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9. Evolution, Ecology and Behavior: The Evolution of Sex
Poziom:
Temat: Edukacja
Prof: Now before I get
going on today's lecture,
which is about the evolution of
sex,
I thought that I would just
share this picture with you,
which I took at ten o'clock on
Saturday morning.
These are the Hamden Golf
Course turkeys,
and they sometimes show up in
my backyard, and they're
absolutely remarkable creatures.
If you look at them,
probably the first thing that
strikes you is how do they make
those iridescent colors,
and is there a different way
perhaps that they make the color
in their neck,
or perhaps on their face?
Their neck is red and their
face is blue.
Is that biomechanically
different?
In fact, these colors are a
diffraction gradient.
There's no dye in them at all,
and the colors in the head,
the blue color,
is actually made by kind of a
fractal matrix of bubbles.
The red color I think is a dye.
So there's some weird stuff
going on in the way that turkeys
make colors.
Why the heck do these turkeys
look like this?
Well the standard explanation
for that,
which may or may not be
true--it hasn't been tested too
explicitly in turkeys,
although it has in pheasants
and in peacocks,
which are both related to
turkeys;
they're all in the family
gallinaceae--
is this is the product of
sexual selection,
and that what you're looking at
is what the female brain of the
turkey finds attractive.
Well there's a deep mystery in
that.
Why should something that a
female turkey thinks is
beautiful also elicit the
sensation of beauty in my brain?
I last shared a common ancestor
with a female turkey about 150
million years ago.
Has the perception of beauty
persisted unaltered in both
lineages for 150 million years?
So you see the contemplation of
turkeys in the snow can take you
a long way.
Now today I want to talk about
the evolution of sex,
which will eventually get us to
sexual selection in a bit over a
week.
And in so doing the messages
that I want to get across are
that this is first a fundamental
question in biology,
because it shapes almost
everything that we study in
biology.
Sex, in the sense that I'm
going to use it today,
in terms of organized diploid
sex, has been around probably
for about one and a half billion
years,
and it's had many,
many consequences.
There is a puzzle about sex,
and we will see that it is
complicated and costly,
and therefore it needs an
explanation.
I think it was the Marquis of
Chesterfield,
or someone like that,
who on advising his son on the
con--
on the issue of sex said,
"It doesn't last very long
and it's extremely
expensive."
>
And we will look at some of the
consequences of sexual
reproduction for large-scale
patterns in the plant and animal
kingdoms.
Now I need to set this up by
distinguishing between
recombination,
reproduction and gender,
because the word sex
often elicits in the minds of
non-biologists a composite of
all three things.
Recombination is the process
that causes offspring to differ
genetically from their parents
and from each other.
Now there are some exceptions
to this.
For example,
armadillos always have
identical quadruplets,
which makes them convenient for
some things.
Identical twins in humans,
of course,
are an exception,
where the recombination has
made them different from their
parents,
but they're still identical to
each other,
and that is because they derive
from an early mitotic event in
development;
so they were originally the
same zygote.
And then we have the
extravagance of polyembryonic
wasps where a parasitic wasp
lays a single egg into a
caterpillar;
the egg starts to develop into
a blastula;
the blastula fragments into
hundreds or even thousands of
pieces, each one of which then
develops into an embryonic wasp.
Some of those sister wasps
differentiate into warrior
castes and go cruising around
the caterpillar,
wiping out other wasps that may
have laid their eggs into the
caterpillar.
They don't make it,
they die, but they clear the
way for the others,
that then eat up the
caterpillar and hatch as wasps,
out of the caterpillar.
So there are always fascinating
biological exceptions to the
idea that recombination makes
siblings different from each
other.
In some cases they are not,
but normally they are.
Reproduction is not the same as
recombination,
and we can see comparatively,
through these contrasting
examples,
why it is that recombination
and reproduction are not always
necessarily coupled.
In us they are,
but if we look at bacteria and
clonal plants,
we can see that they can
reproduce without recombining.
And bacteria can actually
arrange to have sex and not
divide at all.
They can undergo a
recombination event and simply
change themselves genetically,
and then wait for awhile and
divide later.
And, of course,
in plants, clonal plants have
the option, many of them have
the option of either producing
asexually or sexually.
