We spend nearly half of our lives asleep, but many of the physiological aspects involved with regulating shut eye are still a mystery to researchers. Of particular interest to sleep scientists are the molecular mechanisms behind Rapid Eye Movement (REM) sleep, which is characterized by heightened neural activity and the onset of dreams.

In research published today in Cell Reports, a team of Japanese scientists identified two key genes involved with the regulation of REM sleep. Moreover, when these researchers used the gene editing technology CRISPR to “knockout” the genes in mice, they found that they reduced REM sleep “to an almost undetectable level.”

It has been known for decades that a neurotransmitter—a chemical that sends information between brain cells—called acetylcholine was critical to regulating REM sleep. Due to the abundance of acetylcholine released during both wakefulness and sleep and the complexity of the neural networks regulating sleep, however, it was unclear just which acetylcholine receptors were involved in regulating REM sleep.

To tackle this issue, the researchers used the gene editing tool CRISPR, which uses an enzyme called Cas9 to excise small portions of DNA and introduce genetic changes at that location. In this case, the researchers used CRISPR to selectively turn off the genes that encoded acetylcholine receptors.

Want more sleep science? Check out Motherboard’s series “ You’ll Sleep When You’re Dead ,” a deep dive into the future of shuteye.

When the researchers knocked out the genes encoding two acetylcholine receptors called Chrm1 and Chrm3, they found that this induced a “short sleep profile.” In other words, the brain activity of the mice showed that they were cycling through the stages of non-REM sleep, but showed almost no signs of descending into REM sleep.