Taste Receptors Found in Mouse Testicles Linked to Fertility Mice that lacked the key proteins for taste reception could not reproduce.

July 3, 2013 -- While our tongues respond strongly to the sweetness of vanilla ice cream on a hot summer day or the savory umami flavor of a perfectly grilled steak, it turns out those taste receptors do more than simply signal deliciousness -- or awfulness -- in our mouths.

They're also involved in sperm development in the testicles, according to a new study. Bedrich Mosinger, the author of the study that appears in the journal Proceedings of the National Academy of Sciences, noticed that male mice that had malfunctioning taste receptors were effectively sterile.

The origin of the sterility can be traced to two proteins involved in taste reception: TAS1R3 and GNAT3. Both work like puzzle pieces that snap together with other proteins to form either a sweet or umami taste receptor (in the case of TAS1R3) or the protein gustducin (in the case of GNAT3).

If a sugar molecule or a stray amino acid latches onto the taste receptor embedded on a cell's membrane, it relays the signal by producing gustducin.

"You can think of the taste receptor like a microphone and gustducin like its cord," Mosinger told ABC News.

Nipura Chaudhari, a professor of biophysics and physiology at the Miller School of Medicine at the University of Miami in Florida who was not involved in the study, said that taste receptors can express themselves in many parts of the body other than the tongue.

"There are cells in the gut and neurons in the brain that can also detect taste," she told ABC News. Instead of sending a taste sensation to the brain, they might instead send signals to the gut to start the metabolic pathways involved in digesting and absorbing sugars and other nutrients. She said there were other taste receptors whose purpose is less easily explained, such as those in the testes.

Originally, Mosinger wasn't planning on using male mouse fertility as a way to gauge whether the proteins were working properly. He ran into problems, however, when he tried to make a new genetically altered mouse. Although he had one set of mice that lacked the genes to make TAS1R3 and another set that lacked the genes to make GNAT3, he couldn't reliably find one male mouse that lacked both.

"This was unexpected," he said. "There is no reason why we couldn't produce these animals."

That stumbling block led to the surprising discovery. He used a third set of mice that had the human version of TAS1R3 (as opposed to the mouse version), and he added the drug clofibrate to their diet. The clofibrate selectively attaches to the human version of TAS1R3, rendering it useless. Male mice that bred fine before the diet change became sterile once they started eating clofibrate.

Mosinger looked at the testicles underneath the microscope and saw several signs of cellular degeneration. In addition, about 20 percent of their sperm that he could find were abnormal, having either misshapen heads or a tail with tight loops. "These were not normally produced sperm," he said.

It's a bit of a leap to extend these observations beyond mice, but Mosinger said it's not impossible. Genetic surveys conducted in humans reveal that both TAS1R3 and gustducin are also seen in human testicular tissue. Although it's too early to say for sure, Mosinger is willing to entertain the possibility.

"The pathway that we discovered could be part of fertility problems that are described as having an unknown cause," he said.

Chaudhari said she wasn't 100 percent sure either. "We did see at the Chemical Senses Conference that sperm were responding to certain taste compounds," she said. But seeing the proteins implicated in sterility is a first for her.

"This is very cool," she said.