Often they produce sexually in
the parts of them that will then
disperse to another place,
and asexually in the parts of
them that will stay here;
here being more predictable
than there.
Gender is something that is
really not at all the same as
recombination or reproduction.
Gender is maleness and
femaleness.
So it's all of the secondary
sexual characteristics of the
two genders.
And that is something that
originated with the production
of gametes of different sizes.
That didn't happen until after
meiosis originated in evolution,
and it then created a situation
in which sexual selection could
occur;
where there was one kind of
selection on things that made
lots of small gametes--
sperm--and another kind of
selection that operated on
things that made a few large
gametes-- eggs.
So those are three different
things.
I also need a few words,
and I'll refresh your memory or
introduce them to,
depending on where you're
coming from.
Isogamy means that we're
dealing with a species in which
all of the gametes are the same
size.
That happens often in the
protists, in unicellular algae
and protozoa,
that they produce gametes of
the same size.
Anisogamy comes where there are
gametes in two different sizes,
the big ones being eggs and the
small ones being sperm.
So anisogamy is the condition
with which most of you are
familiar.
Syngamy means fusion of gametes
to form a zygote;
that is one step in the process
of sexual reproduction.
Karyogamy is fusion of the two
gametic haploid nuclei.
So the gametes come together,
and then after that happens
their nuclei fuse.
And these things take time.
We will see that those actually
are some of the--the time they
take is some of the cost of sex.
Now mating types occur at this
stage, with isogamous organisms,
and they reduce inbreeding.
Mating types are common in many
unicellular algae and in many
ciliates, like Paramecium.
They are basically a situation
where the organisms of one type
can only mate with organisms of
another type.
So if you are mating Type 1,
you can mate with mating Type 2
but not with mating Type 1.
This, in some sense,
is genetically analogous to
having a large number of sexes
in the population,
but with a rather interesting
pairing rule,
that you can only not mate with
people like yourself.
The population then
differentiates and evolution
produces a huge number of mating
types.
Now the traditional view on why
sex exists was formulated by
August Weismann and then
elaborated by Mueller,
and clarified by Crow and
Kimura, and it goes like this:
recombination is there in
nature basically because it
increases the rate of evolution,
and it does so in two ways.
It increases the rate at which
two advantageous mutations can
be brought together,
and it increases the rate at
which disadvantageous mutations
can be discarded;
and I'll illustrate that with a
few diagrams in a minute.
A consequence of this is that
it decreases the probability of
extinction.
All of that is true,
but it may not be why sex
exists.
So here is the traditional view.
In a large population,
if we contrast a large asexual
population with a large sexual
population,
you should think of the
vertical axis as being the
frequency of a mutation in the
population and the horizontal
axis as being time,
and A, B and C are beneficial
mutations that are arising at
different places in the genome.
They're not alleles with a
single locus.
They are three different genes
whose combination it would be
really cool to have,
because it's going to improve
reproductive success,
defend you against diseases and
so forth.
In the asexual population,
first A pops up and it takes
over the population because it's
advantageous.
Then C, which had occurred once
before but not in combination
with A, happens sequentially in
the same organism that's already
gotten A.
So in the asexual population
the advantageous mutations have
to happen one after another,
in a descendant lineage,
because there's no sex to bring
them together.
AC dies out because shortly
after it arose,
AB came along and AB was
preferential to AC,
and then eventually C arises in
an organism that already has A
and B,
and ABC takes over.
That's a process of clonal
interference.
In the sexual population these
mutations can be conceived of as
occurring at just about the same
time as they did in the asexual
population,
but they are rapidly brought
together by sex and
recombination,
and the combination ABC spreads
through the population much
earlier,
achieving fixation here rather
than here.
Now if we look in small
populations, the advantage of
sex is not nearly as great.
Can anybody tell me why?
You can see a picture there,
but can you interpret it in an
English sentence?
Why is it that in the small
population the advantage of sex
is not so great?
It still can be advantageous,
but it's not as great as it is
in the large population.
Student: You have less
animals.
Prof: Population's
smaller, yes.
Student: You have less
animals
for-->.
Prof: Somebody want to
help Brett out?
He's looking for a word.
Yes?
