[ExI] 3 Stories of Sex and Death in Evolution

Dave Sill sparge at gmail.com
Thu Jun 7 20:51:29 UTC 2018

I've mentioned Josh Mitteldorf here before. Here's his latest blog posting:


*Time and again, evolution has learned (after repeated blind alleys) to do
what is best for the community in the long term and not always what is best
for the individuals in the short term.  But such gains are fragile, easily
lost if a cheater can gain a short-term advantage and its progeny take over
the community.*

*Human societies have rules that encourage cooperation, and enforcement
mechanisms for people who are reluctant to cooperate.  Cooperation in
biology is very old, and it turns out that evolution thought about
enforcement a billion years before Thomas Hobbes.  To see what this has to
do with theories of aging, you’ll have to be patient.*

Story #1: Conjugation and Cell Senescence
Story #2: Sex Required for Reproduction in Plants and Animals
Story #3: Antagonistic Pleiotropy — a Revisionist Theory

To begin, I’m going to ask you to think fresh thoughts about sex.  (Have I
lost you already?)

Sex and reproduction, reproduction and sex.  Go together like a horse and
carriage, right?  Well, how did it come to be that way? Sex is not a way to
reproduce.  Sex is a way to share genes. But sex has become so tightly
linked to reproduction that it requires mental gymnastics to imagine that
it might have been otherwise.

Reproduction without sex—that’s not too hard.  It’s cloning. Or it’s
mitosis, simple cell division which is how bacteria do it.

But sex without reproduction?  What’s that? Remember—sex is the mixing of
genomes between different individuals with different genomes.  Does anyone
do that except as a prelude to reproduction? What would it even look like?

Bacteria share genes willy-nilly.  They shed plasmids, which are little
loops of DNA, and they pick up plasmids from around them.  The plasmid may
be from the same kind of bacteria or another kind of bacteria entirely.
Sometimes the gene they pick up is useful; sometimes, not so much;
sometimes the imported gene kills them. Bacteria can afford this daredevil
lifestyle because there are a lot of them, and their credo is
experimentation. Change or die.  Bacteria are constantly changing, not only
because their generations are measured in hours instead of years, but the
change from generation to generation is also greater than large animals and
plants.  Under stress, they mutate and change even faster. Bacteria are
artists of change, and their genius is figuring out what it takes to
survive in the environment where they happen to be now. For bacteria, sex
is spitting out plasmids and picking them up.

Bacterial plasmid (electron micrograph)

Story #1: Conjugation and Cell Senescence

Protists, or protoctista, are single-cell eukaryotes—far more complex and
structured than bacteria, with a cell nucleus and many more organelles, a
million times bigger than bacteria but still a single cell.  Examples are
amoebas and paramecia. Protists share genes by a process called conjugation
that challenges our idea of the individual.  As promised, sex in protists
is not linked to reproduction…well, maybe indirectly linked, as we’ll see.

(This movie isn’t conjugation; it’s a hunting expedition.)

In conjugation, two paramecia (Dick and Jane) sidle up to each other and
their cell membranes coalesce, forming one big cell.  Then the cell nuclei,
where the chromosomes live, find each other and the two nuclear membranes
open up and merge, just as the cells did.  A double size cell with double
size nucleus, and two copies of each chromosome. Somehow the chromosomes
pair up with the appropriate partner.  Like blind people trying to navigate
a crowded room, how do the chromosomes arrange a meeting place with their
partners? (If chromosomes had telephones, I suppose they would be cell
phones.  OK, it isn’t funny.) Somehow, Dick’s chromosomes finds Jane’s
corresponding chromosome, nearly identical but for the crucial variations
that make them individuals. The chromosomes line up in pairs so they can
swap genes with one another.  Genes cross over until each chromosome
contains about half Dick’s genes and half Jane’s. Then—again using their
cell phones for coordination—the chromosomes segregate. One from each pair
goes north, the other goes south, so that when the nucleus splits in two
again, each half has a full complement.  Two cells go their separate ways,
but the cells that emerge from this process are no longer Dick and Jane.
Each one of them is half Dick and half Jane, in its genes, in its
cytoplasm, and in its mitochondria.

