experiments.
But there is this more important thing.
Is it really that the polar localization
of the transporter, so the fact that they
are on one side of the cell, is that determining
the directionality of the flow?
That was a much more difficult thing.
At that time, pin proteins were also
the only proteins in plants showing
these polar localization.
And then I used Tina, that's post-doc from Poland,
came to my lab, and she wanted to solve the problem.
And she said, well, I have this idea how to do it.
And she said, if we will have a pin on one side of the cell,
we will put oxen, and we will see
how the radioactivity flows.
And then we will put pin on the opposite side of the cell,
like here, and then we will put radioactivity labeled oxen,
and we will see whether it goes in the opposite direction.
If yes, we demonstrated that polarity of the protein
at the cellular level makes the directionality of the flow.
Well, it was a brilliant idea.
What I didn't know how she wanted to do
and what she didn't know how she wants to do
is how to put a pin protein from one side of the cell
to the other side of the cell.
That's not entirely trivial, as you can imagine.
But we solved it.
And the set of experiments, I know, sun is shining
and it's boring, but just time is going.
Give me a chance.
So well, we just thought, if we want
to change the polarity of the pin proteins,
we first need to understand what is deciding
to which side of the cell the pin proteins are going.
And so we just thought, will it be the cell,
or will it be the pin protein itself?
So we took different pin proteins
and put them in the same cell type.
So this is the epidermis cells of the root.
Doesn't matter.
It's just the one cell type in the root.
And then we put pin two there.
And pin two goes up on the upper side of the cell.
And then in the same cell type, we put pin one.
And pin one goes down in the cell.
So that means it's the same cell type,
two different proteins that are very similar,
but not completely identical.
And one goes up and other goes down.
Well, the conclusion is that there
must be something in the protein that is saying,
I am pin one.
I am going down.
Or I am pin two.
I need to go up.
Something where the machinery in the cell will recognize
and accordingly will put the protein on one or other side.
That was already good, because that
meant there are signals in the amino acid
sequence of the protein that remind the polarity.
And so if there are signals within the sequence,
you can just play a lottery and try
to mutate the protein piece by piece
and look what happens with the polarity.
And so we were lucky.
And we got a mutant version of the pin one that went up.
So here we mutated the signal.
It wasn't recognized.
And the protein was mis-sorted to the opposite side
of the cell.
And now we have the situation Eustina
wanted from the very beginning.
We have pin one.
Epidermy cells, epidermy cells.
Once it's down, once it's up.
And now you can test how the auxin flows
in these two different lines.
And so looking at the auxin flow,
if you don't want to use radioactivity,
and the ladies like to use radioactivity even less
than the boys.
So Eustina used this auxin activity reporter.
I'm sorry, guys.
OK.
And so you can gravistimulate the root, as you see here.
And in normal situation, when you put the root like that,
the auxin flux will be redirected to the lower side.
And you have auxin accumulation at the lower side of the root.
Gosh.
Nobody having a laser pointer would really help.
Last chance, no.
OK.
So now we put the pin one on the opposite side.
In the same cells, we do the gravistimulation.
No auxin flow.
No signal at the lower side of the root.
Right?
And then, ah, fantastic.
Thank you very much.
OK.
Feels much better.
So we put pin one on this side.
And there is no flow, no activity.
And now we have the mutated version, which
will put it on the opposite side.
We put the root.
And we have the flux.
And we have the accumulation.
No difference between these two lines.
Only one mutation in the pin one.
That changes the polarity.
And that is enough to change the direction of auxin flow.
And so that was the experiment that
can be summarized on one slide and took
Justyna five years of hard work.
But the important thing is that now we really
have the connection.
We know that whatever signal in the plant
will put a pin protein on the different side of cell.
That will redirect auxin fluxes.
And that will change auxin gradients.
And that has the potential to change the plant development.
And so then, from these experiments,
also our work on the cell polarity in plants
then started.
I will not have the time to talk about that.
But there is a lot of work going
in this direction of cell biology.
So we have these pin proteins.
They mediate auxin fluxes.
And the polarity of the protein determines
where the auxin will flow.
So we have these taxis as the media people
like to say bringing auxin in the different parts of the plant
depending, well, how the wheel is turned.
So and let's now have a look at a few kind of examples
how these fluxes of the signaling molecule
can then change or regulate plant development.
So I will start with embryogenesis.
