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Phosphorylation Hypothesis of Sleep.

Koji L Ode1, Hiroki R Ueda1,2

  • 1Department of Systems Pharmacology, Graduate School of Medicine, The University of Tokyo, Tokyo, Japan.

Frontiers in Psychology
|October 30, 2020
PubMed
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Sleep need, crucial for mammals, is regulated by protein phosphorylation at synapses. Kinase activity increases during wakefulness and sleep deprivation, modifying synaptic proteins to promote sleep.

Keywords:
CaMKIINREM sleepkinasephosphorylationproteomics

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Area of Science:

  • Neuroscience
  • Molecular Biology
  • Sleep Science

Background:

  • Sleep is a fundamental biological process conserved across species.
  • Sleep need, the drive to sleep, is thought to reside in neuronal assemblies, not specific brain regions.
  • The precise molecular mechanisms governing sleep need dynamics remain largely unknown.

Purpose of the Study:

  • To review recent rodent studies on the molecular underpinnings of sleep need.
  • To explore the role of protein phosphorylation, particularly at synapses, in regulating sleep need.
  • To summarize evidence linking kinases and synaptic protein phosphorylation to the sleep-wake cycle.

Main Methods:

  • Review of genetic studies in rodents identifying sleep-promoting kinases.
  • Analysis of proteomic data on synaptic protein phosphorylation.
  • Discussion of kinase activity during wakefulness and sleep deprivation.

Main Results:

  • Genetic studies identified specific kinases that promote sleep.
  • Kinase activity is elevated during the awake state and following sleep deprivation.
  • Proteomic analyses confirm that the sleep-wake cycle influences synaptic protein phosphorylation status.

Conclusions:

  • Protein phosphorylation, especially at synapses, is a key molecular mechanism associated with sleep need.
  • Awake-dependent kinase activation modifies synaptic proteins, contributing to sleep induction.
  • Multisite phosphorylation on protein complexes may explain the slow dynamics and physiological functions of sleep.