THIS is conjugation. It only takes place between protozoa of the same

Conjugation is sex without reproduction.  We started with two cells and
ended with two cells.  They pooled their genes, but didn’t produce
“offspring”.  Both Dick/Jane and Jane/Dick will someday undergo mitosis and
copy themselves, but Dick and Jane have ceased to be, merged instead into
an amalgam.

This has nothing
to do with

The species
is continued
as so many are
(among the smaller creatures)
by fission

(and this species
is very small
next in order to
the amoeba, the beginning one)

The paramecium
achieves, then,
by dividing

But when
the paramecium
desires renewal
strength another joy
this is what
the paramecium does:

The paramecium
lies down beside
another paramecium

Slowly inexplicably
the exchange
takes place
in which
some bits
of the nucleus of each
are exchanged

for some bits
of the nucleus
of the other

This is called
the conjugation of the paramecium.
poem by Muriel Rukeyser

Individual Selection and Group Selection,
Short-term Advantage and Long-term Welfare

Why do cells do this?  Let’s talk about fitness.  In the short term, the
race is to the swift.  Reproduction is everything, especially among
microbes which are always in a tight race with billions of others, and the
one that reproduces fastest is the victor in Darwin’s lottery.  So natural
selection at the individual level motivates Dick and Jane to get on with
the business of copying themselves as fast aspossible.

Why did they take time out to merge their genes?  Dick and Jane
individually must have thought they had a good thing going, each having
survived a long while, and beaten out the competition.  They each had a
combination of genes that work well together. Why would they take a flier
on the off-chance that their genes might do even better in some other
combination?  “Survival of the fittest” at its crudest level simply means
that those who reproduce fastest crowd out everyone else.  Sharing genes
takes time and energy. You can’t afford it.

To make this less abstract:  Imagine a puddle with cells swimming in it,
all the same species.  Suppose some of the cells—the Joneses—go straight to
work reproducing, doubling their numbers, while others—the Smiths—stop
along the way to have sex with other Smiths.  They’re all increasing
exponentially, but the Joneses grow at a faster rate. More doublings of the
Joneses leads to a powerful numerical advantage. Pretty soon, the Joneses
have overwhelmed the Smiths and crowded them out.  The Smiths are a thing
of the past, driven to extinction. We say, “the Joneses have evolved to

Short-term individual selection says “Don’t do it!  Don’t have sex!” But in
the long run, the communal legacy is more robust if they DO share genes.
Having many diverse combinations of genes is insurance against changes in
the environment, and a high-risk investment that just might yield big
dividends if the right opportunity opens up in the future.  But there’s a
danger that the Joneses will crowd out the Smiths in short order, and they
won’t live to see the day when their robust diversity shows to their

After many, many cycles of losing sex in the short term and missing
diversity in the long term, evolution stumbled on an expedient.  A counter
was built into the chromosomes, counting replications. Everyone is allowed
to clone about a hundred times, without sharing genes.  After that, without
conjugation, the cell slows down and dies, stopped dead in its tracks.
Every so often, every cell lineage must take time out for conjugation, or
the lineage dies.

The counter is the telomere.  To enforce conjugation, nature arranged for
telomerase to be locked away (in paramecia and other protists) during
mitosis.  Each act of reproduction makes the telomeres a little shorter.
Only during conjugation is telomerase unlocked, and the counter is reset,
so the lineage can continue to clone.

Twenty years ago, William Clark wrote two books on this subject at a level
accessible to readers of this column.  Sex and the Origins of Death,
followed by A Means to an End.  I read both as they came out, and they had
a profound effect on my thinking about evolution and aging.