Student: Small
population, less genetic
variation.
Prof: There is less
genetic variation in the small
population.
Yes.
Why?
Student: It's a lower
population count,
>.
Prof: Where does
variation come from?
Student: Mutations.
Prof: Mutations. Yes.
You can think of the population
size, all those genomes out
there, as being a net that
catches mutations.
The smaller population is
catching fewer of them,
and therefore there are fewer
things that it could bring
together,
and therefore it takes a longer
time in the small population for
sex to become advantageous,
because it has to wait for that
mutation to come along.
In the large population,
it's there very quickly,
relatively quickly.
Okay, now about the costs of
sex.
In an isogamous organism the
costs are genome dilution,
the amount of time it takes to
have sex,
and the risk of predation,
of sexually transmitted
diseases and of the difficulty
of finding mates.
So let's step through those.
The cost of genome dilution
basically is that by engaging in
sex you've made a decision that
your offspring will only have
50% of your genes,
and it's going to have 50% of
somebody else's genes;
whereas if you were asexual it
would be 100% your genes.
Okay?
So that's what we mean by the
cost of genome dilution.
And I think that you can see,
if you work through it,
that this is indirectly also
the cost of having males.
You don't really need to have
males at all,
if you're asexual,
do you?
As a matter of fact,
we usually think of asexual
species as consisting only of
females, and the reason for that
is that they make eggs.
Okay?
Now you can look at yeast,
which can reproduce either
sexually or asexually,
and experimentally measure this
difference between one hour for
asexual reproduction and eight
hours for sexual reproduction.
So let's do a little mental
experiment here.
We start off a vat of beer,
and we seed it with one asexual
and one sexual yeast organism,
and they happily go to work
starting to make beer for us.
After one hour,
we have two of the asexual,
and we still just have one of
the sexual, don't we?
After two hours,
we have four of the asexual;
we still only have one sexual.
After three hours,
we have eight of the asexual;
we still only have one of the
sexual.
You get the idea.
That timing difference has an
enormous impact on the relative
fitness of the two types.
Just because it can reproduce
faster, the asexual type is
going to sweep through that
population and competitively
exclude the sexual type;
all other things being equal.
So we essentially end up with a
glass of beer that's produced
almost 99.999% by asexual yeast.
The other cost,
of course, is that if you have
to go find a mate and take time
to mate, you expose yourself to
being eaten by a predator.
In the process of mating,
any kind of disease that mate
has could jump into your body or
into your offspring.
It could be a selfish genetic
element that got into your
offspring, coming in through the
genome of your mate.
And it's pretty hard to find
mates at low population density,
which is why we find that
asexuality,
for example,
increases in frequency as we go
into the deep ocean.
And if you look at the
organisms that are specialized
on eating the carcasses of dead
whales,
which drop onto the ocean floor
infrequently and at great
distances from each other,
you discover that they have a
higher rate of being asexual,
or being simultaneous
hermaphrodites,
than do things that say live on
tropical reefs near the surface
at high population density.
Then if you have anisogamy,
in its simplest form,
the cost of males is a twofold
cost.
So if you're a female and you
have the option of being
asexual, and you're wondering,
"Should I be sexual?"
and you ask yourself,
"What's it's going to cost
me?",
basically if you count through
to the number of grandchildren
you have,
you'll have twice as many
grandchildren,
if you don't make any males--if
you only make daughters you'll
get twice as many--
through your female line,
bringing--
and this is because also the
genome dilution effect is coming
in.
Okay?
So anisogamy,
plus genome dilution,
gives you a twofold cost of
sex.
This word Acarophenax is
going to come up several times,
because it's a spectacularly
perverse mite,
and we all are interested in
spectacular perversion.
So Acarophenax is a mite that
has an extreme example of local
mate competition.
And has anybody already run
into this example?
Can you tell me what it is?
Mites, many mites,
not just Acarophenax,
lay their eggs into their
abdomen, where the eggs hatch
out inside the mother,
and the brothers then
impregnate their sisters,
inside the mother,
and the brothers die and the
sisters eat the mother.
That's pretty spectacularly
perverse.
The question is,
if you are the mother,
how many sons should you make
and how many daughters should
you make,
in order to get the maximum
number of grandchildren?
