Science knows a few things about the function of sleep: It makes you feel better, regenerates your cells, consolidates aspects of memory, and may flush waste from the brain. However, sleep researchers have remained largely in the dark about the genetic underpinnings of this most basic behavior. New research on mice published today in Nature, however, indicates that your insomnia, need for extra-long slumber, and the number of dreams you have might be written into your genetic code.

Sleep scientists have previously determined the brain regions responsible for switching between non-dreaming sleep—NREMS (non rapid eye movement sleep)—and dreaming sleep—REMS—but they did not yet understand the molecular and cellular mechanisms that determine a mammal’s likely switch between the two types of sleep.

To determine this, neuroscientists Hiromasa Funato (University of Tsukuba), Masashi Yanagisawa (University of Texas Southwestern Medical Center), and their colleagues looked at the sleep patterns of more than 8000 mice, using a technique known as forward genetic screening. Their method involved first identifying a mouse family that showed a particular heritable sleep abnormality, such as extreme wakefulness, non-REM sleep, or excessive muscle activity during sleep. Next, they identified the gene mutation that caused the sleep abnormality, and induced these mutations by breeding the mice that showed the irregular genes. This created “a mutant pedigree,” as the authors state in the Nature paper.

In order to study sleep and wakefulness time, the mutant mice were attached to electrodes to record electroencephalogram (EEG) and electromyogram (EMG) data 24 hours a day for two consecutive days. The researchers narrowed down their findings into two types of mice: “Sleepy” mice were those that slept more than 3.5 hours longer than the average of all mice, while “Dreamless” mice experienced 44 percent less REM sleep than normal. (They're not entirely "dreamless.")

The "Sleepy" mice all had a mutation in a gene known as Sik3, a kinase that transfers a phosphate group to another protein called a substrate. The Sik3 gene, Funato told mental_floss, “is the first intracellular protein that regulates time spent in sleep.” The researchers believe that the Sleepy mutation in Sik3 increases the animal’s intrinsic sleep need, because, as they write in their paper, “Sleepy mutant mice exhibit (1) a higher density of slow-wave activity, a reliable index of homeostatic sleep need; (2) a larger increase in NREMS delta power after sleep deprivation; and (3) a normal waking response to behavioural or pharmacological arousal stimuli.”

Nalcn, the second gene mutation, showed up in the “Dreamless” mice. The paper's authors write, “Nalcn works in the neuronal groups regulating REMS for the maintenance and termination of REMS episodes.” Nalcn “encodes an ion channel,” says Funato. “When the channel opens, ions can move through the channel between extracellular space and intracellular area.” This gene, he says, “is the first protein that is involved in the termination of an REM sleep episode.” An episode is one “sleep sequence,” of which the average mouse and human has approximately four to six per night.

“The current results suggest there is some genetic factors that determines how long we need to sleep,” Funato says. Of course, what is good for the mouse is not necessarily good for the human. “The genes we found in mice have not been reported in humans,” he notes.

Now, however, scientists have a window into understanding how genetics contributes to sleep—a window that can eventually be used to screen and identify human sleep genes, particularly in order to better understand and treat sleep disorders. Insomnia, for example, is closely associated with mood disorders, as well as one of many risk factors for obesity, diabetes, and dementia.

“This finding is just the first step of the thousand miles’ journey to crack open the mystery of sleep,” Funato concludes.