Cell senescence is programmed death.  Can this be an evolutionary
advantage?  Can programmed death evolve to protect the community from the
fast crowd that doesn’t want to share their genes?  Sure, there is a
long-term advantage, but how was evolution so clever as to arrange this?
How did it happen that telomerase came to be sequestered, available only
during conjugation?  I’ve looked through the evolutionary literature, and
found no explanations, so I have asked this question myself, modeling with
a computer simulation. The model works surprisingly well.  One important
feature of the model is that there is a limited reservoir of the food that
cells need in order to grow. This means that the “cheaters” who avoid
conjugation and reproduce faster don’t have an advantage for long, because
they use up the available food store faster.  Another crucial feature is
that conjugation sometimes leads to combinations of genes that are more
efficient at using food resources.

Here is a preliminary write-up — I plan to finish and publish this work in
the near future.

Story #2: Sex and Reproduction in Plants and Animals

Half a billion years ago, there was an explosion of multicelled life.  Gene
sharing is not so easily arranged when there are billions or trillions of
cells in each fully-grown organism.  Sure, all life passes through an
embryo stage, starting with a single cell. But embryos are hardly in a
position to seek out a partner and share genes.  So evolution needed to
invent anew both the mechanics of gene sharing and a means to enforce it on
individuals whose primary Darwinian motivation was to reproduce as fast as

So nature took the bull by the horns (or perhaps another part of his
anatomy).  She laid down the law: “From now on, it takes two to tango.
Anyone who wants to reproduce is going to have to share genes.”

Sex and reproduction were tied together anatomically, and the connection
was so tight that no would-be cheater could get around the barriers.  For
some (dioecious) species, there were two separate sexes so that no single
individual had the tools to reproduce by itself.  In other (hermaphroditic)
species, each individual could make both eggs and sperm, and there had to
be barriers to self-fertilization, custom-designed for each anatomy.

Exactly how this came about is unknown.  Meiosis is an operation of baroque
complexity, though clearly an outgrowth of both protist conjugation and
mitosis.  Graham Bell (quoting Emerson) called it the Masterpiece of
Nature, but neither he nor anyone proposed an evolutionary pathway that
might have created it.

We know that this whole business of separate sexes and all the cellular and
metabolic complexity that it entails managed to evolve, and we know that it
offers no conventional advantage in terms that neo-Darwinist theory can
understand.  No one doubts that the link between sex and reproduction
femerged from a process of evolution, but the standard mechanisms
recognized by conservative evolutionary theory are at a loss to explain it.

How do we understand evolution of sex?  What is the accepted explanation?

Classical evolutionary theory (neo-Darwinism) is in a bind.  The theory
inherited from R. A. Fisher in the early part of the 20th Century insists
that there is only one mechanism of evolution, and that is
one-mutation-at-a-time.  Each incremental change has to provide a benefit
that is capable of gradually spreading through the gene pool. In other
words, all by itself and immediately it has to offer the bearers (on
average) a faster rate of reproduction.   On the other hand, there are
numerous examples of complex adaptations (like sexual reproduction) that
provide no immediate benefit for reproduction, and that require many
changes to many genes in order to be functional at all.  Classical
evolutionary theory just says, “that’s a tough problem that we haven’t
solved yet.”

But it’s more than that.  The very limited repertoire of mechanisms
recognized by classical evolutionary theory quite obviously can never
explain the provenance of sex, or of aging, or of countless other common
traits.  Classical evolutionary theory is going to have to adapt or die.

I haven’t tried to model the evolution of sex because I can’t think how to
do it.  The problem is just too hard—all the advantage is with the
cheaters, who can reproduce twice as fast because they don’t have two
different sexes to support.  Nevertheless, look around you—somehow nature
managed to arrange most plants and animals in two sexes.