Okay?
And we will run through this
when we have the Sex Allocation
lecture next week,
but I just wonder if any of you
can anticipate that.
Here you are,
you're the mother mite.
You want to maximize the number
of your grandchildren.
You're not worried about
getting eaten,
because your kind have always
had that, that's just a normal
part of life.
The only issue that occupies
you is how many sons should you
make and how many daughters
should you make?
You're a little bit worried
about the lady next door and
what she might be doing.
Any idea?
Student: Only one son.
Prof: You only make one
son, and that's because that one
son can make enough sperm to
inseminate all of his sisters.
And if you made two sons,
you would have some sperm that
was going to waste,
and you could've used that egg
to make another daughter that
got inseminated.
That is, in fact,
the solution chosen by
Acarophenax and all such similar
mites;
one son, many daughters.
Now to go back to this slide,
just to remind you.
I've been telling you lots of
interesting natural history,
but the point of it that sex is
costly.
It takes time,
it dilutes your genome,
and if you are anisogamous it
costs you everything that's
involved in making sons,
who otherwise might be
irrelevant if it weren't for
whatever advantage they might
bring in with sex.
So the paradox of sex is
basically that's it regular,
complicated and costly.
And, as I indicated with the
example of the yeast in the
brewer's vat,
asex should rapidly take over
sexual populations.
Nevertheless,
when we look at the Tree of
Life,
we see that the majority of
organisms are sexual,
and even the ones that we think
of as being asexual,
like bacteria and viruses,
in fact have evolved something
like sex.
So it seems to be a good thing.
We've got this traditional
explanation that sex speeds up
evolution and reduces extinction
probability.
But it has a problem.
It is couched at the level of
the species or the group.
Okay?
And it's not strong enough to
maintain sex against the
invasion of asexual mutants.
The reason is that if you think
of it in terms of being good for
the species because it causes
the species to last a longer
time before it goes extinct,
well the generation times of
species are orders of magnitude
longer than the generation times
of individuals.
Vertebrate species last usually
one to ten million years.
Individuals last months to
years.
So about 10^(6 )difference in
how fast things happen at the
individual and the species
level.
So any individual
advantage--for example,
asex--could be multiplied
thousands or millions of times
before the group or the species
advantage of not going extinct
so frequently could take effect.
The individual advantage of
asex seems to be roughly twofold
each generation,
and that adds up to a big
difference over a lot of
generations.
So asexual mutants should
always be taking over.
But they don't.
Now before I go into the
solution to that problem,
I want to give you a little bit
of what we think is the
evolutionary sequence in matters
sexual.
In prokaryotes,
bacteria and archaea,
probably the repair of
ultraviolet damage to DNA was
very important.
Then mitosis originated and
eukaryotic cell division.
So once the eukaryote ancestor
formed, with the proper
cytoplasm and nucleus,
and we had multiple
chromosomes, mitosis originated.
We're back about probably 1.5
to 2 billion years here.
Then meiosis,
which is really a very,
very complicated symphonic
arrangement, originated by a
duplication and modification of
mitosis.
Then only after we had mitosis
did we get isogamous mating
types, and then we had the
evolution of anisogamy.
Now the evolution of anisogamy
is actually a big deal because
it is what eventually led to the
differences between males and
females.
So sexual selection only starts
to happen after we have things
that make gametes of different
sizes.
So the ideas about why that
happened are kind of
interesting, because they're
right at the origin of
male/female difference.
One of the ideas is that a
bigger egg would improve
offspring survival.
So some of the individuals in
the population,
in the isogamous population,
might be under selection to
produce bigger eggs,
because they could then have
babies that survive better.
They could also produce more
pheromones.
So they could advertise,
so those eggs could advertise
their presence better.
A bigger egg is a better
perfume factory.
So you should think of eggs as
being big, fat perfume
factories.
Okay?
Once this--and this is now
frequency dependent selection--
once some of the organisms
started to make bigger eggs,
the others, some of the others,
could decide,
"Oh, I don't need to make
a big egg and invest a lot of
energy in it because somebody
else is doing that for me;
instead I'll try to inseminate
lots of eggs."
And they got selected to make
sperm.