Well, plants do have embryos.
Be aware of that.
Next time, eating peanuts, think about it.
Oh, yes.
I can do two of them at the same time.
Thank you very much.
OK.
So the main model plant we are working with
is called Arabidopsis thaliana.
It's a small weed.
In our village, it grows mainly in the cemetery.
Well, what can you do?
And so you can find it basically in all these places.
It's small.
It grows fast.
It gives a lot of seeds.
It has a small genomic sequence.
And there is a lot of tools generated by the community.
So it goes really.
You can do many things here, which
you can't do in other plant species.
And that's the Arabidopsis embryogenesis,
which is kind of typical for the Dicotyla edon plants.
So after the zygote division, you
get specification of the small apical cell.
That is the moment when the embryo will know where it's up.
OK, then there will be some divisions.
And then comes the moment when the embryo will
learn where it's down.
And that is the moment when this cell will
change its behavior, its fate, and will
become a founder of the future root.
And that's the moment when the basal end of the apical basal
axis is specified.
And later, you start to generate embryonic leaves.
And that is then the germinated seedling
with a root coming from that and the leaves
coming from those ears.
So that's basically the key moments
in plant embryogenesis.
So the formation of the apical basal axis
and formation of the first pair of leaves of the organs.
And now if you look at auxin, so that is divided zygote.
The auxin is again shown by the activity of the reporter.
I'm really sorry, but zygote is small.
And there is not too much auxin.
But it is clear that already quickly after the division,
you get more auxin in the apical cell.
So this is the cell that gets re-specified and changes
its behavior, right?
Later, at the moment when these cells
needs to get re-specified and become a root, founder cell,
auxin will all of the sudden start to accumulate in this cell.
So there is a coincidence between presence of auxin
in a given cell and the change of the developmental fate
during embryogenesis.
So how auxin gets there?
And then if you look at the different pin proteins,
you will find that one of them, pin 7,
is localized exactly correctly to bring auxin
from the mother to the apical part
and let it accumulate there.
And then later in the embryogenesis,
something very strange happens.
The other pin protein that till that time was not localized
strictly on one side, gets localized on one side.
And that will start to push auxin here.
And that's the accumulation what you see.
So if we try to make the sequence of events,
first you have a flux by pin 7 up.
That makes the upper end.
Then you have polarization of pin 1 down.
That makes the flux down.
And that makes the lower end of the axis.
So schematically with the nice arrows, you have it here.
Didn't do anything?
Right.
Is that really doing the apical basal axis?
Well, if you remove the activity of the pin transporters
in the mutant, so that is the early embryo.
Normally, this upper cell should divide like that.
Here you see the nuclei.
That would be the division.
And that would be the sign that the upper cell knows,
I am upper cell, and I should behave like upper cell.
In pin 7, that doesn't happen.
The division goes like that.
And this cell didn't learn that it's
the uppermost cell of the embryo.
And then later on, you see that the border between apical
and the basal structure is kind of smeary.
It's not as clear as you have in the wild-type embryogenesis.
If you remove activity of all the pin proteins that
are expressed at this stage of embryogenesis,
you get these balls.
The cells will just divide.
And they will not know where is up and where is down.
They will not start to make the structures along the apical basal
axis, because the flux of oxygen cannot get polarized.
And the plant will never make apical basal polarity,
and will stay like a ball.
So that basically showed how the transport makes the gradients
and how the changes in pin polarity
will redirect the fluxes for specifying
and the right moment, the right cells
to convince them to start to do what they should do.
So what about organs?
That was apical basal axis.
But then you go into the formation of organs.
The first moment of organ formation
is at the later stage of embryogenesis,
and that is where the leaves will be.
And again, you see, before the leaves will start to form,
you see the oxygen activity there.
And if you remove the pin proteins,
the oxygen activity will be not there,
and the leaves will not form.
They will be fused.
They will be aberrant numbers.
It will not work.
So it looks like not only apical basal axis,
but also the embryonic leaf formation.
Again, pin pushing the oxygen in the right places,
the cells being specified to become
a founder cells for the organ, and that all goes.
If the pins are not there, it doesn't go,
and you don't have the organs, as they should be.
Well, days and days later, the same point,
all the organs that are formed post-embryonically,
like lateral roots.
Again, the first cell that will make the root
will have oxygen activity.
And there will be pin proteins necessary to do that.
Shoot apiclamoristem.