Story #3: Antagonistic Pleiotropy — a Revisionist Theory

Like sex, aging is a trait that benefits the community in the long run, but
is costly to the individual in the short run.  It’s not as extreme as
sex—the benefit is not so essential, and the cost is much less than the
cost of sex. (Two sexes cuts fitness by half, by the classical definition
of “fitness”.  Time and energy required for the mechanics of sex only add
to the cost.)  So the problem is not as severe as Story #2, but once again,
nature has a problem:  How to make death obligatory, so that there is
population turnover and population diversity and (more important) so the
population doesn’t explode past sustainable levels, leading to population
crashes and extinction.

Nature’s solution was once again to tie together aging with reproduction,
but the link isn’t nearly so tight and consistent as in the case of sex.
In fact, population can be kept within sustainable limits either by
controlling fertility or limiting lifespan, or any combination of the two,
so tying longer lifespan to lower fertility (and vice versa) helps to allow
for diversity and flexible strategies, while guarding against those deadly
population blooms.

The name for nature’s solution is Antagonistic Pleiotropy.  Fertility and
longevity are coded in the genome in such a way that inheritance of
lifespan and fertility are inversely linked.  Higher fertility goes with
shorter lifespan. Lower fertility goes with longer lifespan. As long as the
two vary together in this way, the threat of population explosion can be
kept at bay.

You might be thinking: pleiotropy is everywhere.  We don’t need an
explanation for pleiotropy, because it’s built into the way genomes are
organized.  Very few genes have just one mission. A web of regulation
affects everything at once, so that distinct traits emerges from many
genes, and every gene contributes to many traits.  This is true of the way
that adaptive traits are realized in nature. To think this way, you have to
think of aging as an adaptive trait that nature actively wants to protect.

The Classical view of Antagonistic Pleiotropy

Contrast this with the orthodox theory of Antagonistic Pleiotropy, which
has become the best-accepted theory for the evolution of aging.  In the
orthodox theory, genes for fertility and other traits that are highly
beneficial to the individual are tightly linked to deterioration that we
call “aging”.  Out of the box, the genes work this way, and the forces of
evolution have been unable, over half a billion years, to tease the two
apart. There is a mighty motivation (says classical theory) to separate
aging from fertility so that the individual can have the best of both
worlds, but there are physical limitations or logical connections that make
this impossible.  Hence, natural selection has had to swallow the bitter
pill of aging in order to get the sweet nectar of faster reproduction.

In my version, antagonistic pleiotropy is an evolved linkage, after the
fact.  In the standard version, antagonistic pleiotropy is an inescapable
precondition, a given fact about the way genes work that evolution, with
all her wiles, has been unable to evade.

How do we know that my interpretation of AP is the right one and all the
theorists have it wrong?

Because the classic theory requires that every “aging gene” must have a
benefit that more than compensates, and after 30 years of genetic
experiments, pleiotropic costs.have been identified for only about half of
the known aging genes.
We’ve seen that evolution is capable of some amazing feats.  It just
doesn’t pass muster that evolution has been trying to find a pleiotropy
bypass for half a billion years but doesn’t seem to be able to find one.
Because some of the best-known cases involve quasi-pleiotropic linkages
that can be broken in the lab.  It’s just not that hard to have your cake
and eat it, too. The first example was AGE-1, the first bona fide aging
gene to be discovered (in lab worms, 1989).
When you look at the actual mechanisms of pleiotropy, many of them don’t
seem to be functionally essential, but involve unexpected connections
between unrelated functions.  The most recent example is that methylation
aging seems to be inversely related to telomerase expression.
Of these 3 stories, the story of evolved Antagonistic Pleiotropy (#3) is
the easiest to model and simulate, which is to say that the model requires
few assumptions and works to evolve pleiotropy without a lot of adjustment
or tinkering.  This alone gives me confidence that AP is evolved, and that
the usual interpretation for the meaning of AP is upside down.

I have been working to turn my computer model into an academic article, and
a draft of the paper, not yet submitted, is posted here.
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