Okay?
So they made many small gametes
that could swim fast and were
good at detecting perfume.
That's one idea.
Another idea on anisogamy is
that those big eggs have got
cytoplasmic organelles,
and those cytoplasmic
organelles have got their own
independent genome in them,
that they had when they came in
as mitochondria or as
chloroplasts or as spindle
apparatus.
And you don't want to generate
a situation in which you have
competing cytoplasmic genomes,
because if you do,
you get an uncontrollable
evolution,
microevolutionary process going
on in the cytoplasm that can
cause the takeover of the
cytoplasm by a basically selfish
mitochondrion or a selfish
chloroplast.
There are, in fact,
mitochondrial cancers.
There are cases in which
mitochondria get out of hand and
you end up with cells that are
just packed wall to wall with
mitochondria.
You don't want that.
You want to have the cell to be
a relatively well regulated,
well biochemically balanced
environment.
So one of the consequences of
biparental inheritance,
where you are only getting your
organelles from one of the
parents,
normally the female,
is that you avoid conflicts.
Okay?
This may or may not have been
important at the origin of
anisogamy, but it is certainly
one of the reasons for its
maintenance.
And before I go into mutations
and parasites,
let's recall something that
August Weismann said back in
1892: "Sex has a huge
number of consequences."
It's been around for a long
time, and so when we try to
detect why sex originally
evolved,
we're dealing with a situation
in which the original reasons
are concealed by lots of layers
of adaptations that have built
up since then.
So we have to clearly
distinguish between causes and
consequences of sex.
But this is now very hard to do
because the original causes are
now covered up with so many of
the secondary consequences.
People have been repeatedly
fooled by confusing consequences
for causes.
In a sense I suppose the bottom
line on that slide is we
actually are in a position were
we can talk intelligently and we
can do science on the reasons
for the maintenance of sex,
but we have difficulty--and may
always have difficulty--
in identifying the real reasons
why sex originated,
because that happened a long
time ago,
in a different situation,
and it's had all kinds of
consequences.
Okay, so what kinds of forces
maintain recombination?
When Alex Kondrashov wrote a
paper about this about,
oh gosh, it's fifteen years ago
now,
he came up with forty-three,
and I'm only going to list a
few.
I'm only going to list the ones
that I think remain plausible
and can be demonstrated
experimentally or comparatively.
However, I want you to be aware
that if you decide to write a
paper on this,
and you want to know what are
all the reasons that people have
given for the origin and
maintenance of sex,
that the list is on the order
of forty or fifty hypotheses.
There are two important genetic
hypotheses.
One is repair and the other is
mutations, and in a sense
mutations really are an issue of
repair at the level of the
population.
And there are ecological
hypotheses.
Parasites and pathogens,
and the co-evolutionary problem
that they pose,
are accepted by many now as a
major reason why sex is
maintained in populations.
And it is also true that
recombination spreads risks and
hedges bets in ways that go
beyond the issue of whether your
children are going to be
infected by a particular
pathogen.
You can deal with all sorts of
ecological situations.
So you can think of the reasons
as falling into two general
categories: genetic and
ecological.
So back in prokaryotes,
a lot of repair mechanisms were
evolved, and they are
sophisticated.
They're still in operation;
they're readily studied in
microbiology laboratories.
DNA polymerase itself does
proofreading.
If a nucleotide has been
excised and is missing from the
sequence, then you can use the
complementary strand to patch it
in.
So that happens,
and that needs a
double-stranded DNA,
not a single-stranded RNA.
So if you're just dealing with
a single-stranded RNA virus,
it may very well have
difficulty doing this kind of
repair,
and has a very,
very high mutation rate.
I want you to remember whenever
I say mutation,
that it is often a problem of
inadequate repair.
So the repair mechanisms
actually control the mutation
rates.
In eukaryotes we have this kind
of proofreading,
and we've got a lot more.
There are some repair
mechanisms that actually need
diploidy.
So you have a whole extra
chromosome.
You have two double-stranded
DNA molecules,
and you can go to the alternate
as a backup.
So you can use that to repair
any mutational damage.
But the most interesting kind
is recombinational repair;
well let's put it this way,
to somebody who thinks at the
population level,
the most interesting kind is
recombinational repair,
and that is because it isolates
the defects on a subset of
gametes.