I showed you already this picture.
This will be the cell where the pin will bring oxygen
to convince this cell, you are the cell,
to make a new leaf or flower.
And if it's not there, as in the pin mutant,
there will be no organ formation.
So basically, not to bore you with all
the organogenic processes of plants, all the organs.
If you go out and you see all the leaves, all the flowers,
everything on the plants around, all these organs
started as a cells accumulating oxygen.
And the oxygen was giving the signal
that the organs should form at that time at a given place.
And so that's one of the things which
became clear in the last few years.
And there is this universal way how all the organs are
formed in plants.
And that's the local oxygen accumulation
made by the transport using the pin proteins.
OK, so that's about making axes, making organs,
making the plant as it should be.
But that doesn't really involve yet the integration
of the signals from outside.
And that's where we move now.
So we will go to these plant movements.
And as Darwin got fascinated, it is indeed
an interesting phenomenon.
The shoot will always know where is up.
The root will always know where is down.
Well, the root will be able to seek water.
There is the hydrotropism.
The leaves will turn to the light.
The young leaves will bend towards the light.
I mean, all these changes based on the external signals.
And so what about tropisms?
That's how these movements are called.
And oxygen accumulation and pin proteins.
So basically, for the phototropism,
that's how Darwin started.
It was known pretty early that there
is an asymmetric oxygen distribution,
or asymmetric distribution of oxygen activity.
And there were quarrels.
What is the cause of this asymmetric oxygen distribution?
For the phototropism, there were theories
that the light will chemically destroy oxygen
in the illuminated side.
And that will leave higher oxygen levels in the shaded side.
There are all these nice theories that would work,
but that were not correct.
That happens.
You can have a wonderful theory fitting all the data,
but it can be still wrong.
So be careful about your theories.
I'm sorry.
That's just my pedagogical genes.
So that's the phototropically responding
shoot of Arabidopsis.
That's the asymmetric distribution.
Well, we know that if we inhibit oxygen transport,
the asymmetric distribution will not happen,
and the bending will not happen.
So it's, again, transport-dependent
redistribution.
If it's transport-dependent, we strongly
believe it's spin-dependent, because these
are the guys that are transporting
oxygen-between cells.
And so if you start to look at the different mutants,
meaning plants having switched off function
of different transporters, at some point
you will find a plant that doesn't
like to respond to light so well as the wild type does.
So this is a normal response, and that's
the inhibited response of the mutant.
Then you look where the protein is localized,
and you find out it's, again, a polar localization,
but this time on the lateral side of the cells.
And that is the lateral oxygen redistribution that you need.
So you seem to find found the right one.
And so everything is fine.
We have this pin 3.
The pin 3 will pump oxygen in this direction.
It will make this asymmetry when the light is
coming from that side.
And the asymmetry will promote growth only on this side,
and that will make the bending.
More growth on one side, less growth on other side bending.
Well, yes, that's wonderful.
But there is this one extremely important link missing.
And the link that is missing is how this pin knows
that if the light is coming from here,
that it should pump in the opposite side
to make the asymmetry.
Why it doesn't pump in that side?
So in other words, how the directionality of the light
or of the signal from outside is able,
is translated into the directionality of the oxygen
fluxes in the plant.
And so we found this phenomenon, pin 3, that was 2000, 2001.
And for the phototropism, it took us nine years
till we kind of got a clue how it works.
So I will go to that later.
But first, we got an idea how it might
work from the gravitropism.
So the root growing down.
The gravity is perceived in plants
by sedimentation of a heavy organelles,
so-called statolids.
And this happens in the root cap.
That's in the tip of the root.
And pin 3, the guy that is important for this response,
is also in the same cells.
And it's not polar.
It's on all sides.
And now you turn the root.
So again, you make the gravity stimulation.
And you start to look.
And you count time.
And after five minutes, roughly, you
will start to see asymmetry.
So the localization of the pin protein
change in response to gravity.
And this will probably redirect the flow
to the lower side of the root.
So if we show it schematically, the oxygen is coming from here.
Here are the statolids sedimenting in the cell.
That will bring pin 3 to the lower side of these cells.
And that will redirect the flux to the lower side of the root.
There will be more oxygen accumulating here.
It will inhibit growth in the root.
And that will make the band.
So the external signal is translated
into the redirection of the fluxes
in the way that the transporter's localization
in the cell is changed.
