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Battle of the Sexes: Why Mammals Won’t Lose the Y.

An Op-Ed by Maureen Dowd trying to explain conflicting predictions about the fate of the Y chromosome sent me on an eye-rolling spree. It fits the cultural zeitgeist, I suppose; the image of a war between the genders. Something about women coldly calculating that men are an evolutionary waste of space (due to their inability to bear children) and doing away with the gender. This fact, coupled with the gene-poor nature of the Y chromosome itself, is a reasonably compelling story for science fiction narratives, provided you don’t think about the biology too much.

But really, that’s what I’m here for, right? To think about the biology too much?

Come on, now: they used the word "voluptuous" to describe the X chromosome. Things I never thought I would draw: a voluptuous X chromosome (with mostly accurate banding pattern demarcating mostly-accurate genomic regions...)
Come on, now: they used the word “voluptuous” to describe the X chromosome. Things I never thought I would draw: a voluptuous X chromosome (with mostly accurate banding pattern demarcating mostly-accurate genomic regions…)

So, below, is a bit about the biology of the Y chromosome, a bit about why plants and animals reproduce sexually, and a bit about why mammals in particular aren’t going to do away with males any time soon.

Is Bigger Necessarily Better?

The essential argument that I see parroted around about why men are biologically “disappearing” — at least in the popular press — is because the Y chromosome is so small and gene poor. The X chromosome has hundreds of genes, versus a mere 30-or-so on the Y. Physically, the X chromosome is several times larger than the Y chromosome. This is because the Y chromosome lost genes relatively rapidly, shrinking down to contain only genes that are particularly useful to males.

There are two reasons for this: since roughly half the population lacks a Y chromosome, it can’t have any essential genes. If a gene on the Y significantly increased fitness for both males and females, there would be a large selective pressure for it to migrate to any other chromosome — somewhere that would be present in all individuals. But once a copy of the gene exists outside of the Y, the Y-chromosome copy becomes a backup copy, present in only half of individuals, and thereby loses its utility. Since that particular copy is now redundant, mutations in it will not be as strongly selected against — meaning it may rapidly degrade. And since there’s an energetic cost to replicating long pieces of DNA, (each base added to a DNA strand could be used to provide energy elsewhere in the cell) there is a certain selective advantage towards excising those regions of the Y. So the Y chromosome gets smaller.

And so, the argument goes, what if it shrinks into nonexistence? No more males!

Sociological issues of equating the Y chromosome with the entire male gender aside (and there are many), how does this work biologically? What does the Y chromosome do to “determine gender”? There is one gene on the Y chromosome that becomes active about halfway through mammalian development. It is called SRY (for Sex-determining Region on the Y), and it is a transcription factor: it binds to a bunch of other gene sequences in a bunch of other places in the genome and controls their activity, either turning them on or off. This is a cue for a surge in testosterone production, which in turn signals the developing fetus to alter gonad development.

To be clear: most of the genes that SRY modulates aren’t on the Y chromosome. Many are on the X chromosome. Many have other roles elsewhere. But their concerted effect, in gonadal development, causes the development of testes, instead of ovaries. That’s about it.

And in terms of function, a cassette with a couple of genes on it — SRY included — can function almost as well as a full-length Y chromosome in mice. Which is actually pretty cool when you think about it. Is it plausible that over several hundred thousand years the human Y chromosome could be pared down to something the same size as that cassette? Perhaps.

But the Y chromosome already only has a handful of genes, and there’s a big difference between “an even tinier Y chromosome” and “OMG NO MEN EVER.” That difference has everything to do with how mammals reproduce. If two genders are essential, then the Y chromosome isn’t really going anywhere — it might get smaller, but it won’t disappear. If two genders aren’t essential, then there’s a better evolutionary argument for why males might die out.

Gender Wars

Evolutionarily, what would push males to extinction? And what is stopping that from happening?

To understand what’s going on here, and why it is almost always the male that gets pushed to extinction in this analogy, you first need to understand how biologists classify genders in multicellular organisms. It’s all about the size of the gamete. The individual with larger gametes (see: eggs) is female, the individual with smaller gametes is male (see: sperm). That’s really the only classification that’s used, which is why almost any other trait is malleable, from behavior to physical size to child-bearing and brood behavior. Larger gametes generally contain cellular components that a developing embryo needs to start out: not just nutrients but also the machinery with which to build a new organism. Smaller gametes tend to be almost entirely genetic cargo.

Which reframes the question, a bit: what evolutionary force would work against an individual who only donated genetic cargo, rather than other cellular components?

And it also makes the answer more obvious — if that individual can’t find a mate, it cannot have offspring. But theoretically, at least, the vast majority of the required bits to make an organism already exist in the larger gamete. It’s missing a bit more genetic material, which can be found in another large gamete or perhaps done without entirely. Which is to say: it is always females that can reproduce without males, and not the other way around (sorry, dudes).

Why would this be advantageous? To a population, it comes down to rapid growth: requiring two parents essentially halves the maximum population growth rate. So a population of all females, reproducing via parthenogenesis, can multiply twice as quickly as a population of 50% males and 50% females, reproducing sexually. In fact, insects are more likely to reproduce via parthenogenesis when conditions are ideal — when it’s warm and food is plentiful — because without another external limiting factor on population growth, this intrinsic property becomes more significant.

Parthenogenesis is also advantageous to the mother, from an evolutionary standpoint. That’s because her offspring produced by parthenogenesis will be more genetically related to her (100%) than offspring produced sexually (50%). With one parthenogenetic offspring, she’s probably passed on all of her genes — it would take two offspring via sexual reproduction to do so. So any individual mother reproducing via parthenogenesis is more likely to pass on more of her genetic material to future generations than a mother reproducing via sexual reproduction.