You can have mutations in five
or six genes.
Recombination could put them
all into one set of gametes,
and if those gametes die,
those mutations are gone.
So recombinational repair
isolates and throws away,
through natural selection,
the defects in the genome.
There is a concept here that I
want you all to absorb and
understand,
and it has to do with the way
that mutations will accumulate
in small populations that are
asexual.
And it's important because it
can be shown that this idea is
at least theoretically true--
it can be demonstrated
experimentally in small
populations--
and it is a serious,
long-term problem for anything
that's asexual.
Works like this.
In a small population,
the class of organisms that has
the fewest mutations is
eventually lost by drift.
Okay?
So you should think of this
starting off with a perfectly
clean population of let's say
bacteria.
It's a small one,
there are only ten or twenty of
them.
None of them have any mutations.
Then the first mutation arises,
and eventually it drifts
through the population and it is
fixed.
That will eventually happen.
At that point all the organisms
in the small population have one
mutation.
Because they all have one,
they can't get rid of it.
The process happens again.
Then they have two,
and so forth.
So that leads to an inexorable
increase in the number of
mutations in the class of
organisms that has the fewest.
It goes--the fewest goes from
zero to one to two to three,
and so forth.
And the kinds of organisms that
are afflicted by this would be
mitochondria and chloroplast in
the germ line,
and ancient asexuals like
bdelloid rotifers.
What's going on basically is
that this correlation between
reproductive success and trait
or genetic state gets wiped out
by the Law of Small Numbers.
As you decrease the size of the
population, it becomes less-
natural selection becomes less
and less powerful.
You just get more noise,
simply due to sampling issues;
you just have a smaller number
of organisms,
so the tightness of the
correlation goes away,
it gets noisy.
So the smaller the population,
the more important random
events are.
When it's very small,
natural selection has very
little opportunity to operate,
and the reason it loses its
force is that the correlation of
trait variation with
reproductive success is lost in
the noise of a small number of
arbitrary events.
So that's what's going to go on
when say you start off an oocyte
with two or three mitochondria;
that's a very small number of
mitochondria to go into an
oocyte,
and that's a genetic bottleneck
through which mitochondria will
go in every generation.
There might be 10,000 of them
in your liver cells,
but if they're a small number
in oocytes, then they are going
to experience drift.
So you can think of this as
stochasticity driving a wheel
around,
and there is a lever here that
allows it to go forward but
won't allow it to go back.
The capital letters are
beneficial genes,
and the small letters are
mutations,
and Muller's ratchet will take
this population and at first one
of these genes will get
replaced,
through drift,
by a deleterious mutation;
then two;
then three;
then four;
then five;
and so forth.
And if you plot here,
from few at the top to many on
the bottom,
the number of deleterious
mutations that are carried by
the least loaded genotype--
that is, the type in the
population that has the fewest
deleterious mutations--
it's increasing,
and fitness is going down.
This won't happen in a sexual
population, and it won't happen
in an infinite asexual
population.
The infinite asexual population
is big enough always to have
some individuals in it that
don't have any mutation,
and they will keep taking over.
But in a finite asexual
population, Muller's ratchet
operates.
So it's important in organelle
DNA, and this problem of
Muller's ratchet in organelle
DNA could be solved,
for example,
if mitochondria had sex.
There has been a controversy
over whether mitochondria have
sex,
and if you would like to read a
paper that was written for this
course on that issue,
it's up on the website--it's
called Example Paper--
and it reviews the status of
that issue about two years ago.
In mammals, mutations in
organelle DNA may be solved with
gamete selection through oocytic
atresia.
One of the reasons why female
mammals may make 7,000,000
oocytes,
when they're embryos,
and then kill most of them
before they start menstruating,
is that they are getting rid of
mutations that may have built up
in the mitochondria.
What about the ancient
asexuals, those bdelloid
rotifers?
Well they have really two
possibilities.
One is that they could try and
arrange their physiology so that
they could make the effects of
any mutation more serious.
And that has been suggested as
a hypothesis,
and I find it implausible;
but it's a hypothesis which is
out there.
