The deer mouse is the Don Juan of rodents. Unlike its monogamous cousin, the oldfield mouse, it’s into orgies, and females often rear litters fathered by more than one partner. Now, a comparison of the sperm of these two closely related species has revealed another difference between them: a gene that makes the deer mouse sperm faster and more virile. The secret has to do with an expanded midsection in the sperm’s tail that propels the male mouse’s semen-laden package through the female reproductive tract.
“We are beginning to unravel the genetic architecture of sperm design and function,” says Tim Birkhead, a behavioral ecologist at the University of Sheffield in the United Kingdom who was not involved with the work. Researchers already know that sperm motility—or quality—is an important factor in human fertility, but what genes are involved and how has been a mystery. Thus, the mouse study may shed light even on the genetic basis to human fertility, Birkhead says.
To track the genetic basis of fertility, Harvard University evolutionary biologist Hopi Hoekstra and her colleagues turned to the deer mouse (Peromyscus maniculatus) and the oldfield mouse (P. polionotus). They are so closely related that they can interbreed, yet they have very different mating strategies. In deer mouse orgies, both sexes mate with different partners, sometimes switching to a new one every few minutes, whereas oldfield mice are faithful to their first loves. “To have two closely related species with such different mating systems is an evolutionary biologist’s dream,” Birkhead says.
Hoekstra and her team first examined the two species’ sperm under a microscope. The deer mouse sperm could swim much faster, thanks to tails with expanded midsections. These so-called midpieces are packed full of the mitochondria that fuel the sperm’s swim. To pin down the genetic basis of this difference, the researchers then mated the offspring of hybrid mice and measured the midpiece length of their descendants and the speediness of their sperm. Their studies led them to a gene called PrKar1a.
The protein coded for by PrKar1a is abundant in the tail’s midpiece, suggesting the protein plays an important role in midpiece function. And sure enough, there were differences in the amount of the protein in the oldfield and deer mouse midpieces, Hoekstra and her team reported late last month on the biology preprint server bioRxiv. When the team then bred lab mice with just one copy of PrKar1a, which has also been implicated in male fertility in humans, male mice had sperm with shorter midpieces, leading the researchers to conclude that competition among deer mice sperm has driven that species to have a different level of PrKar1a gene activity, and consequently faster, more competitive sperm.
These results speak to how behavior itself can drive evolution through different mating strategies. When competition is stiff, as is the case among deer mice, expanded midpieces provide an advantage. But, now that there is a specific gene tied to sperm speed, it also hints at a possible genetic influence on male fertility in humans.