In a real snoozer of a scientific discovery, researchers from the University of Tsukuba have zeroed in on the specific position within a protein called SIK3, which underpins excessive sleepiness in mice.

Building on their earlier discovery that mice with a mutant form of SIK3 require more sleep than usual, the researchers found that deleting or mutating just one particular amino acid in the protein impeded the attachment of phosphate tags, a process that normally keeps the activity of the SIK3 in check.

Without this regulatory control, the mice slept more because they had longer durations of non-dreaming sleep. However, rapid-eye-movement sleep — in which the brain is most active, allowing for intense dreams — was largely unaffected. This shows that SIK3 helps mediate the sleep cycle in a stage-specific manner.

The findings could lead to new treatments for people who experience excessive sleepiness and have trouble staying awake.