If you can make any mutation
really serious,
so that it kills anything that
it occurs in,
it has no chance to accumulate.
It's only the deleterious but
not fatal mutations that can
accumulate.
So that's a logical
possibility, but biologically I
find it implausible.
Or they could always maintain a
very large population,
so that drift is not a problem.
And most of the things that are
ancient asexuals do have at
least large populations;
not infinite but certainly
large.
So here's a bdelloid rotifer,
and it's managed to escape
these problems.
Nobody has ever seen a male
bdelloid rotifer.
You could go outside OML and
take some moss off the side of
the building and put it into a
cover slip,
and some bdelloid rotifers
would swim out of it.
They're all over the planet.
Even though it's avoided the
problems with mutations,
we don't know how it's dealt
with pathogens and parasites.
Okay?
And that's this next issue.
Parasites are the principle way
that the idea of co-evolution is
realized in the context of the
evolution of sex.
What happened to the Red Queen,
or what happened to Alice when
she met the Red Queen in Lewis
Carroll's book Through the
Looking Glass?
Did any of you run into that?
Alice sits on a chess board and
she is--
this is kind of in a dream--and
she's trying to march down the
eight squares of the chess board
so that she can be promoted to a
queen.
She's a pawn in the chess game,
and she's trying and trying to
get there,
and the Red Queen comes up to
here and says,
"Alice,
in this game you have to run as
fast as you possibly can,
only to stay in place."
So it's called the Red Queen
Hypothesis,
and the idea is that in
evolution organisms are evolving
as fast as they can,
but they're in fact not
increasing their fitness,
and they are not decreasing
their long-term extinction
probability because the
parasites and pathogens in their
environment are coevolving with
them and keeping up with them.
So it's called the Red Queen,
basically to communicate the
idea that if you are in a
co-evolutionary arms race,
then you may have to run as
fast as you possibly can,
just to stay in the same place.
So what it requires is genetic
variation for resistance in the
host;
genetic variation for virulence
in the pathogen.
We can see that in Daphnia and
its parasites,
and in crop plants and their
pathogens.
So the assumptions appear to be
fulfilled in some well studied
systems, and you can see some of
the data here.
Okay?
So this is a case--this is a
complex table.
I'd like you to be able to
interpret things like this.
Basically what's gone on here
is that ten clones of Daphnia--
or is it nine?--nine clones of
Daphnia have been isolated from
a lake,
and out of each of those clones
a strain of a parasite has been
isolated.
This parasite is Pasteuria
ramosa, and it infects the body
cavity of Daphnia and castrates
it.
Okay?
Often parasites castrate their
hosts.
The numbers are the percentage
infected.
Okay?
If you look at that you can
see, for example,
that this strain of Pasteuria
is really good at infecting the
host that it came out of,
and really lousy at infecting
this other clone of Daphnia
here;
does pretty well in E and G;
and very, very poorly in B,
C, F and H.
So one way to look at it is to
ask, "Where do the
parasites do well?"
And the answer is,
only in some of the clones.
Now if you ask,
"How about the Daphnia,
how are they doing against the
parasites?"
Well you can just go down a
column and you can see that this
Type D here is actually pretty
resistant to almost everything
out there,
and at the worst it gets hit by
this parasite that came out of
clone G, over here.
So from these data you can
conclude that there is genetic
variation for resistance and
there is genetic variation for
virulence,
in a natural population.
The parasites are selecting for
host resistance.
The hosts are selecting for
parasite virulence,
but the parasites have to keep
hopping around,
onto different hosts.
The parasite selection is
happening on a time scale of
days,
and prevalence of a particular
parasite decreases as resistant
host types increase in
frequency.
So that's just what you need to
maintain sex.
Okay?
So that one looks pretty
plausible.
There's another example from
nature that's pretty well
studied,
and that's worms living in
snails and ducks in a beautiful
lake on the South Island of New
Zealand,
and the people who get to go
study this stuff go to one of
the most beautiful parts of the
world,
where they then put on wet
suits and dive into freezing
cold water.
> Okay?
The behavior of scientists is
difficult to explain.
So this is the lifecycle of the
worm.
The adult worms are in the duck.
They make eggs.
The snails pick up the eggs.
