0028 SIK-HDAC4 Signaling Is Required For The Metabolic Regulation Of Sleep

  • Grubbs J
  • Lopes L
  • van der Linden A
  • et al.
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Abstract

Highlights  Sleep is associated with fat mobilization and low ATP levels  Metabolic regulation of sleep requires the SIK homolog KIN-29  KIN-29 acts in sensory neurons upstream of sleep-promoting neurons  KIN-29 acts via the histone deacetylase HDA-4 in the metabolic regulation of sleep  Liberation of energy from fat-storage cells promotes sleep. Combined Manuscript File 2 SUMMARY (146 words) Mechanisms underlying integration of sleep and energy homeostasis are largely unknown. We find that during Caenorhabditis elegans sleep, which is associated with energetically-expensive tasks, fat stores are depleted. Mutants lacking KIN-29, the C. elegans homolog of a mammalian Salt-Inducible Kinase (SIK) that signals sleep pressure, have defective sleep. They also have low cellular ATP levels despite high fat stores, indicating a defect in responding to cellular energy deficits. Liberating energy stores by overexpressing a lipase gene corrects adiposity and behavioral defects of kin-29 mutants. kin-29 acts in sensory neurons upstream of central sleep-controlling neurons. Removing the histone deacetylase hda-4 corrects the kin-29 mutant's sleep defects, suggesting that KIN-29 acts via HDA-4 to regulate sleep. We propose that KIN-29/SIK transduces low cellular energy charge into the mobilization of energy stores from adipocytes, which in turn promotes sleep. SIKs are therefore key nodes integrating sleep and energy homeostasis.

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Grubbs, J. J., Lopes, L. L., van der Linden, A. M., & Raizen, D. M. (2019). 0028 SIK-HDAC4 Signaling Is Required For The Metabolic Regulation Of Sleep. Sleep, 42(Supplement_1), A11–A11. https://doi.org/10.1093/sleep/zsz067.027

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