A single phosphorylation site of SIK3 regulates daily sleep amounts and sleep need in mice.

Research Highlight

You are getting sleepy — specific mutation could explain why

© Clemens Peters/EyeEm/Getty

© Clemens Peters/EyeEm/Getty

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.

Supported content

  1. PNAS 115, 10458–10463 (2018). doi: 10.1073/pnas.1810823115
Institutions FC
International Institute for Integrative Sleep Medicine (WPI-IIIS), University of Tsukuba, Japan 0.61
Laboratory Animal Resource Center, University of Tsukuba, Japan 0.23
Faculty of Medicine, Toho University, Japan 0.05
Human Biology Program (HBP), University of Tsukuba, Japan 0.03
School of Integrative and Global Majors (SIGMA), University of Tsukuba, Japan 0.03
Department of Molecular Genetics, UT Southwestern Medical Center, United States of America (USA) 0.03
Life Science Center for Survival Dynamics, Tsukuba Advanced Research Alliance (LS-TARA Center), University of Tsukuba, Japan 0.03

Return