The worms reproduce in the
snail's body.
Then they are excreted as cysts.
The ducks eat the cysts,
and the life cycle goes around
like this.
Okay?
So anytime this loop can be
completed, the worms can stay
adapted to the snails and to the
ducks.
If this is broken at any point,
then the worms are no longer
adapted to the snails,
or to the ducks.
This is the kind of situation
in this lake in New Zealand.
The ducks are in shallow water,
and the worms come out of the
ducks and infect snails.
They only manage to close the
loop in shallow water,
because the ducks don't dive
very deep to eat the snails.
The worms that are coming out
of the snails and going into
deep water are from a source,
and they're going into a sink,
and they become maladapted to
the snails;
they can't keep up with the
evolution that's going on,
in the snails down here,
because just about everybody
that's getting into the snails
down here,
in fact, is adapted to the ones
in shallow water.
So up here there's more snail
sex, and down here there's less
snail sex.
And that's a very short
distance.
We're only talking about maybe
twenty or thirty meters apart,
for these populations.
The only difference is the
depth of the water,
and whether that loop is
connected or not.
And where the loop is broken,
where the parasite cannot
complete its sexual life cycle,
it loses the arms race with the
snails.
The snails don't need sex.
Asex takes over and spreads
through the population.
So asex hardly ever has an
exactly twofold advantage.
It's a bit more difficult
usually in animals,
and sometimes it's easier in
plants than 2:1.
There are cyclical
parthenogens--Daphnia,
some aphids,
some beetles,
have a series of asexual
generations,
followed by one sexual
generation, and the analysis of
these guys has led us to the
conclusion that you don't need
very much sex,
but you do need a little.
You can have sex about once
every ten to a hundred
generations, and it is almost as
effective as having it every
generation.
And in mammals and birds,
there are no costs of sex,
because the asexual alternative
is impossible,
and that is because early
development requires genes from
each parent to activate in
complementary fashion.
So when you were a very,
very small embryo,
consisting of a few cells,
you had to have some genes from
your father turn on,
and then some genes from your
mother,
and then some genes from your
father,
and then some genes from your
mother,
in sequential fashion,
or development would not occur.
That pretty much means that
asexuality becomes impossible.
Asexuality would only work if
that whole developmental
sequence could be carried
through only by genes from the
mother.
And apparently there has been a
process,
an evolutionary arms race,
probably involving conflict
resolution,
that has led to the kind of
development that birds and
mammals have.
There's an irony in this.
We now have so many advantages
of sex that we have a hard time
explaining asex.
How did those bdelloid rotifers
survive?
We can easily understand why
asexuality would repeatedly
originate and spread.
It can spread like gangbusters.
It has low cost short-term;
big cost long-term.
The long-term cost basically is
pathogens and parasites,
even if it can arrange a
solution to the mutations that
drive Muller's ratchet.
Okay?
So if you look at the Tree of
Life, what we see is that the
asexual types are up on the
twigs and they have sexual
ancestors.
And most of the asexual types
are not too old;
they're usually on the order of
somewhere between 50,000 years
and 10,000,000 years,
and there are very few of them
that are older than that.
It appears that these forces
catch up with them in the
long-term,
and drive them to extinction
more rapidly and more
pervasively than they can drive
sexual types to extinction.
So we have good individual
selection explanations for
recombination.
You don't have to invoke group
selection or species selection.
It has a lot of explanations.
The ones that seem to be pretty
general are repair -- mutations
- and parasites.
Those are certainly
experimentally substantiated.
We do not understand how
ancient asexuals have survived;
that's an open issue.
And sex has had some very
important macroevolutionary
consequences.
Probably the most striking is
the very existence of species.
We would not have things in
nature that we called species if
there were not sex.
Instead we would have clones
that just kept fragmenting and
kept filling in morphospace
fairly continuously.
What sex does is it integrates
populations and causes the
co-adaptation of their genomes,
so that we get breaks
separating the things that we
call species.
They are things that hang
together.
The other is this phylogenetic
distribution of asex.
It's up on the twigs,
it's not down on the main stems
of the Tree of Life.
Next time we're going to
discuss genetic conflict.
It's something that happens,
and it happens much more easily
in sexual than in asexual
species.
