How random is evolution? - Kevin Verstrepen at TEDxFlanders

How random is evolution? This video offers us novel insights in genetics, and how they fit into Darwin's theory. In it, Kevin Verstrepen explains how Lamarckian-like evolution might work and improve evolution theory as a whole.

Alright!

This is a sciene talk,
so please block the exits,

keep people from escaping
and we'll see where we'll end up.

My talk is about evolution and lots of things
have been said about evolution,

lots of things have been done.

I want to make one disclaimer:

I've only been given two and a half hours
to talk about this by the organisers,

so I have to give a short introduction
to some aspects -- to a summary of evolution.

I'm going to skip over things,
going to simplify things,

and you're going to
have to live with it.

But the points I'm making
will hopefully make some sense.

Evolution: everybody knows the theory

or thinks that they know it.

It's a work in progress;
that's very important.

There's many things we understand.

There's many facts
that tell us evolution is right.

There's not a single scientist

that really works
by scientific methods,

that looks at facts and uses theories
that doubts the theory of evolution.

That does not mean that the theory of evolution
is there, that it's not changing.

We always discover more
and we need to adapt our theory.

It's very important.
Some people think

that because we sometimes
discover something

and we need to make
slight changes to our theory

that the theory is not valid.

And instead they come up with a theory
for which there is no proof at all

and they think that's
a much better option.

I don't think so.

Alright!
Let's start with this guy.

As you can tell,
very fashionable: French.

Jean-Baptiste Lamarck.

He was one of the first people to come up
with a coherent theory of evolution.

He's done many more things,
but his theory is quite extraordinary.

And one of the aspects
of his theory is that

he believed in the inheritence
of acquired characteristics.

What does he mean by that is

that, well,
look at these giraffes.

It's a very easy way to explain
this idea by Lamarck.

Everybody knows that a giraffe
has got a remarkably long neck.

How does it get the long neck?
Well --

it's trying to eat leaves on the tree.

And it stretches it's neck.

And therefore the little kiddy giraffes
will have slightly longer necks.

And again this repeats, and that's how
the giraffe got a long neck.

Seems a bit silly to us
but it's actually a great idea.

He was going with
the data he had.

Wonderful theory,
except it's not right.

In came Darwin.

And enough has been said
and done about Darwin

over the last year especially.

He's been great.

One of the things that he did is

he introduced two key concepts

namely variation and selection.

And with variation he just said:

Well, these giraffes
don't stretch their neck

-- well maybe they do, but they are born
with short and longer necks.

There's just this natural variation
amongst giraffes.

And the lucky ones that have the long necks,
can reach more leaves.

And as you know, you only think about sex
after you're not hungry anymore,

so --
(Laughter)

they're going to reproduce because
they're not hungry anymore.

They're going to get little giraffes
with slightly longer necks

and that's how evolution happens.

So, this is the selection part

and then there's natural variation.

He didn't really say how
the natural variation occured,

he didn't really have
answers to that.

He thought about it a lot.

But he really separated
the two processes.

This is also
what made him so controversial,

because it was very cruel,

it's a very cruel way
of having evolution.

There's giraffes dying.

There's poor giraffes
with short necks dying here.

Alright!

And this fellow here looks very stern.

He's German.
(Laughter)

August Weissmann,
great great biologist.

He really -- one of the things he did

is really try to proof
that variation and selection

are completely independent.

And one way he did this

-- so he really sort of tried to kill
the old idea by Lamarck

that the length of the neck of the giraffe
has really nothing to do

with what it did in its lifetime

and its stretching out for trees.

So one of the things he did

-- he's really very famous
for this experiment,

although it's not
his best experiment --

he took mice
as soon as they were born,

cut off the tail
then bred more mice

as soon as the little mice were born

cut off the tail again
and just repeated this.

And in the end
what he noticed was

that all these new mice,
these little mice,

even after he's done this
for 30 generations

still had tails that were just as long
as the original mice.

So it's a great way of disproving Lamarck.

I would say, he should have relaxed,
sit back,

thought about looking
at the Jewish male population

and we wouldn't even had to do
his experiment. (Laughter)

So, he came up with a, I think,
much more important finding, though.