Basically, you move the transporter
to the right side of the cell, depending on the signal.
And that makes the rest.
Well, it didn't solve it completely
because we still have to solve how sedimentation of statolids
is bringing the pin 3 to the one side of the cell.
But we made the farther step.
We know that we can translate the signal from outside
into the developmental response by changing
polar localization of the transporters.
And now, meanwhile, we have also a good clue
how it happens that the statolids can
bring pin on one side.
So and now to the light.
Now, when we know the concept and we
manage to develop tools to visualize the pin protein
correctly, so we are back in this hypothesis.
Structure that is bending towards the light.
This is, again, the pin 3 protein in green.
And that is the moment when we took the plant out of dark.
And we put light from that direction.
If you have trained eyes, which you don't,
but imagine you have, you will see
that this signal is getting much weaker than originally
the signal was there.
You know, during the time that signal is getting weaker,
that's the signal on the side where light comes from.
And the signal on the other side, on the shaded side,
doesn't become weaker.
So again, you generate the asymmetry
in the position of the transporters.
And that will redirect the flow to the shaded side.
And that will make the asymmetric coxin distribution.
And that will make the bending.
And now we also know which light receptor
is responsible for that and how the light receptor is actually
doing it.
Because the light receptor is activated only on this side
and downregulate the activity of a kinase that
is regulating pin localization.
And that makes this change.
So we have now the whole cascade of the old Darwin story.
How light through transcriptional repression
of the regulators through change of pins relocalization
make the redirection of the flux and make the bending.
So and now the complex slide.
And still I try to simplify it.
So basically on the examples I showed you,
we saw these auxin gradients.
That was the first important information
that we have this asymmetric auxin distribution.
And for all these gradients, we can
find the pin proteins being localized
in the proper positions to make it,
to make these distributions here and here.
And then, so you can imagine, you
have like this network of the taxes in the whole plant.
And now depending what signal you get,
you will be bringing auxin to the given destinations.
And the cells that we'll be getting this auxin
will make the switch in developmental program.
So if you will still remember what
I told you at the beginning, which I doubt,
but let's remind you.
So auxin is doing too many things.
Embryogenesis, organogenesis, phototropism, gravitropism,
fruit formation.
I don't know what.
But no, actually auxin is doing only one thing.
Auxin is just coming and saying, now you are the cell.
That's the time.
And you will do it.
And the cell has already pre-programmed what kind
of change of fate she should do.
So meaning this cell knows I'm the cell in the shoot apical
meristem.
I can do leave if I get auxin kicking my ass, saying,
now you do the leave.
The cell, which I didn't put here
because there was not enough space, in the root
will know I am able to do the lateral root.
But there will be 100 cells able to do the lateral root.
And the one which will do it is the one
which will get the kick off from the auxin.
So auxin is basically saying, you now do, but not what.
That is already pre-programmed.
The transcriptional network in the different cell types
is already ready for the change.
So that's the one important thing.
But there is this additional layer to that.
And this is that the signals from outside.
And I put now on the left side because, well,
sun is shining and you don't want
to spend more than 45 minutes with me.
So I just put with the papers the signals which
we were able to show that there are influencing activity
or localization of pin proteins.
Like I mentioned, the gravity, light,
and the developmental context in the embryogenesis,
I will not go into that.
Feedback regulation by auxin itself.
So all these different signals, when
the cell is able to perceive them and respond to them,
get integrated into this taxi network.
All the taxis will start in the given street,
drive away from the light, or they
will start to drive down into the tunnels
when the street has the tunnel.
So basically, that's how the signals get integrated.
And these changes in the global distribution pattern
will then modulate the development accordingly.
So that is the concept.
How can plants basically adapt to different changes
by making more or less organs grow more or grow less,
bend to the light, go direction gravity, and so on.
And basically, now in the last four or five years,
the main aim of the group is to understand
the mechanisms within the cells,
how these different signals are integrated
into the changes of the localization,
how the localization is regulated
to the different side of the cells and these things.
I mean, more cell biological questions
that are still in plants, largely unexplored.
And so I hope using the financial boost
from the Kerberstiftung, I can give you
more exciting results in a few years.
So that's a big thanks to the group,
because without them, it wouldn't be possible.
I made my thanks to Kerber and Hamburg University.
So my thanks that you are not at Lanzarote, but here.
Thank you for coming.
Thank you for attention.