Some species of whiptail lizards, such as this desert grassland whiptail lizard, reproduce exclusively via parthenogenesis. Image By Ltshears (Own work) [CC-BY-SA-3.0 (], via Wikimedia Commons
Some species of whiptail lizards, such as this desert grassland whiptail lizard, reproduce exclusively via parthenogenesis. Image By Ltshears (Own work) [CC-BY-SA-3.0 (], via Wikimedia Commons

All of which makes it seem a bit like the males of the species are a bit of an awkward afterthought, likely to be discarded in the dust bin of evolution before too long. And it might be true, almost, if most organisms developed and lived in a perfectly uniform environment without external pressures.

Unfortunately, that environment doesn’t exist. And in a rapidly fluctuating environment with myriad external pressures, it becomes advantageous to sacrifice rapid growth and genetic identity in order to be more variable and flexible yourself. Sexual reproduction, then, acts as a melting pot into which the genes of a species are thrown.

First, a bit of a reminder: genes don’t really exist in isolation. They exist in organisms. And even an incredibly advantageous trait, something that in isolation would be highly selected for, can occur in an otherwise bad genetic milieu, where it is counterbalanced, negated, or doesn’t even come to light. A bacterium reproducing asexually, with a mutation to double its production of glucose transporters (which would make it grab more food more easily), and another mutation to slow its metabolism (so it needs more food to get the same amount of energy), isn’t going to take over a population.

But with sexual reproduction, those two traits could separate. And then the gets-more-food trait, alone, would be selected for and would help the population as a whole.

Every other kind of combination analogy works as well. Sexual reproduction is valuable because it can reveal and weed out unproductive combinations of genes. It can bring two novel variants together which have a synergistic effect.

Now, bacteria get around some of this with a process called “horizontal gene transfer”, in which they directly share genetic information. Which works pretty well if you have a small genome and only one cell. But for a multicellular organism, especially a large multicellular organism, sexual reproduction is faster and more effective. Which means that sexual reproduction is here to stay — as long as the animal and plant kingdoms, at least.

Every (Mammalian) Child Needs a Mother and a Father

If parthenogenesis is an advantage because it allows the mother to maximize the evolutionary return (in genes passed on) for her nutritional contribution (in gamete size), then it would seem to make sense that the species with the greatest maternal contribution also would be the most likely to reproduce via parthenogenesis. Right? Like, if something is seriously life-threatening for an organism, it had better have a really big evolutionary bang-for-the-buck.

Can you see where I’m going with this line of reasoning? It suggests that mammals, (where maternal contribution is very high) and in particular humans (where childbirth for a long time was incredibly dangerous and retains its danger today even with modern medicine) should really look into parthenogenesis. (Since evolution totally works like a lending library: check out this new behavior/trait/novel!)

In reality, the opposite is true.

Why could that be?

This is about to get incredibly hypothetical, so bear with me for a second. In my opinion, the most likely reason for this is that live birth, and big babies, and all the things that create the increased maternal contribution that defines the mammalian lineage, wasn’t driven by selection on females. It was driven by selection on males.

And to understand how male DNA could alter female reproductive patterns, let me introduce you to a little bit of background on placental development.

The placenta sits between a mammalian mother and fetus. It pulls nutrients away from the mother and diverts them to the fetus. It is made up of both maternal and fetal cells. And it starts forming when fetal cells invade the uterine wall and start proliferating in maternal tissue. Those cells remodel the maternal tissue, guide blood supply to the embryo, and send signals to the mother’s body to facilitate pregnancy and birth.

Really, they do a lot of the same things that pathogens do: they invade into the mother’s body (in humans, they get as far as the brain, which is really disturbing when you stop to think about it and possibly explains why everyone’s mother is a little bit weird); they suppress the mother’s immune system (often by co-opting the remnants of viruses that infected humans millenia ago); they pull blood supply just like a tumor. In reality, they don’t do much good for the maternal body, and there’s correlative evidence to suggest that some of the painful realities of being a female human (like menstruation) happen because our placental cells are just so invasive and aggressive.

So, what does dad have to do with this? Well, a more invasive placenta means a bigger baby, which would be more likely to survive after birth. So far, both mom and dad are fans: increased survival of offspring is a winner, evolutionarily. There’s a caveat when it gets to the point of mammalian birth, though: it’s also more likely to kill the mother, or to render her sterile for future births. Which dad might not care about, because he’s more genetically similar to the offspring than the mother, but mom definitely cares about.

Which means that live birth, and placentation, and many of the hallmarks of mammals, are things that are much more advantageous to males than they are to females. We see that in the very nature of the placenta, and we see it molecularly as well, at individual genes — many genes that drive early placental development and proliferation are expressed only from the copy inherited from the father.

And those genes aren’t just on the Y chromosome; they’re scattered throughout the autosomes.

Igf2 is a gene in mice and humans which is expressed only from the paternal allele. It is a potent growth factor, and when disrupted in mice leads to tiny pups. Image courtesy of the NIH.
Igf2 is a gene in mice and humans which is expressed only from the paternal allele. It is a potent growth factor, and when disrupted in mice leads to tiny pups. Image courtesy of the NIH.

So the Y chromosome might get even smaller, but it’s not going anywhere — as mammals, we’re probably stuck with it for the long haul, just like we’re stuck with men.

Elizabeth Finn

Elizabeth is a geneticist working for a shady government agency and therefore obliged to inform you that all of the views presented in her posts are her own, and not official statements in any capacity. In her free time, she is an aerialist, a dancer, a clothing designer, and an author. You can find her on tumblr at, on twitter at @lysine_rich, and also on facebook or google+.

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