And really amazing work that he did.

Where he actually said that,

even early in our lives,
and I'm talking about embryo's,

what he called our germ cells,

these are the cells
that are used to reproduce,

are separated from
the rest of the embryo.

You can see them here
as little dots.

And they separate and we all know
where they end up in the end.

And the strong point in that --

he was totally right about this --

and the strong point about this is that --

pretty much what he was saying is --

when the giraffe stretches its neck,
it's not stretching its testicles.

So how can this have
any effect on your germ cells.

It's a very strong point, then again,

at least for complex organisms,

he set apart variation and selection.

The forces that will select you

are independent
of this variation that you have.

Again a bit later

these two fine gentlemen here,
Luria and Delbrück,

were working in Cold Spring Harbor in the U.S.

where they were doing
multiple amazing experiments

and one of them
got them the Nobel Prize.

And they were working on
this virus here,

which looks a bit like a Moon lander

but it's a little bit smaller than it.

It's called a bacteriophage.

This is good news for all of you.

All of you non-scientists might not realize

that these bacteria that make us sick

they actually also get sick,
they also have virus infections.

The only organisms
that gets away without being sick

are the viruses themselves.

But so, bacteria do get virus infections

and they actually die from it

and that's what these guys were studying.

And they also wanted to
look at this idea:

is variation independent of selection.

And they came up with
a very smart experiment.

What they did is, they said, "Well, let's start
from one bacterial cell.

And let's give it lot of food
so it will make lots of little bacteria."

And they always divide as you know,

bacteria they grow or they multiply
by just dividing themselves into two

and they make clones of themselves,

genetically identical,
and so this is what happens.

And they said --

so these are the bacteria here,
always dividing --

and they said, "Well, at some point
we're going to introduce a virus

and we're going to see what happens."

Because they've noted that when you introduce
a virus to lots of bacteria

there's always a few bacteria
that manage to survive.

They are genetically, because
their little children bacteria are also surviving,

so it's clearly a genetic trait

something has happened to their DNA,
to their genetic material.

So something has happened.

Some of these bacteria are resistant.

And now the question is --

this variation, because that's what it is,

does it occur before the bacteria
are ever in contact with the virus?

Or is it when we infect this culture,

this hundred of millions of cells,

that suddenly a few manage
to become resistant?

It's a very interesting question.

And they were very smart.

They said, "Well, supose there is a mechanism

by which, when you infect
the bacteria with the virus,

it tries to become resistant some way.

There's a mechanism.

Then, if you do this to
a hundred million cells,

and you do it a few times
to a hundred million cells,

you sort of expect
that a similar number of bacteria

will always become resistant

that manage to get there, right?
The lucky few.

Whereas, suppose that some bacteria
become resistant

while they're multiplying
-- the blue dots here --,

You can have vastly diferent numbers
when you repeat this experiment.

Because, what can happen is:

here we have a bacterium
that becomes resistant to the virus

very late in the reproduction.

And there's only one
in this whole population

that's resistant,
that's not killed by the virus.

Here though, you have
what is called a jackpot event,

and the name comes exactly
from what you think it comes from.

Very early in the reproduction
of this first cell here

one of two kids becomes --

or maybe the parent becomes resistant

and it starts dividing.
And now half of your culture --

but we're talking millions
of cells here -- are resistant.

So you have this huge variation.

So they've done the experiment

and what they found was this.

And so they concluded:

Clearly -- and they've shown this matematically --

clearly some bacteria in this population

were resistant to a virus
that they've never seen before.

And again, variation must be
independent of selection.

Now, I would claim,
and other people have claimed,

that the experiment does contain
a pretty serious flaw.

And I'm not saying that they
didn't deserve the Nobel Prize,

at all, they definitely deserved it.

But one problem with their experiment is clearly

that, well, they introduce a deadly virus

maybe the bacteria have a mechanism
to develop resistance

or tolerance to this virus,

but not to one
that kills them instantaneously.

Maybe they should have used
some milder stress,

some milder selection.

So that's the problem there.

