Here’s a fun biological fact: men pass on less DNA to their children than women do. The reason for this has been a long-standing mystery, though a study published today leads us closer to understanding.

When humans reproduce, women are the only ones who pass on a type of DNA called mitochondrial DNA. Unlike most of our genetic material, this kind of DNA comes from tiny cellular subunits, called mitochondria, located inside the cell's cytoplasm, but outside the nucleus. That DNA is crucial because mitochondria provide energy to the rest of the cell. Both men and women have this kind of DNA, but like I said — women are the ones who pass it on.

Men pass on less DNA to their children than women do

Now, a roundworm study published in Science reveals that sperm produce an enzyme that attacks the sperm’s mitochondrial DNA shortly after it merges with the female egg. And when the paternal mitochondria stick around for longer than they should during an embryo’s development, that embryo is a greater risk of dying. Because of this, the researchers speculate that it’s evolutionarily advantageous for roundworms — and other organisms like humans — to do away with that extra dad DNA.

Mitochondrial DNA is actually just a tiny part of what makes people who they are. In total, mitochondria contain 37 genes — which is a lot less than the 25,000 other genes that a mother contributes to her child. Still, mutations in mitochondrial DNA can lead to serious health conditions in humans, such as blindness, heart problems, and liver disease. That’s why researchers are so interested in it; despite its tiny contribution, the sum of its properties make it unique.

In the study, the researchers used electron microscopes to observe roundworm embryos as they developed. They found that when sperm merges with an egg to make an embryo, paternal mitochondria inside the sperm gets attacked by an enzyme called endonuclease G. The enzyme enters the mitochondria and starts cutting away at the paternal DNA. And that, in turn, makes it easier for mechanisms provided by the egg to finish off the sperm’s mitochondria — and all the paternal DNA it contains. "So there's a collaboration to coordinate the rapid removal of this paternal mitochondria," says study co-author Ding Xue, a molecular genetic at the University of Colorado Boulder.

So why do sperm spend so much energy sabotaging themselves? The answer to that probably has to do with the fact that paternal mitochondrial DNA is a lot more prone to mutations than its maternal counterpart, Xue says. "If mutated paternal mitochondrial DNA isn’t removed promptly, then mutations can accumulate through generations" — and that can cause problems for the species.

It's a coordinated attack

To prove their point, the researchers used sperm that contained mutated mitochondria. As expected, when these mitochondria hung around in the embryos, those embryos were more likely to die. And that, Xue says, might also be true for humans, because our species also produce this enzyme. "So, if this mechanism is not there, then you basically increase the chance that a human embryo potentially will have problems," he says. But that’s just speculation.

The finding is "of great importance," says Kateryna Makova, a geneticist at Penn State University who wasn’t involved in the study. Even though many animals — including humans — pass only their maternal mitochondria on to the next generation, researchers haven’t spent a lot of time studying how paternal mitochondria are destroyed, or what the evolutionary consequences might be, she says. So, gaining a better understanding of what’s going on is welcome — a sentiment echoed by Ken Sato, a molecular biologist at Gunma University in Japan. The questions surrounding why only the maternal version is inherited to offspring are "very mysterious and attractive," he says, and today’s paper provides some interesting answers.

There’s a lot more to figure out, still. For one thing, it’s not clear how endonuclease G manages to distinguish paternal mitochondria from maternal mitochondria, Makova says. The study also didn’t demonstrate that the same mechanism takes place in humans. But now that the role of endonuclease G has been discovered, researchers will probably start looking into its role in humans, too. And that could prove very interesting, she says.