And then of course, later

after Watson and Crick
and Rosalind Franklin here

discovered the structure of DNA

and the whole molecular research
started taking off

we sort of put everything together
of the evolution theory

into what is called 'the new synthesis'.

And that's sort of our
current theory of evolution

where you have changes in the DNA code

that are more or less random,

they are independent of selection

and they give you diferences,

that's what's causing all
these differences between us

and that's why some of us cannot get AIDS
and most of us can.

Which is true, by the way.

And so this is pretty much our theory.

Now, I don't want to end here.

What we've seen is that

more and more evidence is emerging that

the story is a bit more complex.

And maybe variation and selection

are not so completely independent
as some people believed.

And I got to know about this

while studying this year

I did my PHD in a beer brewing lab.

You know, it's one of the better places

to start your research as a student.

And I was stuying yeast cells,

great genetic model organism by the way,

so actually one of the frustrations I have

is, try to be taking seriously
by the people who need to fund you

or at the conference,
when you're working on beer.

And you go like, "Trust me, I'm doing
real serious genetic experimenting."

Alright, so one of the things
I was studying is

yeast cells that are clumping together.

It's called flocculation.

So what you see here
is a bunch of yeast cells

that stick to each other and they settle out
in this in this culture here.

This is important for beer because
it happens at the end of fermentation.

This is what pretty much makes
the difference between a clear beer,

that doesn't have
any yeast cells in it,

and what we call
a 'witbier' or a 'weizenbier'

that has yeast cells
still floating around in it.

And we were trying
to find the genetics of this.

What we found is this one gene here

flow one,
which stands for flocculation one.

It's a gene,
and what is so special about this gene

is that it contains a middle part

that is extremely unstable.

So this gene is of course
made of DNA, like any gene.

And the middle part of the DNA
is extremely unstable.

It changes much more
than any other DNA.

And what it is in particular

is that it contains these things
which are called 'tandem repeats'.

It's pretty much a piece of DNA
that's repeated time and time again.

It's much longer than what you see here
but you get the basic idea.

And what makes it unstable is

that the number of these repeats
changes very quickly.

Every time the DNA is copied

you have a pretty high chance that the number
will be different from what it was.

This has been known for a long time

except people don't really expected
too much within genes.

Usually you find these
tandem repeats outside of genes.

But here and in some other
genes you find this.

So, what you have here
is a piece of DNA

or a particular gene that's changing
more rapidly than other genes.

And in this case it means
that flocculation is changing,

so this characteristic of the yeast,
this specific thing,

compare it to a long neck,
if you will,

is changing more rapidly
than some other properties of the yeast.

Now if you think that this is

-- well, this doesn't matter --

if you think that this is specific
for yeast cells you are wrong.

Pretty much around the same time
we were publishing our story,

there was a great story
published about dogs.

And I don't know
if you've thought about this

but dogs are some of
the most variable creatures

on the face of the Earth.

Especially when it comes to their shape.

Just look at, you know,

this Chihuahua and this St. Bernard here.

They're the same species.

In principle.
And I say 'in principle.'

These things can breed.

You just hope that the Chihuahua
is not a female.

(Laughter)

Now, these are bred by humans.

We have made these dogs
by selection and whatever.

But we didn't even use so much time for it.

And in evolutionary terms
these things are new.

They are brand new
and they were, sort of --

they developed in a very short time.

And one of the things that was found

is that one of the key regulators that regulates --

and again I'm talking about the gene --

it's a regulating gene and it regulates
the shape of the skull.

Basically the shape of the dog as well.

And it also has this
unstable tandem repeats in it.

And what these researchers found is

that there's a nice correlation between

how many repeats you have in this gene

and how curved your snout is

or how long your snout is.

And they also found that some
other changes in another regulatory gene

give you a sixth finger.

Sort of this little extra thumb here.

And, I didn't know this
but this is a characteristic

of a specific breed of Great Dane dogs.

And that's why this actually happened.

It sort of happened in a very short time

and now people see
this sixt claw, if you will,

as a characteristic.

So clearly it's not just happening in yeast.

And there's more.

One of the other things that people
have known for a while

and we are also researching

is that the end of chromosomes

-- chromosomes are basically packages of DNA,

that's how our DNA sits in the cell --

well, the ends of chromosomes -- here,

the very ends --
they change much more quickly.

There's higher mutation rates.

The DNA is not as stable.

And so the genes that lie there,
again, evolve.

And if you're wondering in humans
which genes are lying there.

It's the genes that, for example,

the genes that make us smell.

And of course we have to recognize
lots of different smells

and these genes are copying themselves

and they are changing very quickly.

In plants: a whole different mechanism.

And this is a bit more complicated.

I will try to fly through it.

There's this particular protein.

And, this is a bit like your mother.

This protein is the mother of the cell.

It sort of checks
all the other little proteins

and it goes like, "Are you okay?

You don't look very good.
Here, here's your coat.

You should behave this way,
don't behave that way."

It's sort of like a teacher mother.

And, so the protein really takes care

that even if there's small mutations,

changes in other proteins,
that they still behave right.

And if they don't behave right,
they get degraded.

Now what you see is that,
in times of stress

-- and plants also have stress,

stress is a biological word for selection.

It means you're not adapted to a condition.

It means that you feel the burden of evolution

pressing down on you, pretty much.

So, in times of stress, this protein,
this function of the mother protein,

gets dialed down a little bit.

And suddenly these plants start disbehaving.

You know, they become weird.

And that's because some mutations
that you previously couldn't see

now suddenly emerge.

And, although it's not proven,
it seems like a likely theory

that maybe this could serve as a mechanism

to try and escape the stress.

Because suddenly it's good to
try and be different

from what your mother was.

And so maybe a few of these plants

are better at surviving the stress.

And they will cope.
And maybe this mutation can get fixed.

And this and that.

Another thing, another example
comes from bacteria.

And I'm just skimming over it again,

but bacteria -- in times of stress, again

they activate --
and this is just to impress you

it's not very important --
in times of stress

what they do is, they activate
a different protein to copy their DNA.

And of course a protein to copy your DNA
is a very important protein.

Because it shouldn't make
too many mistakes.

Because that's how you get changes in DNA

and that's how you get natural variation.

So you need a little bit of them
but you don't want to much of them

because most of the variation is not good.

It wouldn't be so great if a giraffe
got a neck that was three times as long

because the heart couldn't cope with it.

But in times of stress, again

it's obvious sometimes you need to chose
between dying or gambling.

And bacteria may be gambling.

They activate this gene that's very sloppy.

And so the DNA gets copied,
but it has lots more changes in it.

And maybe,
although it's hard to prove it,

maybe this is a strategy of bacteria
to try and beat the selection,

the evolutionary pressure
that's pushing down on them.

An even nicer example,
I think, is the waterflea here.

Again, it's pretty mysterious still.

But waterfleas, swimming around,
beautiful organisms,

they have predators.
And when they get -- you know,

there's a family of waterfleas
and dad gets eaten,

there's some chemicals released in the water

and it induces the formation of the stickle here,
which is called a 'spina'.

And the stickle makes the waterflea
a little bit less attractive for predators.

Now that's all great,
thats not so special

a chemical induces
some morphological change.

The weird thing is that the kids
of this waterflea will also have the spina.

Even if they've never seen a predator.

Even if you take all the predators away.

They will still have this for quite a while,

for a few generations.

So this comes very close to Lamarck, right?

There is something happening
in the course of the life of this organism.

It changes something and it's giving
that information to its kids.

It's getting pretty close to Lamarck.

So, this is, the conclusion of the talk
-- and this is important --

does this mean that our theory of evolution
really needs a major overhaul?

I would say: not at all.

And, people have often misunderstood

I guess the things I have said and published.

And it happened recently in this Flemish,
or Dutch, magazine here, where I wrote a piece

telling, or writing about the same things
that I'm telling you now.

And this is the cover they came up with.

I wasn't so happy because it looks like
I'm sort of sawing the ground under Darwin.

No.

Here, this is what Darwin wrote literally

about variation and selection.

He says, pretty much he says,

I have spoken as if this natural variation
was totally random in my book.

Like it was just pure chance.

But of course I didn't mean to imply that.

It just means that I don't really
know what's happening.

And maybe there is a mechanism
It's much more complex.

Darwin was extremely clever.
He thought about his theory.

He knew exactly where the holes were

and where he shouldn't really speak
for one possibility or the other.

So he actually incorporated --

it's only later that maybe we've gone
a bit too far away from Lamarck.

He didn't really dislike
Lamarck's theory that much.

Although, this is not to say
that Lamarck's theory was right.

I mean,
I still think that it's mostly random

but there's some small changes
here and there

that make it a little less random
than completely random.

So, what I'm saying is that
through evolution, mechanisms

have developed that make evolution
not a complete chance.

And then you might start wondering

how can this be right.

And there I would argue this just happens
through the process of evolution.

Suppose a gene becomes very unstable

and it's a housekeeping gene

it's a gene that doesn't need to change.

Or it doesn't need to change as quickly.

Or when it changes
it's mostly detrimental.

Now, if such a gene becomes unstable

it's going to be a huge disadvantage
for the organism that has it.

And so it will be selected away.

However, if a gene

for example, a gene that makes
your skull a bit more flexible,

like in a giraffe,
and maybe you can, you know,

you get more giraffes with longer necks.

If such a gene arises, by pure chance --

and this is pure chance.

Maybe it becomes an advantage
for the organism and it stays there.

It stays unstable like it was.

And maybe that's
how these things have evolved.

Now again, like I said,
my work sometimes gets misinterpreted.

Sometimes it's quite funny.
Especially when it's the people

that believe in creationism
as a more intelligent design that take our work.

This was [one of] the more funny things.

This is a website called 'uncommon descent.'

And if you think about it, you know,

the title says it all. These people
don't believe in the common descent,

that's of course at core
of our evolution theory.

So we published a paper,

a coleague in the U.S. -- when I was
still working in the U.S. -- and I.

And we were, again in this paper, it's a more
in-depth discussion of what I'm telling you know,

and we were aware of the fact
that some people might misinterpret this.

So, in the abstract,
in the summary of the paper,

which is pretty much the thing
that everybody will read,

we wrote, specifically, that our ideas
do not go against Darwin.

And then these guys here read the article,

still wanted to use it for their ideas.

And they said, "Well, to publish this
in a reputed scientific journal

the authors needed to write something
that their ideas do not go against Darwin,

but they don't mean it.

It's just a secret handshake
to get into this good journal."

So that's the secret handshake here.

So luckily there was --

oh, then it becomes quite funny
because there's reactions on this forum

of people, and, well, I can barely
read it myself, but I'll try.

So this is one of the people
reacting to this, and he says --

they quote some of the parts
that we write in the paper --

and he says like:
"Error-prone DNA copying enzymes

produce bursts of
variability in times of stress.

These mechanisms seem to tune
the variability of a given characteristic

to match the variability of the selection."

That's something that we wrote.

And he says, "Gee, it almost seems
like a built-in response mechanism.

Who would've thunk. Darwin is sooo dead!"
That's what he writes.

Anyway, so there's some people
who did not misunderstand our paper

and they reacted to this.

And it's also fun to read this discussion

because then the 'intelligent design' people get on.

It's all one great family.

It's kind of fun to have this --
I really like these discussions.

I have nothing against people who come up
with different theories.

They're just wrong, but, you know,

it makes it fun to discuss with them.

Alright, this brings me
to the acknowledgements.

And I have to acknowledge
pretty much all these people here,

which are the people who are doing
all the hard working in my lab,

probably as we're speaking now
they're getting more results

so I can give another great talk
and, you know, be the hero for this audience.

They are chained to their benches.

I have to remember to feed them tonight.

But, they really are the heroes of the lab.

And there are many more of them, of course,

our group is definitely not
the only one doing this work.

For people who are scientists
and want to know more about this

these are some of the publications.

This is the major one, where we really
sort of discuss all these things.

There's more information on the website.

And this is very impotant as well,

these are the people that are paying us.

Well not me, but, more, the research.

Thanks.